Introduction
IBD is a chronic intestinal disorder that primarily manifests as a
specific immune response of the mucosal immune system towards intestinal
pathogenic microorganisms. Human IBD can be divided into two types:
ulcerative colitis (UC) and Crohn’s disease (CD)
[1]. UC typically involves Th2- and
Th17-type inflammation, and the superficial portion of the colon is
prone to ulcers. CD is primarily based on Th1-type inflammation, and the
lesions are typically transmural and may spread throughout the intestine
[2]. Compared to developing countries,
the incidence of inflammatory bowel disease in developed Western
countries is relatively high. This phenomenon can be explained by the
“hygiene hypothesis”, which describes how improved sanitary conditions
reduce the chances individuals will come into contact with pathogenic
organisms, increasing the incidence of autoimmune and inflammatory
diseases [3-5]. Antiparasitic drugs
and good hygiene practices in developed countries have effectively
controlled parasitic infections, but with the elimination of parasitic
infections, the incidence of immune diseases, including inflammatory
bowel disease, has also increased [6].
As a non-invasive organism, C. rodentium uses attaching and
effacing (A/E) lesion formation as its major tissue-targeting mechanism,
resulting in infection. This approach is consistent with the mechanisms
observed in other enteropathogenic pathogens, such asEscherichia coli (EPEC) and
enterohaemorrhagic E. coli (EHEC). As a natural mouse pathogen,C. rodentium provides an excellent in vivo model to study
A/E lesion-forming pathogens, including EPEC and EHEC, because both EHEC
and EPEC are poorly pathogenic in mice. However, infection with C.
rodentium has also been investigated as a model for studying IBD,
because the colonic pathology of the mouse shares several similarities
with clinical IBD [7]. In addition,
this model provides potential mechanisms for increasing the
understanding of how host immunity that plays a role in limiting the
infection of the mucosal epithelium of the colon and clearing pathogens
[8].
Parasitic infection can induce an immune response in the host, causing
polarization towards a Th2-type response, which is characterized by the
expression of the Th2-type cytokines IL-4, IL-5 and IL-13
[9]. Parasites downregulate T and B
cell responses with respect to Tregs, anti-inflammatory cytokines IL-10
and transforming growth factor
TGF-β and regulates the Th1- and
Th2-type immune responses [10].
Parasites can establish a parasitic lifestyle by regulating the host
immune response, which simultaneously protects the host from excessive
inflammation that causes damage to tissues and organs
[11]. In recent years, experimental
and clinical studies have shown that parasitic infections can protect
the host from inflammatory bowel disease. For example, the intestinal
parasites T. spiralis , Swine whipworm (Trichuris muris )
and Hymenolepis diminuta can provide protection to IBD in mice
[12,
13]. Similarly, UC and CD symptoms in
IBD patients infected with T. muris are alleviated
[14]. The mechanism of intestinal
parasite treatment of IBD is not yet clear, and many aspects of this
process remain to be elucidated. In the present study, we constructed an
experimental mouse enteritis model induced by C. rodentium ,
studied the immune system effects of T. spiralis treatment on
inflammatory bowel disease in mice, and elucidated the effects ofT. spiralis intervention in IBD at the molecular and cellular
levels to identify the potential immunological mechanisms involved to
provide a theoretical basis for clinical treatment of human IBD.