Abstract:
:Osteoarticular complications are common in human brucellosis, but the pathogenic mechanisms involved are largely unknown. In this manuscript, we described an immune mechanism for inflammatory bone loss in response to infection by Brucella abortus. We established a requirement for MyD88 and TLR2 in TNF-α-elicited osteoclastogenesis in response to B. abortus infection. CS from macrophages infected with B. abortus induced BMM to undergo osteoclastogenesis. Although B. abortus-infected macrophages actively secreted IL-1β, IL-6, and TNF-α, osteoclastogenesis depended on TNF-α, as CS from B. abortus-infected macrophages failed to induce osteoclastogenesis in BMM from TNFRp55⁻/⁻ mice. CS from B. abortus-stimulated MyD88⁻/⁻ and TLR2⁻/⁻ macrophages failed to express TNF-α, and these CS induced no osteoclast formation compared with that of the WT or TLR4⁻/⁻ macrophages. Omp19, a B. abortus lipoprotein model, recapitulated the cytokine production and subsequent osteoclastogenesis induced by the whole bacterium. All phenomena were corroborated using human monocytes, indicating that this mechanism could play a role in human osteoarticular brucellosis. Our results indicate that B. abortus, through its lipoproteins, may be involved in bone resorption through the pathological induction of osteoclastogenesis.
journal_name
J Leukoc Bioljournal_title
Journal of leukocyte biologyauthors
Delpino MV,Barrionuevo P,Macedo GC,Oliveira SC,Genaro SD,Scian R,Miraglia MC,Fossati CA,Baldi PC,Giambartolomei GHdoi
10.1189/jlb.04111185subject
Has Abstractpub_date
2012-02-01 00:00:00pages
285-98issue
2eissn
0741-5400issn
1938-3673pii
jlb.04111185journal_volume
91pub_type
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journal_title:Journal of leukocyte biology
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