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在异辛烷诱导的炎症中白细胞向脾脏和腹腔募集的调节。

Regulation of Leukocyte Recruitment to the Spleen and Peritoneal Cavity during Pristane-Induced Inflammation.

机构信息

Department of Basic Medicine, Haihe Clinical College of Tianjin Medical University, Tianjin, China.

Key Research Laboratory for Infectious Disease Prevention for State Administration of Traditional Chinese Medicine, Tianjin Institute of Respiratory Diseases, Tianjin Haihe Hospital, Tianjin 300350, China.

出版信息

J Immunol Res. 2017;2017:9891348. doi: 10.1155/2017/9891348. Epub 2017 Oct 19.

Abstract

Chronic inflammation is associated with an increased number of leukocytes in the spleen, which are then redirected to the site of inflammation. However, it remains unknown how leukocyte recruitment is regulated. Herein, chronic inflammation was induced by intraperitoneal injection of pristane into mice. Leukocytes in the spleen or in the peritoneal cavity were quantified by flow cytometry. We found that the loss of IL-6 decreased macrophage recruitment to the spleen and the peritoneal cavity during pristane-induced inflammation. The loss of TNF delayed the recruitment of neutrophils and macrophages to the spleen and inhibited the recruitment of neutrophils, macrophages, B cells, and T cells. The recruitment of neutrophils and macrophages into the spleen or peritoneal cavity was largely inhibited in the absence of LT. The loss of TNF receptor 1/2 resulted in reduced recruitment of neutrophils, macrophages, and dendritic cells into the spleen, but only neutrophil recruitment was inhibited in the peritoneal cavity. Similarly, a lack of B cells significantly impeded the recruitment of neutrophils, macrophages, and dendritic cells to the spleen. However, only macrophage recruitment was inhibited in the absence of T cells in the spleen. These data provide insight into the development of chronic inflammation induced by noninfectious substances.

摘要

慢性炎症与脾脏中白细胞数量的增加有关,这些白细胞随后被重新定向到炎症部位。然而,白细胞募集的调节机制尚不清楚。在此,通过向小鼠腹腔内注射降植烷来诱导慢性炎症。通过流式细胞术定量分析脾脏或腹腔中的白细胞。我们发现,IL-6 的缺失减少了巨噬细胞向降植烷诱导的炎症的脾脏和腹腔的募集。TNF 的缺失延迟了中性粒细胞和巨噬细胞向脾脏的募集,并抑制了中性粒细胞、巨噬细胞、B 细胞和 T 细胞的募集。在缺乏 LT 的情况下,中性粒细胞和巨噬细胞向脾脏或腹腔的募集受到了极大的抑制。TNF 受体 1/2 的缺失导致中性粒细胞、巨噬细胞和树突状细胞向脾脏的募集减少,但仅在腹腔中抑制中性粒细胞的募集。同样,B 细胞的缺失显著阻碍了中性粒细胞、巨噬细胞和树突状细胞向脾脏的募集。然而,仅在脾脏中缺乏 T 细胞时才抑制巨噬细胞的募集。这些数据为非传染性物质引起的慢性炎症的发展提供了深入了解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b420/5671734/405d2f2e9fc6/JIR2017-9891348.001.jpg

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