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Review
. 2021 Jul 22;10(8):925.
doi: 10.3390/pathogens10080925.

Trichuris muris Model: Role in Understanding Intestinal Immune Response, Inflammation and Host Defense

Yeganeh Yousefi  1   2 , Sabah Haq  1   2 , Suhrid Banskota  1   2 , Yun Han Kwon  1   2 , Waliul I Khan  1   2
Affiliations
Review

Trichuris muris Model: Role in Understanding Intestinal Immune Response, Inflammation and Host Defense

Yeganeh Yousefi et al. Pathogens. .

Abstract

Several parasites have evolved to survive in the human intestinal tract and over 1 billion people around the world, specifically in developing countries, are infected with enteric helminths. Trichuris trichiura is one of the world's most common intestinal parasites that causes human parasitic infections. Trichuris muris, as an immunologically well-defined mouse model of T. trichiura, is extensively used to study different aspects of the innate and adaptive components of the immune system. Studies on T. muris model offer insights into understanding host immunity, since this parasite generates two distinct immune responses in resistant and susceptible strains of mouse. Apart from the immune cells, T. muris infection also influences various components of the intestinal tract, especially the gut microbiota, mucus layer, epithelial cells and smooth muscle cells. Here, we reviewed the different immune responses generated by innate and adaptive immune components during acute and chronic T. muris infections. Furthermore, we discussed the importance of studying T. muris model in understanding host-parasite interaction in the context of alteration in the host's microbiota, intestinal barrier, inflammation, and host defense, and in parasite infection-mediated modulation of other immune and inflammatory diseases.

Keywords: Trichuris muris; enteroendocrine cells; epithelial cells; goblet cells; host defense; host–parasite interaction; immune response; intestinal helminth; smooth muscle cells.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
Host intestinal immune response against T. muris infection. Representative schematic of the helminth detection and immune response induction. (1) T. muris larvae breach the intestinal epithelium and release Ags. (2) IRF4-dependent CD11b+ DCs up-take T. muris Ags (3) Upon T. muris invasion, intestinal epithelial cells produce alarmins that recruit immune cells. (4) DCs present T. muris Ags to adaptive immune cells in the mesenteric lymph node on day 7 p.i. and activate Th2 cells (the main source of Th2 cytokines). Th2 cells stimulate B cells that synthesize and secret IgA, IgG1 and IgE. (5) Innate immune cells also present Ags to adaptive immune cells in the mesenteric lymph node. (6) Innate immune cells (basophils, eosinophils, ILC2s and NK cells) release Th2 cytokines and promote Th2 immune response. The effects of Th2 immune response are: (7) Activation of mast cells to release mast cell protease, which increases epithelial cell permeability, (8) development of alternatively activated macrophages, which cause tissue repair and helminth detection, (9) goblet cell hyperplasia and increased mucins (Muc2 and Muc5ac) secretion. (10) T. muris affect microbiota composition, which subsequently can influence mucin secretion and barrier function, (11) increase production of 5-HT and AMPs from EC cells and goblet cells, respectively, and (12) increase smooth muscle contraction. (13) All these Th2 responses lead to T. muris expulsion.
Figure 2
Figure 2
Overview of the role of T. muris in inflammatory and immunogenic diseases. T. muris modulates immunopathological and inflammatory disorders by triggering Th1/Th2/Tregs immune responses [9]. Acute T. muris infection results in mounting Th2 immune responses, which are associated with worm expulsion and reduced severity of chemical-induced colitis [135]. However, the effect of T. muris infection in colitis in genetically susceptible individuals remains to be determined. Chronic T. muris infection leads to Th1 immune responses resulting in worm survival and protection against allergic airway diseases [146]. Chronic T. muris infection model can also be used as a model of experimental colitis [144]. T. muris infection also induces regulatory Tregs, and consequently these cells, by releasing anti-inflammatory cytokines, reduce inflammatory disorders [141].
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