Problems with your eyes, sign of gut inflammation?

[Chu]

Given that Laura and others have been talking about probiotic enemas recently (start reading here), the following articles might be helpful in connection to that, IF you have eye problems. They suggest that one should not only look for causes related to the common ocular diseases. The root cause might be, as often happens, in your gut!

Ocular manifestations of inflammatory bowel disease.

Abstract

The association between inflammation of the eyes and the intestine is not often recognized by ophthalmologists. We report two patients who developed peripheral corneal ulcers, episcleritis, and scleritis just prior to the onset of Crohn's disease. The severity of the eye disease paralleled that of the intestinal symptoms, and both conditions subsided after treatment with topical steroids, oral prednisone, oral sulfasalazine, and hydrocortisone retention enemas. Inflammatory bowel disease should always be included in the differential diagnosis of scleritis and uveitis, as the patient may be benefited greatly by appropriate, early therapy of this gastrointestinal disorder.

(The whole text is not available for free).

Ocular complications of inflammatory bowel disease.

Abstract

Though inflammatory bowel disease (IBD) has a specific predilection for the intestinal tract, it is a systemic inflammatory disorder affecting multiple organs, including the eye. Ocular complications directly related to IBD are categorized as primary and secondary. Primary complications are usually temporally associated with IBD exacerbations and tend to resolve with systemic treatment of the intestinal inflammation. These include keratopathy, episcleritis, and scleritis. Secondary complications arise from primary complications. Examples include cataract formation due to treatment with corticosteroids, scleromalacia due to scleritis, and dry eye due to hypovitaminosis A following gut resection. Some ocular manifestations of IBD can lead to significant visual morbidity and temporally associated complications can also be a herald of disease control. Furthermore, ocular manifestations of IBD can occasionally manifest before the usual intestinal manifestations, leading to an earlier diagnosis. Thus, it is important to understand the clinical presentation of possible ocular manifestations in order to initiate appropriate treatment and to help prevent significant visual morbidity.

Full text here.

Managing IBD outside the gut: ocular manifestations.

Abstract

Extraintestinal manifestations are common in inflammatory bowel disease (IBD), being reported in over 25% of patients. Ocular complications of IBD occur in around 10% of cases, but may precede systemic symptoms and are usually nonspecific. Complications of therapy, such as cataracts or glaucoma from steroid use or keratoconjunctivitis sicca related to 5-aminosalicylic acid medications, may also involve the eyes. The pathogenesis remains unclear, but factors such as the extent of intestinal disease, disease activity, and the presence of associated arthritis have been associated with ocular involvement. Conjunctivitis, episcleritis, scleritis and uveitis are by far the most common ophthalmic complications of IBD. However, posterior uveitis, intraretinal hemorrhages, vasculitis, choroiditis, optic neuropathy, and vaso-occlusive phenomena may also occur. The most frequent severe ocular manifestation is anterior uveitis (more common in women). It usually presents as a mild anterior nongranulomatous uveitis (60% of the cases). The inflammation in the eye and the inflammation in the gut are rarely correlated. Patients with uveitis, scleritis, and other anterior segment inflammation usually respond to steroids (topical, periocular or systemic). If the inflammation is resistant to steroids, or if appreciable steroid adverse effects are encountered, systemic immunosuppressive treatment should be considered; this is more likely in HLA-B27-positive patients with uveitis. Evaluation of the eye should be a routine component in the care of patients with IBD.

(The whole text is not available for free).

The prevalence of ocular involvement in patients with inflammatory bowel disease.

Abstract
PURPOSE:
The aim of this prospective randomized clinical study was to evaluate the prevalence of ocular involvement in patients with inflammatory bowel disease (IBD).

MATERIALS AND METHODS:
We prospectively evaluated 116 patients who went to the gastroenterology clinic with endoscopically proven IBD between December 2001 and February 2005. All patients were examined for evidence of ocular manifestations of IBD. Twenty patients had Crohn's disease and 96 had ulcerative colitis. The examination consisted of slit-lamp examinations, tonometry, visual acuity, and indirect ophthalmoscopy.

RESULTS:
The mean age of the 116 patients with IBD who were enrolled was 40.6 +/- 14.4 years (range 16 to 75). Twelve of 20 patients (60%) with Crohn's disease and 22 of 96 patients (22.92%) with ulcerative colitis had ocular involvement. The most common ocular findings were conjunctivitis (8.62%) and blepharitis (6.9%) followed by uveitis (5.17%), cataract (5.17%), and episcleritis (3.45%). Extraintestinal complications were seen in 12 (35.3%) of 34 patients with ocular involvement and in 16 (19.5%) of 82 patients without ocular involvement.

CONCLUSION:
Because the ocular complaints of IBD patients are often nonspecific, it may be helpful to performed eye examinations as a routine component in the follow-up of these patients. It is well-known that early diagnosis and treatment of ocular involvement may prevent serious ocular complications that could be associated with significant visual morbidity. In addition, clinicians should be aware that some ocular diseases, such as uveitis and scleritis, might precede a diagnosis of ulcerative colitis or Crohn's disease.

In uveitis, bacteria in gut may instruct immune cells to attack the eye

The inflammatory eye disorder autoimmune uveitis occurs when a person’s immune system goes awry, attacking proteins in the eye. What spurs this response is a mystery, but now a study on mice suggests that bacteria in the gut may provide a kind of training ground for immune cells to attack the eye. The study was conducted by researchers at the National Eye Institute (NEI), part of the National Institutes of Health.

Evidence increasingly suggests that there is an association between the microbiota in the gut – bacteria, fungi and viruses – and the development of autoimmune disorders. Findings from this study suggest how that association may be made and therefore have implications about the origins of autoimmune diseases not only in the eye, but also elsewhere in the body, said Rachel R. Caspi, Ph.D., a senior investigator at NEI whose lab led the study.

Autoimmune uveitis accounts for more than 10 percent of severe visual disability in the United States. Corticosteroids provide a blanket approach to the disorder by quelling inflammation, but their long-term use can lead to adverse side effects.

Understanding what spurs autoimmune uveitis is fundamental to the development of safer long-term therapies and possibly even strategies for preventing it, said Reiko Horai, Ph.D., a staff scientist at NEI and a lead author of the study, published in the journal Immunity. Carlos R. Zarate-Blades, Ph.D., a postdoctoral fellow at NEI, is the other lead author.

The eye is one of the places in the body that has immune privilege meaning it is protected by a blood-tissue barrier that physically separates it from the rest of the body and minimizes the exchange of substances and blood-borne cells going in and out of the eye.

In the case of autoimmune uveitis, immune cells (T cells) are thought to penetrate through this blood-ocular barrier. But first, they must become activated, which occurs when they come in contact with the protein that they are pre-programmed to recognize. This is how T cells fight an infection and some types of cancer – by targeting proteins on bacteria, viruses and cells. And herein lies a paradox that’s been puzzling uveitis researchers. The proteins believed to be targeted in autoimmune uveitis are sequestered in the eye; they don’t exist elsewhere in the body. So what activates the T cells and allows them to cross the blood-ocular barrier?

The researchers asked this question by studying mice genetically engineered to develop autoimmune uveitis, due to a high level of retina-reactive T cells in their bodies. Before the mice had developed signs of the disease, the team searched their bodies for activated T cells and made an interesting discovery. Levels of activated T cells were not elevated in the lymph nodes (the glands that tend to swell during infections), but they were abundant in the intestines. What’s more, the T cells in the gut produced a protein shown in previous studies by Dr. Caspi’s team to augment the damage in autoimmune uveitis.

“These discoveries support the idea that activation of T cells in the gut may actually precede the first signs of the disease,” she said. To test that idea, the researchers gave the mice an antibiotic cocktail designed to wipe out a broad spectrum of bacteria in the gut and by rearing them in a germ-free environment. They found that mice without gut bacteria developed autoimmune uveitis much later, and with less severity, compared to control mice with normal gut flora.

There was a similar delay in uveitis and decline in its severity when the uveitis-prone mice were raised in an environment free of bacteria and other germs. But when the same mice were later moved into normal housing, where they acquired normal gut bacteria, the uveitis roared in at full strength.

So how do bacteria in the gut activate T cells against cells in the eye? The researchers theorize that bacteria in the gut produce a molecule that, to T cells, looks similar to a protein in the retina. This gives the T cells marching orders to look for that retinal protein and attack it. Consistent with this idea, the researchers found that they could activate retina-specific T cells by exposing them to a soup of bacterial proteins extracted from mouse intestines. When those activated T cells were injected into normal mice (not prone to uveitis), the mice developed uveitis.

“Given the huge variety of bacteria in our intestines, if they can mimic a retinal protein, it is conceivable that they could also mimic other self-proteins in the body. So we believe that normally harmless bacteria in the gut could be involved in promoting other autoimmune diseases as well,” Dr. Caspi said.

The results don’t have immediate implications for patients, but will help inform further research to understand the disease and help to develop new therapies, Dr. Caspi said. Eliminating bacteria from our bodies isn’t a treatment option, and a bacteria-free state would not be feasible. However, if scientists could one day identify the bacteria specifically involved in promoting autoimmune uveitis, it might be possible to target only those of interest.

About the National Institutes of Health (NIH): NIH, the nation's medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit www.nih.gov.

From the gut to the eye: commensal microbes as potential triggers of autoimmune uveitis

Autoimmune uveitis is a group of inflammatory diseases that affect the retina of the eye and related tissues and constitute a major cause of human blindness. It is believed that the disease is triggered by the activation of circulating lymphocytes capable of recognizing the proteins (antigens) that are unique to the eye, whereupon they gain the ability to invade the healthy eye and induce uveitis. How and where these lymphocytes become activated has been a long-standing mystery, because the proteins that they are programmed to recognize which would activate them are inside the eye and are not accessible. Questions such as these cannot be studied in humans for reasons that are both ethical and practical (the patient comes to the clinic after disease has already developed). Therefore, researchers rely on animal models to study disease related processes in a setting that can be controlled and manipulated experimentally.
lymphocyte activation

Fig. 1. Schematic representation of lymphocyte activation in the intestine on commensal microbiota, which endows them with the ability to induce uveitis. (Adapted from press release by the National Eye Institute).

In traditional animal models of uveitis, experimental mice or rats are immunized with proteins from the eye (incorporated into an emulsion of oil containing heat-killed tuberculosis bacteria, known as complete Freund’s adjuvant, which amplifies immune responses). Their lymphocytes then become activated and the animals develop uveitis. However, these models are not appropriate to study natural causes of disease, as the trigger is provided by the researcher in the form of immunization. We, therefore, developed a new model of autoimmune uveitis in genetically engineered mice that develop the disease spontaneously as a consequence of having an increased number of circulating retina-specific lymphocytes.

By studying these mice, which additionally contained a fluorescent reporter molecule to show lymphocyte activation, we observed that the retina-specific lymphocytes became activated in the intestine. This occurred even before the animals developed clinically apparent uveitis, and was still present in mice that had the retinal antigen genetically deleted. Treatment of the mice with antibiotics, or rearing them in germ-free conditions, resulted in strongly delayed and attenuated development of disease, pointing to bacteria in the intestine as a potential trigger. Indeed, further experiments demonstrated that circulating retina-specific lymphocytes isolated from the genetically engineered mice could be activated by culture with extracts of bacteria-rich intestinal contents. Moreover, these lymphocytes induced uveitis when subsequently injected into genetically normal recipients, whereas lymphocytes that were cultured by themselves, did not. Extracts from germ free animals did not have an activating effect. In the aggregate, these findings indicated that bacteria in the intestine make something (which we identified as a protein) that to the retina-specific lymphocytes “looks” similar to the retinal antigen that they are programmed to recognize. These lymphocytes then enter the circulation and make their way to the eye, which they are able to infilatrate due to their ativated state, and cause uveitis (Figure 1).

Due to the complexity of the intestinal microbiome, it has not yet been possible to identify the responsible organism(s) and to characterize their product. Bioinformatic and biological methods may help us achieve this, but there is still much work to be done. Irrespective of that, however, our findings have clear implications for the etiology of human uveitis. Furthermore, in view of the almost infinite variety of microbes living in and on our bodies, if they can mimic a retinal antigen, it is possible that they may produce substances that mimic tissue antigens involved in other autoimmune diseases. If that is true, commensal microbes might be a more common trigger of autoimmune diseases than is currently appreciated.

While the knowledge gleaned from these studies can help us understand the biology of the disease, the conclusions cannot yet be applied clinically. In view of what we know about the importance of microbiota for proper development and functioning of immunity, host defense and metabolism, prophylactic treatment with broad spectrum antibiotics is not feasible. Furthermore, we are not yet able to identify the individuals at risk for uveitis with sufficient certainty. However, as our knowledge advances and as our ability to control undesirable immunological responses in an increasingly selective fashion develops, specific immunological interventions or introduction of appropriate probiotics and prebiotics might become possible.

 

[MusicMan]

Thank you Chu for this valuable information. I currently am under treatment with antibiotics (for a lung condition) however I believe I also have incipient auto-immune problems (dry eyes, dry mouth) and have had for some time, not being able to figure out the problem. I thought it may be old age creeping up, but perhaps you have thrown new light upon the subject. Perhaps a holistic approach may provide a solution. I'm getting the probiotics in as much as I can.

 

[Eboard10]

Thanks for sharing Chu, that was a very interesting read. The links between the gut microbiome and the body keep on being discovered, stressing the importance of following an optimal diet and keeping a healthy gut flora.

The last two papers reveal something very telling, that certain bacteria found in the gut produce a protein that the lymphocites of the retina (T-cells) recognise as being similar to a protein in the retina. These T-cells will then activate and mobilise themselves by moving through the blood-tissue barrier that protects the eye and attack the real retina protein, causing autoimmune uvetitis.

As to what actually informs these bacteria in the gut to produce these lymphocites, it looks like more studies need to be done, but I wonder if it might be caused by specific foreign invaders that infect certain bacteria in the gut informing them to produce said proteins as a way of attacking and weakening one of the body's most important sensory functions, i.e. sight...?

Furthermore, as the studies point out, what's even more concerning is that bacteria in the microbiota could potentially mimic antigens of other tissues and organs in the body.


In uveitis, bacteria in gut may instruct immune cells to attack the eye

The eye is one of the places in the body that has immune privilege meaning it is protected by a blood-tissue barrier that physically separates it from the rest of the body and minimizes the exchange of substances and blood-borne cells going in and out of the eye.

In the case of autoimmune uveitis, immune cells (T cells) are thought to penetrate through this blood-ocular barrier. But first, they must become activated, which occurs when they come in contact with the protein that they are pre-programmed to recognize. This is how T cells fight an infection and some types of cancer – by targeting proteins on bacteria, viruses and cells. And herein lies a paradox that’s been puzzling uveitis researchers. The proteins believed to be targeted in autoimmune uveitis are sequestered in the eye; they don’t exist elsewhere in the body. So what activates the T cells and allows them to cross the blood-ocular barrier?

The researchers asked this question by studying mice genetically engineered to develop autoimmune uveitis, due to a high level of retina-reactive T cells in their bodies. Before the mice had developed signs of the disease, the team searched their bodies for activated T cells and made an interesting discovery. Levels of activated T cells were not elevated in the lymph nodes (the glands that tend to swell during infections), but they were abundant in the intestines. What’s more, the T cells in the gut produced a protein shown in previous studies by Dr. Caspi’s team to augment the damage in autoimmune uveitis.

“These discoveries support the idea that activation of T cells in the gut may actually precede the first signs of the disease,” she said. To test that idea, the researchers gave the mice an antibiotic cocktail designed to wipe out a broad spectrum of bacteria in the gut and by rearing them in a germ-free environment. They found that mice without gut bacteria developed autoimmune uveitis much later, and with less severity, compared to control mice with normal gut flora.

There was a similar delay in uveitis and decline in its severity when the uveitis-prone mice were raised in an environment free of bacteria and other germs. But when the same mice were later moved into normal housing, where they acquired normal gut bacteria, the uveitis roared in at full strength.

So how do bacteria in the gut activate T cells against cells in the eye? The researchers theorize that bacteria in the gut produce a molecule that, to T cells, looks similar to a protein in the retina. This gives the T cells marching orders to look for that retinal protein and attack it. Consistent with this idea, the researchers found that they could activate retina-specific T cells by exposing them to a soup of bacterial proteins extracted from mouse intestines. When those activated T cells were injected into normal mice (not prone to uveitis), the mice developed uveitis.

“Given the huge variety of bacteria in our intestines, if they can mimic a retinal protein, it is conceivable that they could also mimic other self-proteins in the body. So we believe that normally harmless bacteria in the gut could be involved in promoting other autoimmune diseases as well,” Dr. Caspi said.

From the gut to the eye: commensal microbes as potential triggers of autoimmune uveitis

By studying these mice, which additionally contained a fluorescent reporter molecule to show lymphocyte activation, we observed that the retina-specific lymphocytes became activated in the intestine. This occurred even before the animals developed clinically apparent uveitis, and was still present in mice that had the retinal antigen genetically deleted. Treatment of the mice with antibiotics, or rearing them in germ-free conditions, resulted in strongly delayed and attenuated development of disease, pointing to bacteria in the intestine as a potential trigger. Indeed, further experiments demonstrated that circulating retina-specific lymphocytes isolated from the genetically engineered mice could be activated by culture with extracts of bacteria-rich intestinal contents. Moreover, these lymphocytes induced uveitis when subsequently injected into genetically normal recipients, whereas lymphocytes that were cultured by themselves, did not. Extracts from germ free animals did not have an activating effect. In the aggregate, these findings indicated that bacteria in the intestine make something (which we identified as a protein) that to the retina-specific lymphocytes “looks” similar to the retinal antigen that they are programmed to recognize. These lymphocytes then enter the circulation and make their way to the eye, which they are able to infilatrate due to their ativated state, and cause uveitis (Figure 1).

Due to the complexity of the intestinal microbiome, it has not yet been possible to identify the responsible organism(s) and to characterize their product. Bioinformatic and biological methods may help us achieve this, but there is still much work to be done. Irrespective of that, however, our findings have clear implications for the etiology of human uveitis. Furthermore, in view of the almost infinite variety of microbes living in and on our bodies, if they can mimic a retinal antigen, it is possible that they may produce substances that mimic tissue antigens involved in other autoimmune diseases. If that is true, commensal microbes might be a more common trigger of autoimmune diseases than is currently appreciated.

 

[Gaby]

That is very interesting research.

Here is a summary of the autoimmune diseases which have an eye manifestation. I think all of them might fit the infection profile of autoimmune reactions manifesting in the eyes, although there might be a few exceptions and/or a different mechanism.

Missing in the summary are the ones already mentioned above: Inflammatory bowel diseases.

Ocular Manifestations of Autoimmune Disease

_http://www.aafp.org/afp/2002/0915/p991.html

Rheumatoid arthritis, juvenile rheumatoid arthritis, Sjögren's syndrome, the seronegative spondyloarthropathies, systemic lupus erythematosus, multiple sclerosis, giant cell arteritis, and Graves' disease are autoimmune disorders commonly encountered by family physicians. These autoimmune disorders can have devastating systemic and ocular effects. Ocular symptoms may include dry or red eyes, foreign-body sensation, pruritus, photophobia, pain, visual changes, and even complete loss of vision. Because a number of these diseases may initially present with ocular symptoms, physicians should maintain a high index of suspicion to make a timely diagnosis. [...]

Patients with autoimmune diseases are frequently encountered by family physicians. It is important to understand not only the systemic effects of these diseases but also their ocular manifestations (Table 1). Most ocular complications involve the cornea but may also include the conjunctiva, uvea, sclera, retina, and surrounding structures (Figure 1). The majority of these diseases will ultimately need to be referred to an ophthalmologist.

Disease Ocular manifestations

Rheumatoid arthritis

Keratoconjunctivitis sicca, scleritis, episcleritis, keratitis, ulcerative keratitis, choroiditis, retinal vasculitis, episcleral nodules, retinal detachments, macular edema

Juvenile rheumatoid arthritis

Uveitis

Sjögren's syndrome

Keratoconjunctivitis sicca

Ankylosing spondylitis

Uveitis

Reiter's syndrome

Conjunctivitis, uveitis, keratitis

Enteropathic arthritis

Uveitis, episcleritis, peripheral ulcerative keratitis

Psoriatic arthritis

Uveitis, conjunctivitis, keratitis

Systemic lupus erythematosus

Keratoconjunctivitis sicca, conjunctivitis, uveitis, episcleritis, scleritis, keratitis, retinal hemorrhages, retinal vasculitis, proliferative retinopathy, optic neuritis, ischemic optic neuropathy, hemianopia, amaurosis, internuclear ophthalmoplegia, pupillary abnormalities, oculomotor abnormalities, visual hallucinations

Multiple sclerosis

Afferent: optic neuritis, retrobulbar neuritis, visual field defects

Efferent: internuclear ophthalmoplegia, dysmetria, nystagmus, cranial nerve palsies

Giant cell arteritis

Amaurosis fugax, diplopia, vision loss

Graves' disease

Proptosis/exophthalmos, lid lag and retraction, keratitis, decreased visual acuity, reduced visual fields, relative afferent pupillary defect, loss of color vision

Myasthenia gravis

Diplopia, eyelid ptosis

Sarcoidosis

Uveitis, conjunctival nodules, cranial nerve palsies, enlarged lacrimal glands, optic neuropathy

Wegener's granulomatosis

Proptosis/exophthalmos, orbital cellulitis, uveitis, corneal ulcers, optic neuropathy

Behçet's syndrome

Uveitis, hypopyon

Antiphospholipid syndrome

Vaso-occlusive retinopathy, ischemic optic neuropathy

Polyarteritis nodosa

Episcleritis, scleritis, optic neuropathy

Takayasu's arteritis

Vaso-occlusive retinopathy, ischemic optic neuropathy, cataracts

Dermatomyositis

Eyelid/conjunctival edema, retinopathy, uveitis

[...]

The link has a review of each disease and its eye condition.

There might be episcleritis and/or other inflammatory diseases of the eyes when everything else is seemingly okay too.

 

[Gaby]

Here is another possible mechanism involving fungi (i.e. candida), traditionally linked with leaky gut and autoimmune diseases.

IL-17–Mediated Immunity to the Opportunistic Fungal Pathogen Candida albicans

_http://www.jimmunol.org/content/195/3/780.full

IL-17 (IL-17A) has emerged as a key mediator of protection against extracellular microbes, but this cytokine also drives pathology in various autoimmune diseases. Overwhelming data in both humans and mice reveal a clear and surprisingly specific role for IL-17 in protection against the fungus Candida albicans, a commensal microbe of the human oral cavity, gastrointestinal tract, and reproductive mucosa. The IL-17 pathway regulates antifungal immunity through upregulation of proinflammatory cytokines, including IL-6, neutrophil-recruiting chemokines (e.g., CXCL1 and CXCL5), and antimicrobial peptides (e.g., defensins), which act in concert to limit fungal overgrowth. This review focuses on diseases caused by C. albicans, the role of IL-17–mediated immunity in candidiasis, and the implications for clinical therapies for both autoimmune conditions and fungal infections.

Full article in the link above.

Dry eye disease: an immune-mediated ocular surface disorder

_http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3677724/

Dry eye disease is a multifactorial disorder of the tears and ocular surface characterized by symptoms of dryness and irritation. Although the pathogenesis of dry eye disease is not fully understood, it is recognized that inflammation has a prominent role in the development and propagation of this debilitating condition. Factors that adversely affect tear film stability and osmolarity can induce ocular surface damage and initiate an inflammatory cascade that generates innate and adaptive immune responses. These immunoinflammatory responses lead to further ocular surface damage and the development of a self-perpetuating inflammatory cycle. Herein, we review the fundamental links between inflammation and dry eye disease and discuss the clinical implications of inflammation in disease management.

IL-17 and other inflammatory pathways are related to dry eyes.

A role for IL-17 in age-related macular degeneration

_http://www.nature.com/nri/journal/v13/n9/full/nri3459-c1.html

It seems that stealth infections can literally cause a lot of chaos and regulating gut health is really the key to regain health.

 

[Chu]

The last two papers reveal something very telling, that certain bacteria found in the gut produce a protein that the lymphocites of the retina (T-cells) recognise as being similar to a protein in the retina. These T-cells will then activate and mobilise themselves by moving through the blood-tissue barrier that protects the eye and attack the real retina protein, causing autoimmune uvetitis.

It's always amazing to me how some of these processes are similar to what is described in Ponerology and in other studies on psychopathology. It's like ponerology at a microbiological level. Cells with a "mask of sanity", "ponerization" of previously healthy process, etc.

 

[Lilou]

This is quite interesting and it's the first time I hear of it! Researchers are using Probiotic Eye Drops to treat allergic and inflammatory eye conditions. Continued research is trying to identify which strain is best for which condition. The following study was for allergic vernal conjunctivitis using L. Acidophilus. {Current standard treatment for this is a steroid drop.}

http://www.eyeworld.org/article.php?sid=4964

Probiotics also may have an intriguing place in ophthalmology, particularly to help treat allergic conjunctivitis and inflammation from ocular rosacea or inflammatory dry eye......

The most important safety and efficacy issue right now is discovering which strain of probiotic is best to treat specific conditions.....

A study led by Dr. Iovieno and published last year in Graefes Archives of Clinical and Experimental Ophthalmology tested the use of a probiotic eye drop with Lactobacillus acidophilus for a month to treat seven patients with signs and symptoms of vernal keratoconjunctivitis. Investigators measured conjunctival hyperemia, chemosis, secretion, Trantas dots, and superficial punctuate keratitis, and their symptoms. They also performed impression cytology to evaluate the expression of ICAM-1 and TLR-4.

Investigators diluted Lactobacillus acidophilus into a saline solution to create the eye-drop solution.

Symptoms in all six patients who completed the study (one patient dropped out) were significantly improved at two weeks and four weeks. Clinical signs were also significantly better after four weeks (although not at the two-week mark). The impression cytology, which was performed in three patients, showed a down regulation of ICAM-1 and TLR-4 in two patients. “We were fairly surprised by the fact that every patient, regardless of statistically significant clinical improvement, described a positive effect of Lactobacilli eye drops on their symptoms, and none of them reported discomfort or the occurrence of side effects,” Dr. Iovieno said. He and fellow investigators are now analyzing the effects of prolonged oral consumption of Lactobacilli for more mild forms of eye allergies.

 

[sebbe]

It's always amazing to me how some of these processes are similar to what is described in Ponerology and in other studies on psychopathology. It's like ponerology at a microbiological level. Cells with a "mask of sanity", "ponerization" of previously healthy process, etc.

It is very true. It is like the "That which is below is like that which is above & that which is above is like that which is below" thing, very helpful.

Thank you for this thread.

 

[Eboard10]

The last two papers reveal something very telling, that certain bacteria found in the gut produce a protein that the lymphocites of the retina (T-cells) recognise as being similar to a protein in the retina. These T-cells will then activate and mobilise themselves by moving through the blood-tissue barrier that protects the eye and attack the real retina protein, causing autoimmune uvetitis.

It's always amazing to me how some of these processes are similar to what is described in Ponerology and in other studies on psychopathology. It's like ponerology at a microbiological level. Cells with a "mask of sanity", "ponerization" of previously healthy process, etc.

Yeah, it really looks like these ponerological processes that happen at the human level are also reflected at the microbiological level. When we allow psychopathological life forms to influence us both in terms of interaction with psychopaths and information we absorb through the food we ingest and process, it messes up the proper functioning of our system at the energetic and physical levels. Hence why knowledge of these topics and objectivity are such important tools to counter these processes.

 

[Oxajil]

Very interesting information, thank you for starting this thread Chu!

 

[loreta]

Very interesting information, thank you for starting this thread Chu!

Yes! Thank you Chu! I have eyes problems, always little "flies" in my eye but the oculists are so insipide: they always say it is normal. Thank you for the information.

 

[dantem]

Many thanks Chu! Got really tired eyes from last winter and on, and some days it's like I never wake up entirely. Even while my body is up and not sleepy at all, my eyes feel like it's early morning or late at night for the whole day. 50% of the day are always itchy, sometimes it's even more...

This stated in tandem with symptoms of high salivation, to the point that all that is going to get quite annoying to put it mildly!

I've skipped a lot of Forum's healthy threads from some time, having been busy with a job change and a lifestyle a bit tumultuous here. Time to get back to probiotics it seems.

 

[Chu]

Many thanks Chu! Got really tired eyes from last winter and on, and some days it's like I never wake up entirely. Even while my body is up and not sleepy at all, my eyes feel like it's early morning or late at night for the whole day. 50% of the day are always itchy, sometimes it's even more...

This stated in tandem with symptoms of high salivation, to the point that all that is going to get quite annoying to put it mildly!

I've skipped a lot of Forum's healthy threads from some time, having been busy with a job change and a lifestyle a bit tumultuous here. Time to get back to probiotics it seems.

Well, when you have a bit of time to catch up, do read up on probiotic enemas (links provided above), not just oral intake. It makes a big difference, I think! Usually when you take probiotics by mouth, by the time they reach your gut they're probably very weak after all the stomach juices.

I've done it once so far, and it feels very different. It might be a bit early to tell, but I already feel more clearer headed, with a happier tummy, my eyes aren't dry, my mood is better. It's hard to describe with words, actually. Worth a try, IMO!

Here's a simple step-by step guide posted on the iodine thread:

http://pronutrics.net/probiotic-enema-benefits/

Here’s a step by step guide on how you can self-administer a probiotic enema, ensuring that there are no lumps in your enema mixture:

Step 1. Fill a glass or bowl with 1-2 tablespoons of water

Step 2. Depending on your need, pop open two or three probiotic capsules. Add them to the water and mix with a spoon. Crush and squash lumps against the side of the bowl or glass to form a smooth paste.

Step 3. Add two more tablespoons water, stir again until the capsules dissolves. Set aside for at least eight hours. [One or two hours seem to work just fine for some!]

Step 4. Get a clean enema bag, pour in the probiotic mixture and clamp the enema firmly into place. Shake the enema bag from time to time to keep lumps from sinking on the bottom.

It’s advisable to perform a probiotic enema in the morning.

[As you see, it's a very small amount of water, a cup at the most. So Ideally, you would retain it and not flush it. If you can't, you may need previous flush with a coffee enema.]

Some people recommend different positions for better absorption:

http://thepowerofpoop.com/epatients/fecal-transplant-instructions/

Refresh your memory by looking at the diagram of the colon.
Lie on your left side for 10 minutes. Massage the FMT gently up your colon.
Lie on your stomach for 10 minutes.
Lie on your back for 10 minutes. Massage the FMT gently across your colon.
Lie on your right side for 10 minutes. Massage the FMT gently down your colon.
If you are having trouble holding it in, don’t panic. It doesn’t matter if you lose a little. That’s what the big brown towel and paper towels are for. Try doing a little at a time, massaging, and then doing some more.
Try and hold it in for at least 6 hours.

You can use something like this: _https://www.amazon.com/Premium-Silicone-Comfortable-Medical-Douche/dp/B01HIQ0CLU/ref=sr_1_1_s_it?s=hpc&ie=UTF8&qid=1473019531&sr=1-1&keywords=enema

instead of a whole big bag and all that. There's no need, for such a small amount of liquid.

As for the type of probiotics to use, as far as I understand, the best thing is to get as high a strength as possible. For example:

_https://www.amazon.fr/Bio-Kult-F7056-B-Protexin-120-Capsules/dp/B004SGO4DG/ref=sr_1_1?ie=UTF8&qid=1473076907&sr=8-1&keywords=biokult

(I used 2 capsules of that one, and one of the ones we got at the local pharmacy, containing "l-rhamnosus" which is supposed to be super good. But others may have better "recipes").

 

[Persej]

I've done it once so far, and it feels very different. It might be a bit early to tell, but I already feel more clearer headed, with a happier tummy, my eyes aren't dry, my mood is better. It's hard to describe with words, actually. Worth a try, IMO!

So far I did 4 coffee enemas and 3 probiotic. For first probiotic I used too much water so I had to flush it, but the two after I was able to hold it.

But I can't say that I feel any different. In the third one I combined two different local types so I had 8 strains of bacteria and one yeast, for a total of 58 billion microorganisms. And so far nothing, except that I feel unusual movements in my bowels.

But I don't feel bad also, so I will continue with the experiment. I want to try some different probiotic from the iherb, but I don't want to order it during the summer because they are sensitive to heat.

As for the type of probiotics to use, as far as I understand, the best thing is to get as high a strength as possible. For example:

_https://www.amazon.fr/Bio-Kult-F7056-B-Protexin-120-Capsules/dp/B004SGO4DG/ref=sr_1_1?ie=UTF8&qid=1473076907&sr=8-1&keywords=biokult

(I used 2 capsules of that one, and one of the ones we got at the local pharmacy, containing "l-rhamnosus" which is supposed to be super good. But others may have better "recipes").

That one is actually very low in strength. Just 2 billions? But the number of strains is good, 14.

 

[Gaby]

I did my second probiotic enema last Saturday with L.rhamnosus, 4 sachets, after finishing a specific cycle with antibiotics. I used 400cc of distilled water and read a book for like 30 minutes while holding the enema. The next day I lost like a kilo in fluid retention. I was also able to concentrate better on my tasks.

I've been doing saunas, 15 minutes per day for the last 3-4 days. So that may have contributed as well.

After finishing a specific protocol for heavy metal detox/stealth infection, I'll give the mini-probiotic enema a try. It might work better when it is concentrated.