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Impaired osteoclastogenesis by staphylococcal lipoteichoic acid through Toll-like receptor 2 with partial involvement of MyD88


Impaired osteoclastogenesis by staphylococcal lipoteichoic acid through Toll-like receptor 2 with partial involvement of MyD88



Journal of Leukocyte Biology 86(4): 823-831



ISSN/ISBN: 0741-5400

PMID: 19602669

DOI: 10.1189/jlb.0309206

Degenerative bone disease, marked by excessive loss of calcified matrix, is often associated with bacterial infections. Osteoclasts, which mediate the bone-resorptive process, are derived mainly from myeloid precursor cells of the monocyte/macrophage lineage, from which cells with phagocytic and inflammatory capacities may alternatively arise. Here, we investigated the effect of LTA, a major cell-wall virulence factor of Gram-positive bacteria, on osteoclast differentiation. Osteoclast precursors were prepared from C57BL/6 mouse BM using M-CSF and RANKL. When osteoclastogenesis was induced in the presence of staphylococcal LTA, LTA dose-dependently inhibited the differentiation of osteoclast precursors to mature osteoclasts. A corresponding inhibition of bone-resorptive function was observed in the reduced resorption area on calcium phosphate-coated culture plates. In contrast, the phagocytic and inflammatory potential of the osteoclast precursors increased in the presence of LTA. TLR2, known to recognize LTA, might be essential for the LTA inhibition of osteoclastogenesis, as the inhibition did not occur in the precursors from TLR2-deficient mice. Importantly, MyD88-dependent and MyD88-independent pathways would participate in the inhibition, as determined using MyD88-deficient cells. Moreover, LTA inhibited phosphorylation of ERK and JNK in osteoclast precursors stimulated with M-CSF and RANKL, concomitantly with a decreased DNA-binding activity of AP-1. These results suggest that staphylococcal LTA inhibits osteoclast differentiation primarily through TLR2 but also in part through MyD88 signaling, which in turn, inhibits activation of ERK, JNK, and AP-1.

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Accession: 053730228

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