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人类腹腔感染的局部炎症反应:细胞因子、巨噬细胞和其他白细胞的调节作用。

The local inflammatory responses to infection of the peritoneal cavity in humans: their regulation by cytokines, macrophages, and other leukocytes.

机构信息

Department of Internal Medicine, Erasmus Medical Center, Centrumlocatie, P.O. Box 2040, 3000 CA Rotterdam, The Netherlands.

出版信息

Mediators Inflamm. 2012;2012:976241. doi: 10.1155/2012/976241. Epub 2012 Feb 26.

DOI:10.1155/2012/976241
PMID:22481867
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3317024/
Abstract

Studies on infection-induced inflammatory reactions in humans rely largely on findings in the blood compartment. Peritoneal leukocytes from patients treated with peritoneal dialysis offer a unique opportunity to study in humans the inflammatory responses taking place at the site of infection. Compared with peritoneal macrophages (pMϕ) from uninfected patients, pMϕ from infected patients display ex vivo an upregulation and downregulation of proinflammatory and anti-inflammatory mediators, respectively. Pro-IL-1β processing and secretion rather than synthesis proves to be increased in pMϕ from infectious peritonitis suggesting up-regulation of caspase-1 in vivo. A crosstalk between pMϕ, γδ T cells, and neutrophils has been found to be involved in augmented TNFα expression and production during infection. The recent finding in experimental studies that alternatively activated macrophages (Mϕ2) increase by proliferation rather than recruitment may have significant implications for the understanding and treatment of chronic inflammatory conditions such as encapsulating peritoneal sclerosis (EPS).

摘要

人体感染引起的炎症反应研究主要依赖于血液组分的发现。腹膜透析患者的腹膜白细胞为研究感染部位炎症反应提供了一个独特的机会。与未感染患者的腹膜巨噬细胞(pMϕ)相比,感染患者的 pMϕ分别表现出促炎和抗炎介质的上调和下调。体外研究表明,感染性腹膜炎患者的 pMϕ中 pro-IL-1β 的加工和分泌而非合成增加,提示体内 caspase-1 的上调。已经发现 pMϕ、γδ T 细胞和中性粒细胞之间的串扰参与了感染期间 TNFα 表达和产生的增加。在实验研究中最近发现,增殖而不是募集会增加选择性激活的巨噬细胞(Mϕ2),这对于理解和治疗慢性炎症性疾病如包裹性腹膜硬化症(EPS)可能具有重要意义。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c903/3317024/445b496c503a/MI2012-976241.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c903/3317024/48a6652981c8/MI2012-976241.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c903/3317024/39403f94dec1/MI2012-976241.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c903/3317024/445b496c503a/MI2012-976241.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c903/3317024/48a6652981c8/MI2012-976241.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c903/3317024/39403f94dec1/MI2012-976241.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c903/3317024/445b496c503a/MI2012-976241.003.jpg

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