Unconjugated
Parasitic helminth and their products can suppress or modulate the host immune response for long-term survival and continued infection. Commonly, helminth can induce conditional T helper cell type 2 (Th2) response, regulatory T cell and cytokines, and altered function of antigen presentation cells by modulating toll-like receptors (TLRs). The helminth Trichinella spiralis establishes chronic infection in skeletal muscles of a wide range of mammalian hosts. We infected mice with T. spiralis and investigated Th1/Th2/Th17 cytokine profiles in serum and expression of TLRs and related signal molecules in spleen at various times post-infection. The infection evoked a mixed Th1/Th2 and inhibited Th17 immune response, with initial predominance of a Th1 response in intestine stage and subsequent predominance of a Th2 response in muscle stage. Different stages of infection had different impacts on the expression of TLRs and related signaling molecules. In the adult stage of infection, TLR1 and TLR4 were upregulated and the MyD88-dependent signal pathway was activated. The muscle larvae inhibited TLR4 and TRIF-dependent signal pathway. Our results implied that T. spiralis infection may regulate Th1/Th2/Th17 cytokine production through TLRs.
