Open AccessSchistosome infection promotes osteoclast-mediated bone loss
Author(s) -
Wei Li,
Chuan Wei,
Lei Xu,
Beibei Yu,
Ying Chen,
Di Lu,
Lína Zhang,
Xian Song,
Liyang Dong,
Sha Zhou,
Zhipeng Xu,
Jing Zhu,
Xiaojun Chen,
Chuan Su
Publication year - 2021
Publication title -
plos pathogens
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.719
H-Index - 206
eISSN - 1553-7374
pISSN - 1553-7366
DOI - 10.1371/journal.ppat.1009462
Subject(s) - rankl , osteoclast , osteoprotegerin , bone remodeling , immunology , context (archaeology) , biology , bone resorption , activator (genetics) , receptor , medicine , endocrinology , paleontology
Infection with schistosome results in immunological changes that might influence the skeletal system by inducing immunological states affecting bone metabolism. We investigated the relationships between chronic schistosome infection and bone metabolism by using a mouse model of chronic schistosomiasis, affecting millions of humans worldwide. Results showed that schistosome infection resulted in aberrant osteoclast-mediated bone loss, which was accompanied with an increased level of receptor activator of nuclear factor-κB (NF-κB) Ligand (RANKL) and decreased level of osteoprotegerin (OPG). The blockade of RANKL by the anti-RANKL antibody could prevent bone loss in the context of schistosome infection. Meanwhile, both B cells and CD4 + T cells, particularly follicular helper T (Tfh) cell subset, were the important cellular sources of RANKL during schistosome infection. These results highlight the risk of bone loss in schistosome-infected patients and the potential benefit of coupling bone therapy with anti-schistosome treatment.