I´m late to the party, but some people seem to be jumping too conclusions rather quickly regarding mTOR, namely those who are suggesting that non-macrolide antibiotics may have caused their ME. From a quick search, the inhibitory effects seem to be limited to the macrolides, and even then mainly to Rapamycin (which I doubt that anyone had heard of before the mTOR stuff came up) and Azithromycin: in the study below, it took 4 times more Clarithomycin than Azithromycin to have the same inhibitory effect. The study also seems to suggest that the positive effects observed from Azithromycin use in some people with ME may be due to the same mechanism, whereby the mTOR inhibition results in an antiflammatory effect:
http://www.nature.com/articles/srep07438#abstract
´Several clinical studies on diseases with an auto-inflammatory or auto-immune background have described a therapeutic effect for AZM and CLM, which could not be explained by its anti-bacterial properties
13,
15,
17. Interestingly, although T-cells are strongly involved in the regulation of virtually any immune response, the immunomodulatory effects of macrolides on T-cells have to date not been thoroughly characterized. In this respect, we have shown for the first time that AZM and CLM directly exert suppressive effects on the activation of purified CD4+ T-cells.´
´In conclusion, a remarkable difference in the immunosuppressive potency between AZM and CLM on highly purified CD4+ T-cells was shown for the first time. These effects of AZM seem to be translated by specific inhibition of mTOR kinase activity in an FKBP12 independent fashion.´
Perhaps some of the other mTOR inhibitors that people have found helpful may work in a similar way.
I also found this paragraph quite pertinent:
´Septic patients frequently present with an overwhelming reaction of the immune response, and therefore the administration of macrolides has shown beneficial results in septic patients, especially when the sepsis is secondary to pneumonia
59,
60. A suppressed immune status marked by lymphopenia
61, associated with a higher mortality rate
62, is also frequently observed in the course of a severe sepsis. In particular, CD4+ T-cells are affected from an increased apoptosis rate, leading to an elevated risk of viral co-infection
63,
64,
65. In the light of the immunosuppressive function of AZM and CLM, it might be necessary to re-evaluate respective treatment regimens. Therefore, it might be preferable to switch to other antibiotics which do not suppress the effector functions of CD4+ T-cells. In this context, further
in vitro and
in vivo studies with other commonly used antibiotics (e.g. beta-lactam antibiotics, fluorochinolones, macrolides) are necessary.´
