Staphylococcus Aureus Tames Nociceptive Neurons to Suppress Synovial Macrophage Responses for Sustained Infection in Septic Arthritis

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Abstract The interaction between the nervous system and immune system during chronic bacterial infection remains unclear. Here, it is reported that Staphylococcus aureus ( S. aureus ) infection induces calcitonin gene‐related peptide (CGRP) secretion from intra‐articular transient receptor potential cation channel subfamily V member 1 positive (TRPV1 + ) nociceptive nerves through its pore‐forming toxin (PFT) α‐hemolysin. The released CGRP then inhibits the production of chemotactic cytokines by CX3CR1 + tissue‐resident synovial lining macrophages via receptor activity modifying protein 1 (RAMP1) receptors at the onset of septic arthritis. During the subsequent chronic course of infection, the continuous release of CGRP triggered by pain has a lasting effect on the antimicrobial capabilities of macrophages, thereby promoting bacterial survival and joint damage. This evidence suggests a critical role for neuroimmune regulation in S. aureus‐ induced chronic septic arthritis. CGRP receptor antagonism may reduce joint destruction, thus providing a new option for treating bone and joint infections.

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