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巨噬细胞和半乳糖凝集素 3 控制急性和亚急性鼠伤寒菌血症中的细菌负荷，进而决定慢性肾脏纤维化。

Macrophages and Galectin 3 Control Bacterial Burden in Acute and Subacute Murine Leptospirosis That Determines Chronic Kidney Fibrosis.

机构信息

Laboratory of Animal Viruses, Institute of Biotechnology and Molecular Biology, UNLP-CONICET, La Plata, Argentina.

Laboratory of Experimental Thrombosis, Institute of Experimental Medicine, National Academy of Medicine-CONICET, Buenos Aires, Argentina.

出版信息

Front Cell Infect Microbiol. 2018 Oct 30;8:384. doi: 10.3389/fcimb.2018.00384. eCollection 2018.

DOI:10.3389/fcimb.2018.00384
PMID:30425972
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6218566/
Abstract

Previous studies have suggested that macrophages may contribute to acute dissemination, as well as having a major role in kidney fibrosis. Our aim was to characterize the role of macrophages and galectin 3 (Gal-3) on the survival, clinical course, bacterial burden, interstitial nephritis, and chronic kidney fibrosis in serovar Copenhageni (LIC)-induced experimental murine leptospirosis. C57BL/6J mice depleted of macrophages by liposome-encapsulated clodronate treatment and infected with LIC presented a higher bacterial burden, had reduced subacute nephritis and enhanced chronic kidney fibrosis relative to untreated, infected mice. Moreover, LIC infection in mice whose Gal-3 was disrupted () had a higher bacterial burden and enhanced subacute nephritis and chronic kidney fibrosis when compared to C57BL/6J wild-type mice. Chronic fibrosis did not correlate with higher transcription levels of TGF-β1 or IL-13 in the kidneys. Kidney fibrosis was found in chronically infected rats as well as in wild infected rats. On the other hand, human fibroblast cultures exhibited enhanced differentiation to myofibroblasts after treatment with LIC. Our results demonstrate that macrophages and Gal-3 play a critical role in controlling the LIC burden but has a minor role in subsequent fibrosis. Instead, kidney fibrosis was better correlated with bacterial burden. Taken together, our results do not support a role for macrophages to disseminate leptospires during acute infection, nor in chronic kidney fibrosis.

摘要

先前的研究表明，巨噬细胞可能有助于急性播散，并在肾脏纤维化中起主要作用。我们的目的是描述巨噬细胞和半乳糖凝集素 3（Gal-3）在血清型哥本哈根（LIC）诱导的实验性小鼠钩端螺旋体病中的生存、临床过程、细菌负荷、间质性肾炎和慢性肾脏纤维化中的作用。用脂质体包裹的 clodronate 处理耗尽巨噬细胞并感染 LIC 的 C57BL/6J 小鼠与未经处理的感染小鼠相比，具有更高的细菌负荷，亚急性肾炎减少，慢性肾脏纤维化增强。此外，与 C57BL/6J 野生型小鼠相比，Gal-3 缺失（）的 LIC 感染小鼠具有更高的细菌负荷，亚急性肾炎和慢性肾脏纤维化增强。慢性纤维化与肾脏中 TGF-β1 或 IL-13 的转录水平升高无关。慢性感染的大鼠和野生感染的大鼠肾脏均有纤维化。另一方面，人成纤维细胞培养物在用 LIC 处理后表现出向肌成纤维细胞的增强分化。我们的结果表明，巨噬细胞和 Gal-3 在控制 LIC 负荷方面起着关键作用，但在随后的纤维化中作用较小。相反，肾脏纤维化与细菌负荷更好相关。总之，我们的结果不支持巨噬细胞在急性感染期间传播钩端螺旋体，也不支持其在慢性肾脏纤维化中的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7e9/6218566/d52ce3871176/fcimb-08-00384-g0009.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7e9/6218566/c637bcf84d5a/fcimb-08-00384-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7e9/6218566/39f05712c8a5/fcimb-08-00384-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7e9/6218566/549592544070/fcimb-08-00384-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7e9/6218566/abcd25d98f60/fcimb-08-00384-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7e9/6218566/4eb2f7e9a7e9/fcimb-08-00384-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7e9/6218566/e5face52d184/fcimb-08-00384-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7e9/6218566/8e479ed83044/fcimb-08-00384-g0007.jpg
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