Brucella abortus-infected macrophages modulate T lymphocytes to promote osteoclastogenesis via IL-17.

GIAMBARTOLOMEI GH; SCIAN R; ACOSTA RODRIGUEZ EV; FOSSATI CA; DELPINO MV

AMER SOC INVESTIGATIVE PATHOLOGY, INC

Año: 2012 p. 887 - 887

he pathogenic mechanisms of bone loss caused by Brucella species have not been completely deciphered. Although T lymphocytes (LTs) are considered important to control infection, the mechanism of Brucella-induced T-cell responses to immunopathological features is not known. We present in vitro and in vivo evidence showing that Brucella abortus–induced inflammatory response leads to the activation of LTs, which further promote osteoclastogenesis. Pre-activated murine LTs treated with culture supernatant from macrophages infected with B. abortus induced bone marrow–derived monocytes (BMMs) to undergo osteoclastogenesis. Furthermore, osteoclastogenesis was mediated by CD4 T cells. Although B. abortus–activated T cells actively secreted the proosteoclastogenic cytokines RANKL and IL-17, osteoclastogenesis depended on IL-17, because osteoclast generation induced by Brucella-activated T cells was completely abrogated when these cells were cultured with BMMs from IL-17 rece