Rook GAW; Review series on helminths, immune modulation and the hygiene hypothesis: The broader implications of the hygiene hypothesis. Immunology Volume 126 Issue 1, Pages 3-11. December 8 2008

Cooke A; Review series on helminths, immune modulation and the hygiene hypothesis: How might infection modulate the onset of type 1 diabetes? Immunology Volume 126 Issue 1, Pages 12-17. December 8 2008

Jackson JA, Friberg IM, Little S, Bradley JE: Review series on helminths, immune modulation and the hygiene hypothesis: Immunity against helminths and immunological phenomena in modern human populations: coevolutionary legacies? Immunology Volume 126 Issue 1, Pages 18-27. December 8 2008

The depressing thing about MAP, is like most mycobacteria, it is exceptionally hard to kill. Triple antibiotic therapy, usually for a course of many years, is required, and it is similar in leprosy in that one may never eliminate the infection, as it is even slower growing.

So how would helminths alter an existing infection? I was just reading Weinstock’s and Elliott’s patent on all use of helminths for all autoimmune diseases, and it mentions in the mouse model, that those mice infected with an existing mycobacterial infection, given helminths, have altered response to that infection:

“The immune response to helminthic parasites promotes Th2 responses to unrelated antigens. Infestation with helminthic parasites, which all induce Th2-type inflammation, can modulate the Th1 immune response to unrelated concomitant parasitic,
bacterial and viral infections (Kullberg et al., 1992, J. Immunol. 148:3264).

Animal experimentation supports this contention. Mice infected with Mycobacterium avium develop chronic Th1-type granulomatous inflammation in the lungs and liver. Splenocytes and granuloma cells from these infected animals normally produce
IgG2a and IFN-γ, and no IL-4 or IL-5. However, mice infected with S. mansoni after the establishment of Mycobacterium avium infection form mycobacterial granulomas containing eosinophils. Also, splenocytes and granuloma cells from co-infected
mice secrete more IgG1 and much less IgG2a. The cytokines released from these cells both constitutively or after mycobacterial antigen stimulation include IL-4 and IL-5, and much less than normal quantities of IFN-γ.

Th1 responses promote IgG2a production, whereas Th2 reactions enhance IgG1 and IgE. FIG. 3 shows that mice infected with M. avium have high serum IgG2a levels. Yet, co-infected animals have normal serum IgG2a concentrations, but increased IgG1
and IgE levels.

These data taken together show that a Th2 response to a helminthic infection can down-modulate the ongoing host response to even a strong Th1-inducing organism like M. avium.”

For those of us possibly infected with MAP, helminth infection should down-modulate the immune response. At least according to this patent.