Adult Hymenolepis nana and its excretory–secretory products elicit mouse immune responses via tuft/IL-13 and FOXM1 signaling pathways
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Background
Hosts typically elicit diverse immune responses to the infection of various parasitic worms, with intestinal epithelial cells playing pivotal roles in detecting parasite invasion. Hymenolepis nana ( H . nana ) is a zoonotic parasitic worm that resides in the host’s intestine. The contribution and underlying mechanisms of tuft cell-mediated immune reactions against H . nana remain unexplored.
Methods
This study endeavors to examine the immune responses in the mouse intestine elicited by the adult H . nana and its excretory–secretory products (ESP). Ileal tissue alteration was detected using hematoxylin and eosin (H&E) staining, changes in the number of intestinal stem cells, goblet cells, tuft cells, and Paneth cells were detected by immunohistochemistry (IHC), immunofluorescence (IF), etc., and changes in the expression of type 2 cytokines and FOXM1 were detected by Western blotting (WB) or real-time quantitative polymerase chain reaction (RT-qPCR).
Results
The presence of adult H . nana and its ESP enhanced the number of tuft cells and goblet cells while fostering the production of type 2 cytokines. Furthermore, the surge in Paneth cells and FOXM1 triggered by H. nana aids in maintaining intestinal stem cells homeostasis and proliferation. Notably, the FOXM1 inhibitor RCM-1 dampened intestinal stem cells differentiation and type 2 cytokines secretion, potentially impeding the host's capacity to eliminate H . nana .
Conclusions
The adult H . nana and its ESP stimulate the immune responses in mice through tuft/interleukin (IL)-13 and FOXM1 signaling pathways and promote the elimination of H . nana from the host through the differentiation of intestinal stem cells into tuft cells, goblet cells, and Paneth cells, as well as the activation of type 2 immune responses. Meanwhile, RCM-1 inhibits the immune responses to H . nana in mice, thus affecting the excretion of H . nana by host.
