During Schistosoma
infection, lack of B cells results in more severe
granulomas,
inflammation, and
fibrosis in the liver, but the mechanisms underlying this pathology remain unclear. This study was to clarify the mechanisms underpinning the
immunomodulation of B cells in mice infected with Schistosoma japonicum (S. japonicum). We found that B cell deficiency led to aggravated liver pathology, as demonstrated by increases in the size of the egg-associated
granulomas,
alanine transaminase levels, and
collagen deposition. Compared with infected wild-type (WT) mice, infected B cell-deficient (μMT) mice showed increased infiltration of Ly6Chi monocytes and higher levels of proinflammatory
cytokines and
chemokines. Furthermore, B1 cells were increased significantly in the liver of WT mice following S. japonicum
infection. Adoptively transferring B1 cells, but not B2 cells, to μMT mice significantly reduced liver pathology and liver infiltration of Ly6Chi monocytes. Additionally, secretion of
IL-10 from hepatic B cells increased significantly in infected WT mice and this
IL-10 was mainly derived from B1 cells. Adoptively transferring B1 cells purified from WT mice, but not from IL-10-deficient mice, to μMT mice significantly reduced liver pathology and liver infiltration of Ly6Chi monocytes. These reductions were accompanied by decreases in the expression levels of
chemokines and inflammatory
cytokines. Taken together, these data indicated that after S. japonicum
infection, an increased number of hepatic B1 cells secrete
IL-10, which inhibits the expression of
chemokines and
cytokines and suppresses the infiltration of Ly6Chi monocytes into the liver thereby alleviating liver early
inflammation and late
fibrosis.