Today, during pharmacology lecture I heard that interferon, beside being an anti-viral agent, is being used as an anti-toxoplasmosis treatment for dogs (which is curious, since it is a protozoan parasite). Now, I don't know how it is in other countries, but here, indeed, dried and pulverized interferon is being used as an immunostimulant and prophylactic of influenza and other viral infections. For best effect it should be taken about 10 days before the potential exposure to the virus.
Last year someone recommended it to me, so before trying it out I searched the net for more info, and found out that in human medicine interferon primarily is being given intravenously to people on hepatitis C therapy, and apparently there are some serious side effects to be considered, including depression, bad sleep, hair loss, thyroid problems, ect. Well, I didn't know in what quantities it is usually being given to the people on this therapy, and obviously the effects would be stronger when given intravenously than intranasally, and considering the fact that I was constantly getting sick and searched for possible ways to boost my immune system, I decided to try it out.
There were no pronounced side effects, and nothing really serious beside slight irritation and dryness of the nasal mucous membrane. But then, maybe there were and I didn't notice, because was already pretty much restless and stressed!
In any case, it seems to work, but only if it is combined with other common sense solutions as good sleep and not getting upset or taking things too seriously. ;)
But back to the toxoplasmosis. I searched the web, and found couple of papers on the topic:
Interferon y blocks the growth of Toxoplasma gondii in human fibroblasts by inducing the host cells to degrade tryptophan
_http://www.pnas.org/content/81/3/908.full.pdf
The mechanism of interferon-gamma induced anti Toxoplasma gondii by indoleamine 2,3-dioxygenase and/or inducible nitric oxide synthase vary among tissues.
_http://www.ncbi.nlm.nih.gov/pubmed/15206721
The research is too complex for my current level of understanding, so I am not sure if interferon could or would have any effect on toxoplasma antibodies, but it seems that it does. There is the following, very detailed article, that talks among other things about interferon-y being the essential mediator of the immune response to control Toxoplasma in the brain and how it is
able to maintain the latency of chronic infection.
_http://schizophreniabulletin.oxfordjournals.org/content/33/3/745.full
It also mentions the following regarding the onset of schizophrenia:
Elevated anti-T. gondii IgG antibody levels have been reported in patients with first-onset schizophrenia,29,30 suggesting an involvement of this parasite in the etiology of schizophrenia. Elevated serum levels of IL-1β have also been detected in individuals with acute schizophrenia, but not chronic schizophrenia,31 and there were no differences in IL-1β or IL-6 serum or cerebro-spinal fluid levels in medicated patients compared with a control group.32 Because tachyzoites induce more pronounced inflammatory cytokine responses in host cells than do bradyzoites, as described above, proliferation of tachyzoites in the brain may be related to the onset of schizophrenia.
The lack of elevated IL-1β or IL-6 in medicated patients could be due to the antitoxoplasmic activity of some antipsychotic drugs.33,34 Interestingly, anti-T. gondii IgM antibody, a key indicator of acute acquired infection, is not elevated in the sera of patients with first-onset schizophrenia,29,30 implying that the patients are not in the acute stage of a newly acquired infection.
Therefore, a reactivation of chronic infection with the parasite (proliferation of tachyzoites caused by cyst rupture) in the brain might be involved in the onset of the disease. In support of this possibility, expression levels of proinflammatory cytokines, including IL-1β and IL-6, are higher in the brains of a mouse strain in which tachyzoite proliferation occurs in this organ during the later stage of infection compared with the brains of another mouse strain that prevents tachyzoite proliferation during chronic infection.35
It is noteworthy that individuals with congenital T. gondii infection often develop ocular toxoplasmosis later in life,36 and the disease is considered to be due to reactivation of infection. The onset of toxoplasmic chorioretinitis is most frequent during the ages of 20–30,36 correlating well with the age of onset of schizophrenia.37 Therefore, congenital infection with T. gondii may be involved in the etiology of schizophrenia.