PDF(Pubmed)
Abstract：
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.
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.
摘要：
背景：神经系统和免疫系统之间的相互作用可以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善治疗策略。
结果：在这项研究中，我们发现，在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，金黄色葡萄球菌可以促进体外瞬时受体电位阳离子通道亚家族V成员1（TRPV1）神经元CGRP的释放。TRPV1神经元的存在抑制了中性粒细胞向感染区域的募集，并调节了巨噬细胞向M2的极化，同时抑制了向M1的极化。这降低了感染区域的炎症水平，这加剧了局部感染。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标，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，使它们成为治疗金黄色葡萄球菌皮肤感染的潜在疗法。
结论：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。
结果：在这项研究中，我们发现，在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，金黄色葡萄球菌可以促进体外瞬时受体电位阳离子通道亚家族V成员1（TRPV1）神经元CGRP的释放。TRPV1神经元的存在抑制了中性粒细胞向感染区域的募集，并调节了巨噬细胞向M2的极化，同时抑制了向M1的极化。这降低了感染区域的炎症水平，这加剧了局部感染。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标，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，使它们成为治疗金黄色葡萄球菌皮肤感染的潜在疗法。
结论：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。
