Conventional wisdom suggests that Th2 response (aka, type II immunity) developed in response to worms (helminths). At the same time, notoriety of Th2 response comes from its involvement in allergies [that is spreading far and wide in western-style living environments]. Strangely enough, the same people enjoying western-style living conditions suffer minimally or not at all from helminths. This is by definition a paradox. If Th2 is directed towards helminths, then what activates Th2 response in total absence of such parasites? crazy, right? Here another paradox for you. It appears that presence of helminths are actually beneficial against allergy. What?!
New paper in journal Immunity has some interesting story to tell about all these. This study showed that in mice, helminth infection modifies endogenous gut microflora to drive allergy down via production of microbe-derived short-chain fatty acids.
Initially, the authors showed that helminth[Hpb]-infected mice showed reduced inflammation in response to house dust mite (HDM) allergen [eosinophils↓, IgG1↓, IL-5↓, H&E↓].
Interestingly, antibiotic treated mice infected with helminth failed to show attenuated allergic response to HDM.
Parallel experiment showed that helminth infection modified mouse gut flora composition and increased gut concentration of short chain fatty acids (propionate, butyrate, acetate).
Finally, mice deficient for GPR-41 (Ffar3-/-), a receptor for short chain fatty acids, also failed to down-regulate allergic response to HDM allergen after helminth infection.
In summary, this study proposed that helminth infection could modify host's allergic phenotype by its influence on gut flora-derived short chain fatty acids. If application of short chain fatty acids alone could reproduce the key observation of this study, it could potentially provide easily available dietary supplements for allergy treatment.
David Usharauli
Interestingly, antibiotic treated mice infected with helminth failed to show attenuated allergic response to HDM.
Finally, mice deficient for GPR-41 (Ffar3-/-), a receptor for short chain fatty acids, also failed to down-regulate allergic response to HDM allergen after helminth infection.
In summary, this study proposed that helminth infection could modify host's allergic phenotype by its influence on gut flora-derived short chain fatty acids. If application of short chain fatty acids alone could reproduce the key observation of this study, it could potentially provide easily available dietary supplements for allergy treatment.
David Usharauli
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