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共生微生物群失调引发白细胞介素-8信号传导,从而驱动皮肤纤维化疾病。

Commensal microbiome dysbiosis elicits interleukin-8 signaling to drive fibrotic skin disease.

作者信息

Zhang Wenyu, Peng Qili, Huang Xian, Huang Qing, Zhang Zhiliang, Li Fuli, Zheng Naisheng, Shi Binsheng, Fan Zhihong, Maj Tomasz, Chen Rui

机构信息

Institute of Molecular Medicine, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Pujian Road 160, Shanghai 200240, China.

Department of Surgery, Division of Plastic and Reconstructive Surgery, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Pujian Road 160, Shanghai 200240, China.

出版信息

PNAS Nexus. 2024 Jul 30;3(7):pgae273. doi: 10.1093/pnasnexus/pgae273. eCollection 2024 Jul.

DOI:10.1093/pnasnexus/pgae273
PMID:39081787
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11287872/
Abstract

Wound healing is an intensely studied topic involved in many relevant pathophysiological processes, including fibrosis. Despite the large interest in fibrosis, the network that is related to commensal microbiota and skin fibrosis remains mysterious. Here, we pay attention to keloid, a classical yet intractable skin fibrotic disease to establish the association between commensal microbiota to scaring tissue. Our histological data reveal the presence of microbiota in the keloids. 16S rRNA sequencing characterizes microbial composition and divergence between the pathological and normal skin tissues. Moreover, the data show elevation of interleukin-8 (IL-8) in both the circulation and keloid tissue, which elicited the collagen accumulation and migratory program of dermal fibroblasts via CXCR1/2 receptor. Our research provides insights into the pathology of human fibrotic diseases, advocating commensal bacteria and IL-8 signaling as useful targets in future interventions of recurrent keloid disease.

摘要

伤口愈合是一个经过深入研究的课题,涉及许多相关的病理生理过程,包括纤维化。尽管人们对纤维化有着浓厚的兴趣,但与共生微生物群和皮肤纤维化相关的网络仍然神秘莫测。在这里,我们关注瘢痕疙瘩,一种典型但棘手的皮肤纤维化疾病,以建立共生微生物群与瘢痕组织之间的关联。我们的组织学数据显示瘢痕疙瘩中存在微生物群。16S rRNA测序表征了病理皮肤组织和正常皮肤组织之间的微生物组成和差异。此外,数据显示循环系统和瘢痕疙瘩组织中白细胞介素-8(IL-8)水平升高,其通过CXCR1/2受体引发真皮成纤维细胞的胶原蛋白积累和迁移程序。我们的研究为人类纤维化疾病的病理学提供了见解,提倡将共生细菌和IL-8信号作为复发性瘢痕疙瘩疾病未来干预的有用靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c96f/11287872/e27075a86648/pgae273f7.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c96f/11287872/a14ef4427ddc/pgae273f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c96f/11287872/4e3163533b9e/pgae273f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c96f/11287872/e27075a86648/pgae273f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c96f/11287872/38dcdc49c870/pgae273f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c96f/11287872/9e53d9de9c48/pgae273f2.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c96f/11287872/e27075a86648/pgae273f7.jpg

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