Mario M. Zaiss 1 , Alexis Rapin 1 , Luc Lebon 1 , Lalit Kumar Dubey 1 , Ilaria Mosconi 1 , Kerstin Sarter 2 , Alessandra Piersigilli 1 , 3 , Laure Menin 4 , Alan W. Walker 5 , 6 , Jacques Rougemont 7 , Oonagh Paerewijck 8 , Peter Geldhof 8 , Kathleen D. McCoy 9 , Andrew J. Macpherson 9 , John Croese 10 , 11 , Paul R. Giacomin 11 , Alex Loukas 11 , Tobias Junt 12 , Benjamin J. Marsland 13 , Nicola L. Harris 1 , ∗
17 November 2015
Intestinal helminths are potent regulators of their host’s immune system and can ameliorate inflammatory diseases such as allergic asthma. In the present study we have assessed whether this anti-inflammatory activity was purely intrinsic to helminths, or whether it also involved crosstalk with the local microbiota. We report that chronic infection with the murine helminth Heligmosomoides polygyrus bakeri (Hpb) altered the intestinal habitat, allowing increased short chain fatty acid (SCFA) production. Transfer of the Hpb-modified microbiota alone was sufficient to mediate protection against allergic asthma. The helminth-induced anti-inflammatory cytokine secretion and regulatory T cell suppressor activity that mediated the protection required the G protein-coupled receptor (GPR)-41. A similar alteration in the metabolic potential of intestinal bacterial communities was observed with diverse parasitic and host species, suggesting that this represents an evolutionary conserved mechanism of host-microbe-helminth interactions.
Intestinal helminths are well known to possess potent immunomodulatory capacities. Harris and colleagues demonstrate in mice that helminth infection alters the bacterial microbiota and increases the concentration of short chain fatty acids (SCFAs), which reduce allergic asthma via GPR41. Increased intestinal SCFA concentrations were conserved across multiple parasite and host species.