Discussion
2,4,6-Trinitrobenzene sulfonic acid (TNBS) and dinitrobenzenesulfonate
(DNBS) mouse models are early-stage IBD animal models
[18]. The damage caused in these
models is highly concentrated, the course of the disease is acute, and
the onset is short. Rat and mouse models of intestinal inflammation
induced by the oral administration of dextran sulfate sodium (DSS) are
also used. The DSS animal model is primarily an injury model, which is
primarily used to study the influencing factors of promoting and
inhibiting intestinal epithelial healing
[19,
20]. In the present study, mice were
administered C. rodentium to induce IBD animal models. C.
rodentium is an adhesion and shedding pathogen of the family
Enterobacteriaceae to which gerbils and mice are susceptible, whereas
hamsters and rats are not. This model has been widely used to study the
immunoprotective role of E. coli and the mechanism of the host
immune response against intestinal pathogens. C.
rodentium -induced animal model mice showed obvious inflammatory
symptoms in the colon, and the pathological characteristics were
consistent with the IBD animal model.
Compared with the TS group, the TS+CR group showed a higher survival
rate, reduced intestinal damage, decreased DAI score, and significantly
reduced symptoms of intestinal inflammation, indicating that T.
spiralis infection could alleviate colitis caused by C.
rodentium . This finding is consistent with that observed in other worm
infection studies [21,
22].
To better understand how worms suppress the occurrence of
immunomodulatory diseases, recent research has focused on the
interaction between the Th2- and Th1-type immune responses
[23]. Th1 cells primarily secrete
IL-2, IFN-γ, IFN-α, and TNF-β, while Th2 cells primarily release IL-4,
IL-5, IL-6 and IL-10 [24]. IL-12
plays an important role in Th1 cell-mediated immune response and
inflammatory diseases [25]. IL-17 is
a pro-inflammatory cytokine produced by T cells and is an early
initiating factor of inflammatory responses induced by T cells
[26]. In this study, IFN-γ and IL-4,
IL-10 were selected as representatives of Th1- and Th2-type cytokines.
The number of Th cells was assessed by flow cytometry, and the results
showed that T. spiralis infection could reduce the expression of
IFN-γ, IL-17 and IL-12 and increase that of IL-4 and IL-10 in colitis
mice. These results showed that T. spiralis infection causes a
colitis mucosal immune response to switch from a Th1-type response to a
protective Th2-type response. ELISA results showed changes in the levels
of IgG1 and IgG2a in mouse serum, indicating that the levels of Th2-type
cytokines caused by T. spiralis infection have an inhibitory
effect on C. rodentium -induced Th1 type inflammation. These
reactions reduce the intensity of the Th1-type immune response, thereby
alleviating intestinal inflammation, and these results are consistent
with the expected experimental results. From another perspective,
colitis was also shown to stimulate the switch from a Th2-type immune
response induced by T. spiralis larvae infection into a Th1-type
immune response, reduce the intensity of the Th2-type immune response,
and possibly alleviate the pathological changes attributed to the
parasite infection in the body. T. spiralis and C.
rodentium interact together to maintain immune balance in mice.
Tregs have a wide range of immunosuppressive effects. By producing
regulatory cytokines, these cells maintain the balance of the immune
system and prevent the development of autoimmune diseases
[27]. Foxp3 is a marker molecule for
CD4+CD25+Tregs
[28]. The results showed that
compared with that observed in the control group, the number of
CD4+CD25+Foxp3+Tregs
in the spleens and MLNs of mice in the TS group was increased, showing
that T. spiralis infection could induce
CD4+CD25+Foxp3+Tregs
production in mice In contrast, compared with that observed in the TS
group, the number of CD4+CD25+Foxp3+Tregs in the spleens and MLNs of mice in the
TS+CR group were decreased, showing that C. rodentium infection
can affect Tregs in the immune response induced by T. spiralis .
The results of the present study are consistent with those of a previous
study of worm infections that showed increased levels of
Foxp3+Tregs in mouse MLNs and intestinal mucosa lamina
propria, inhibiting the mouse colon inflammatory response, as reported
by Maloy et al [29].
In summary, the results of the present successfully showed that the
effect of T. spiralis intervention on C. rodentium -induced
colitis in mice is achieved by regulating the Th1/Th2 type immune
response balance of the host.