Trichuris muris: a model of gastrointestinal parasite infection

Abstract

Infection with soil-transmitted gastrointestinal parasites, such as Trichuris trichiura, affects more than a billion people worldwide, causing significant morbidity and health problems especially in poverty-stricken developing countries. Despite extensive research, the role of the immune system in triggering parasite expulsion is incompletely understood which hinders the development of anti-parasite therapies. Trichuris muris infection in mice serves as a useful model of T. trichiura infection in humans and has proven to be an invaluable tool in increasing our understanding of the role of the immune system in promoting either susceptibility or resistance to infection. The old paradigm of a susceptibility-associated Th1 versus a resistance-associated Th2-type response has been supplemented in recent years with cell populations such as novel innate lymphoid cells, basophils, dendritic cells and regulatory T cells proposed to play an active role in responses to T. muris infection. Moreover, new immune-controlled mechanisms of expulsion, such as increased epithelial cell turnover and mucin secretion, have been described in recent years increasing the number of possible targets for anti-parasite therapies. In this review, we give a comprehensive overview of experimental work conducted on the T. muris infection model, focusing on important findings and the most recent reports on the role of the immune system in parasite expulsion.

Transcriptomics identified a critical role for Th2 cell-intrinsic miR-155 in mediating allergy and antihelminth immunity

“…Unlike H. polygyrus, expulsion of the intestinal whip worm Trichuris muris is critically dependent on a highly polarized Th2 response (48), and a mixed Th1/2/17 response leads to chronic infection (49). Therefore we tested whether mice with miR146a −/− T cells could mount the polarized Th2 response required for proficient antihelminth immunity.…”

Immunity to Helminths: Resistance, Regulation, and Susceptibility to Gastrointestinal Nematodes

“…For example, T. muris differs from the other nematodes discussed above in that it requires the activation of a Th1 response and IFN-γ production to progress to chronic infection (89,90). The activation of these processes is not required for chronic infection by H. polygyrus bakeri, and N. brasiliensis is essentially studied as an acute-resolving infection in mice.…”

Eosinophils in Helminth Infection: Defenders and Dupes

“…Best understood in the intestine, in some instances goblet cells are critical [1], in others mast cells [2] or antibodies [3–5] play important roles in host defense. Immune mediators may cause displacement [3, 4], deprive the worm of energy or nutrients [1], or disrupt the habitat [6]. By a similarly varied array of mechanisms, worms evade or co-opt the immune response in order to complete their life cycles and be transmitted to the next host [7].…”