Immunopathology in osteoarticular Brucella infection

Abstract

Osteoarticular brucellosis, the most common form of human brucellosis, primarily manifests as sacroiliitis, spondylitis, and peripheral arthritis. Recent research has elucidated the molecular mechanisms underlying bone damage caused by Brucella abortus. This bacterium induces bone damage through pathways involving TNF-α and receptor activator of nuclear factor kappa B ligand, engaging inflammatory cells such as monocytes/macrophages, neutrophils, Th17 CD4 + T cells, and B cells. B. abortus disrupts bone homeostasis by inhibiting osteoblasts, promoting matrix metalloproteinases and cytokine secretion, and increasing osteoclast activity, leading to heightened bone resorption. Furthermore, B. abortus infects and replicates in synoviocytes, inducing chemokine and proinflammatory cytokine production and inhibiting apoptosis. These insights into the molecular mechanisms highlight the intricate interactions between B. abortus and host cells, which contribute to joint and bone damage in osteoarticular brucellosis.