Spleen atrophy related immune system changes attributed to infection of Angiostrongylus cantonensis in mouse model.

The spleen is one of the most important peripheral immune organs, which is frequently affected in infectious diseases. Infectious diseases can induce splenic alterations including splenic atrophy and functional alteration, while splenic atrophy may in turn interferes with recovery of infectious diseases. Angiostrongyliasis is an infectious disease by Angiostrongylus cantonensis (A. cantonensis), which invade non-permissive hosts, such as humans and mice, to cause severe damage to the central nervous system (CNS) and acute inflammatory response. A. cantonensis infection-induced CNS injury has been confirmed to be due to profound immunopathology derived from peripheral immune components. However, the mechanism of immunopathology remains largely unknown. Here, we found that A. cantonensis invaded non-permissive hosts such as mice in the brain, but not in the other peripheral organs. However, this infection induced severe spleen atrophy. We further recognized that this atrophy is associated with a decrease of total splenocyte number and disruption of splenic structure due to reduced proliferation and increased apoptotosis. These also resulted in deterioration of T cell profile in the periphery with a low CD4/CD8 ratio and B/T cell ratio, and increased ratio of CD4(+)CD25(+)Foxp3(+) Treg, CD8(+)CD28(-) T, and CD38(+)T lymphocyte of spleen. Albendazole treatment can alleviate spleen atrophy and set T cell immune reconstitution in some extend. Our data showed that A. cantonensis infection can cause splenic atrophy. These results are suggested to put more emphasis to improve the function of immune system. Meanwhile, infection and treatment model will be useful to evaluate new therapeutic approaches which can prevent or reverse immunosuppression and infectious complications.