Pathogenesis and pathobiology of zoonotic brucellosis in humans

BALDI, PABLO CESAR; GIAMBARTOLOMEI, GUILLERMO

REVUE SCIENTIFIQUE ET TECHNIQUE DE L4OFFICE INTERNATIONAL DES EPIZOOTIES

OFFICE INT EPIZOOTIES

Lugar: París; Año: 2013 vol. 21 p. 117 - 125

0253-1933

Although human brucellosis has protean clinical manifestations, affected tissues usually exhibit signs of inflammation. The cellular and molecular bases of some immunopathological phenomena probably involved in Brucella pathogenesis have been recently unraveled. Human osteoblasts and fibroblast-like synoviocytes produce cytokines, chemokines and matrix-metalloproteinases (MMPs) in response to Brucella infection and/or to stimulation by Brucella-infected monocytes. In turn, the released cytokines promote the secretion of MMPs and induce osteoclastogenesis. These phenomena may underlie the bone loss and cartilage degradation found in brucellar arthritis and osteomyelitis. B. abortus and its lipoproteins elicit an inflammatory response in the CNS of mice, leading to astrogliosis, a characteristic feature of neurobrucellosis. Brucella can also replicate in human endothelial cells, inducing an inflammatory response with increased expression of chemokines, IL-6, and adhesion molecules. The long-lasting infection of the endothelium would support brucellar endocarditis and other vascular manifestations. Therefore, while the inflammatory phenomena triggered by Brucella are relatively mild, they are long-lasting due to the prolonged intracellular persistence of the bacterium in infected tissues, eventually leading to tissue damage.