The interaction between the nervous system and the immune system can affect the outcome of a bacterial infection. Staphylococcus aureus skin infection is a common infectious disease, and elucidating the relationship between the nervous system and immune system may help to improve treatment strategies. In this study, we found that the local release of calcitonin gene-related peptide (CGRP) increased during S. aureus skin infection, and S. aureus could promote the release of CGRP from transient receptor potential cation channel subfamily V member 1 (TRPV1+) neurons in vitro. The existence of TRPV1+ neurons inhibited the recruitment of neutrophils to the infected region and regulated the polarization of macrophages toward M2 while inhibiting polarization toward M1. This reduces the level of inflammation in the infected area, which aggravates the local infection. Furthermore, this study demonstrates that TRPV1 may be a target for the treatment of S. aureus skin infections and that botulinum neurotoxin A (BoNT/A) and BIBN4096 may reverse the inhibited inflammatory effect of CGRP, making them potential therapeutics for the treatment of skin infection in S. aureus. In S. aureus skin infection, TRPV1+ neurons inhibit neutrophil recruitment and regulate macrophage polarization by releasing CGRP. BoNT/A and BIBN4096 may be potential therapeutic agents for S. aureus skin infection.

中文翻译：

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TRPV1+ 神经元通过影响巨噬细胞极化和中性粒细胞募集来改变金黄色葡萄球菌皮肤感染结果

神经系统和免疫系统之间的相互作用会影响细菌感染的结果。金黄色葡萄球菌皮肤感染是一种常见的感染性疾病，阐明神经系统和免疫系统之间的关系可能有助于改进治疗策略。在本研究中，我们发现金黄色葡萄球菌皮肤感染期间降钙素基因相关肽（CGRP）的局部释放增加，并且金黄色葡萄球菌可以促进瞬时受体电位阳离子通道亚家族V成员1（TRPV1+）释放CGRP体外的神经元。TRPV1+神经元的存在抑制了中性粒细胞向感染区域的募集，并调节巨噬细胞向M2的极化，同时抑制向M1的极化。这会降低感染区域的炎症水平，从而加重局部感染。此外，这项研究表明，TRPV1 可能是治疗金黄色葡萄球菌皮肤感染的靶点，而肉毒杆菌神经毒素 A (BoNT/A) 和 BIBN4096 可能逆转 CGRP 的抑制炎症作用，使其成为治疗皮肤感染的潜在疗法。金黄色葡萄球菌感染。在金黄色葡萄球菌皮肤感染中，TRPV1+ 神经元通过释放 CGRP 抑制中性粒细胞募集并调节巨噬细胞极化。BoNT/A 和 BIBN4096 可能是金黄色葡萄球菌皮肤感染的潜在治疗剂。