AbstractThis study aimed to investigate whether class A1 scavenger receptor (SR-A1) regulated macrophage polarization and gut microbial alteration during intestinal inflammation of colitis. A murine colitis model was established by feeding with dextran sulfate sodium (DSS), and treatment groups were injected intravenously with SR-A1 antibody.

摘要本研究旨在探讨A1类清道夫受体（SR-A1）在结肠炎肠道炎症过程中是否调节巨噬细胞极化和肠道微生物改变。。

Results showed a preventive effect on colitis symptoms and fewer inflammatory cell infiltrates in treatment groups. Down-regulation of inflammatory cytokines and up-regulation of anti-inflammatory cytokine related to macrophages were seen in murine PBMC and LPMC after injected with SR-A1 antibody. The percentage of M2 macrophages was also elevated in treatment groups.

结果显示，治疗组对结肠炎症状有预防作用，炎症细胞浸润较少。注射SR-A1抗体后，在小鼠PBMC和LPMC中观察到炎性细胞因子的下调和与巨噬细胞相关的抗炎细胞因子的上调。治疗组M2巨噬细胞的百分比也升高。

In addition, SR-A1 antibody treatment resulted in the decreased apoptosis and increased proliferation of colonic epithelial cells. Other findings indicated that SR-A1 antibody injection could mediate its anti-inflammatory effect via inhibiting TLR4-MyD88-NF-kB signaling pathway and alterating the gut microbiota composition.

此外，SR-A1抗体治疗导致结肠上皮细胞凋亡减少和增殖增加。其他研究结果表明，SR-A1抗体注射可通过抑制TLR4-MyD88-NF-kB信号通路和改变肠道微生物群组成来介导其抗炎作用。

Our research identified SR-A1 as a potential therapeutic target in inflammatory bowel disease (IBD)..

我们的研究确定SR-A1是炎症性肠病（IBD）的潜在治疗靶点。。

IntroductionAs a first-line housekeeper of complex innate immune system, monocyte-derived mononuclear phagocyte, particularly macrophage, plays a variety of roles to the maintenance of gut homeostasis in the steady state1,2. On one hand, macrophages rapidly eliminate apoptotic cells and life-threatening pathogens by direct phagocytosis and production of inflammatory cytokines and soluble factors.

引言作为复杂先天免疫系统的一线管家，单核细胞衍生的单核吞噬细胞，特别是巨噬细胞，在稳态下对维持肠道稳态起着多种作用1,2。一方面，巨噬细胞通过直接吞噬作用和炎性细胞因子和可溶性因子的产生迅速消除凋亡细胞和危及生命的病原体。

On the other, they also recognize food-derived antigens or commensal microbiota in a tolerating manner in the absence of co-stimulatory signals3,4. Intestinal microenvironmental alterations determine the polarization of macrophages into different phenotypes, including classically activated (M1) macrophages and alternatively activated (M2) macrophages, and simultaneously act as pro-inflammatory or anti-inflammatory function.

另一方面，他们还在没有共刺激信号的情况下以耐受的方式识别食物来源的抗原或共生微生物群3,4。肠道微环境的改变决定了巨噬细胞极化为不同的表型，包括经典激活的（M1）巨噬细胞和交替激活的（M2）巨噬细胞，并同时起到促炎或抗炎功能的作用。

Failure to achieve this polarized balance between tolerance and responsiveness in intestinal lamina propria can lead to development of chronic immune disorder such as inflammatory bowel disease (IBD)5. Therefore, targeting of macrophage-related regulatory switches may offer a new approach to the immune treatment of IBD.Like most tissue macrophages, intestinal macrophages exert their removal and cytokine secretion effects by stimulation of pattern recognition receptors (PRR) activation.

未能在肠道固有层的耐受性和反应性之间实现这种极化平衡可能导致慢性免疫疾病的发展，如炎症性肠病（IBD）5。因此，靶向巨噬细胞相关的调节开关可能为IBD的免疫治疗提供新的方法。像大多数组织巨噬细胞一样，肠巨噬细胞通过刺激模式识别受体（PRR）激活发挥其去除和细胞因子分泌作用。

Class A1 scavenger receptor (SR-A1), also known as SCARA1, CD204 or macrophage scavenger receptor 1, is a prototypic member of PRRs family primarily expressed in macrophages6. SR-A1 was initially identified by its ability to mediate the formation of foam cells, functioning as regulating the process of atherosclerosis in cardiovascular diseases7.

A1类清道夫受体（SR-A1），也称为SCARA1，CD204或巨噬细胞清道夫受体1，是主要在巨噬细胞中表达的PRRs家族的原型成员6。SR-A1最初是通过其介导泡沫细胞形成的能力来鉴定的，其功能是调节心血管疾病中动脉粥样硬化的过程7。

Subsequent lines of evidence reveal that SR-A1 is implicated in other disease pathogenesis by modulating macrophage activity and pola.

随后的证据表明，SR-A1通过调节巨噬细胞活性和pola参与其他疾病的发病机制。

Data availability

数据可用性

The datasets used and/or analyzed during current study are available from the corresponding author upon reasonable request.

。

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Download referencesAcknowledgementsThis work was supported by Natural Science Foundation of Fujian Province of China (2021J011323) to J.S., Natural Science Foundation of Fujian Province of China (2020J011205), and Xiamen Guidance Programs of Medicine and Health (3502Z20214ZD1054) to C.X.Author informationAuthors and AffiliationsDepartment of Gastroenterology, Zhongshan Hospital of Xiamen University, School of Medicine, Xiamen University, No.201-209, Hubinnan Road, Siming District, Xiamen, 361004, Fujian Province, ChinaJingling Su, Lupeng Liu, Yandan Ren, Yutong Gan, Yumei Lin & Chenxi XieAuthorsJingling SuView author publicationsYou can also search for this author in.

下载参考文献致谢这项工作得到了中国福建省自然科学基金（2021J011323）对J.S.，中国福建省自然科学基金（2020J011205）和厦门市医学与健康指导计划（3502Z20214ZD1054）对C.X的支持。作者信息作者和附属机构厦门大学医学院厦门大学中山医院消化内科，厦门市思明区湖滨南路201-209号，福建省厦门市361004，中国苏静玲，刘鲁鹏，任燕丹，甘玉彤，林玉梅和陈曦Sjingling SuView作者出版物您也可以在中搜索此作者。

PubMed Google ScholarLupeng LiuView author publicationsYou can also search for this author in

PubMed Google ScholarLupeng LiuView作者出版物您也可以在

PubMed Google ScholarYandan RenView author publicationsYou can also search for this author in

PubMed Google ScholarYandan RenView作者出版物您也可以在

PubMed Google ScholarYutong GanView author publicationsYou can also search for this author in

PubMed Google ScholaryUton GanView作者出版物您也可以在

PubMed Google ScholarYumei LinView author publicationsYou can also search for this author in

PubMed Google ScholarChenxi XieView author publicationsYou can also search for this author in

PubMed Google ScholarChenxi XieView作者出版物您也可以在

PubMed Google ScholarContributionsMain experiments performance and manuscript drafting: J.S.; animal model establish and data analysis: L.L. and Y.R.; experiments cooperation and data analysis: Y.G. and Y. L. Experimental design and guidance: C.XCorresponding authorCorrespondence to.

PubMed谷歌学术贡献主要实验表现和手稿起草：J.S。；动物模型建立和数据分析：L.L.和Y.R。；实验合作和数据分析：Y.G.和Y.L.实验设计和指导：C.X相应的作者对应。

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Reprints and permissionsAbout this articleCite this articleSu, J., Liu, L., Ren, Y. et al. Class A1 scavenger receptor antibody improves murine colitis by influencing macrophage and gut microbiota.

转载和许可本文引用本文Su，J.，Liu，L.，Ren，Y。等人。A1类清道夫受体抗体通过影响巨噬细胞和肠道微生物群来改善小鼠结肠炎。

Sci Rep 14, 18618 (2024). https://doi.org/10.1038/s41598-024-69656-1Download citationReceived: 20 April 2024Accepted: 07 August 2024Published: 10 August 2024DOI: https://doi.org/10.1038/s41598-024-69656-1Share this articleAnyone you share the following link with will be able to read this content:Get shareable linkSorry, a shareable link is not currently available for this article.Copy to clipboard.

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KeywordsDSS-induced colitisClass A1 scavenger receptorMacrophage polarizationGut microbial alteration

关键词DSS诱导的结肠炎A1类清道夫受体巨噬细胞极化肠道微生物改变

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