ArticleBone & joint research2026
CXCL5 suppresses osteoclastogenesis and protects against lipoteichoic acid-induced bone loss by modulating PLCγ2 and c-Fos signalling in gram-positive periprosthetic joint infection.
Article in Bone & joint research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Aims: Periprosthetic joint infection (PJI) is known to disrupt bone metabolism. Unlike lipopolysaccharide (LPS) from Gram-negative bacteria (GNB), lipoteichoic acid (LTA) from Gram-positive cocci (GPC) induces minimal osteoclast activation and bone resorption. Clinically, patients with Gram-positive bacterial component-associated PJI (GPC-PJI) exhibit less osteolytic activity than those with Gram-negative bacterial PJI (GNB-PJI), suggesting a milder disruption of bone homeostasis. In this study, we identified elevated levels of chemokine (C-X-C motif) ligand 5 (CXCL5) in the synovial fluid (SF) of GPC-PJI patients and investigated its regulatory role in osteoclast signalling and bone remodelling. A murine bone loss model was employed to assess its in vivo function. Methods: SF samples from patients with PJI and aseptic loosening (AL) were analyzed using cytokine protein arrays and enzyme-linked immunosorbent assay (ELISA) to compare CXCL5 expression in the AL, GPC-PJI, and GNB-PJI groups. In vitro, MC3T3-E1 osteoblasts were used to examine CXCL5 induction following LTA stimulation, while RAW264.7 macrophages were used to evaluate the effects of CXCL5 on receptor activator of nuclear factor kappa-B ligand (RANKL)-induced osteoclast differentiation. In vivo, a mouse model received intra-articular LTA and intraperitoneal CXCL5 neutralizing antibody to investigate the role of CXCL5 in maintaining bone integrity under infectious conditions. Results: CXCL5 was significantly upregulated in PJI patients, particularly in GPC-PJI cases. LTA stimulation increased CXCL5 secretion from osteoblasts in a dose-dependent manner. Functionally, CXCL5 inhibited osteoclast formation and reduced nuclear factor of activated T-cells cytoplasmic 1 (NFATc1) expression. Kinase profiling revealed that CXCL5 suppressed osteoclastogenesis via PLCγ2 phosphorylation and c-Fos downregulation. In vivo, CXCL5 neutralization exacerbated LTA-induced bone loss. Conclusion: CXCL5 is highly expressed in GPC-PJI and protects bone by inhibiting osteoclast differentiation through PLCγ2 and c-Fos signalling. In vivo evidence confirms its key role in preserving bone homeostasis during Gram-positive bacterial infection.
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