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地塞米松与肠炎沙门氏菌免疫淋巴细胞因子对肠炎沙门氏菌器官侵袭及体外多形核白细胞功能的相互作用

Interaction of dexamethasone and Salmonella enteritidis immune lymphokines on Salmonella enteritidis organ invasion and in vitro polymorphonuclear leukocyte function.

作者信息

McGruder E D, Kogut M H, Corrier D E, DeLoach J R, Hargis B M

机构信息

Department of Veterinary Pathobiology, College of Veterinary Medicine, Texas Agricultural Experiment Station, Texas A and M University, College Station 77843, USA.

出版信息

FEMS Immunol Med Microbiol. 1995 Mar;11(1):25-34. doi: 10.1111/j.1574-695X.1995.tb00075.x.

DOI:10.1111/j.1574-695X.1995.tb00075.x
PMID:7599601
Abstract

We used an anti-inflammatory dose of dexamethasone (DEX) and Salmonella enteritidis (SE)-immune lymphokines (ILK) followed by oral SE challenge to chicks to determine the effects of these treatments on SE organ invasion and in vitro function of PMNs derived from peripheral blood. Endpoints included percent protection against SE organ invasion, numbers of peripheral blood PMNs, and in vitro PMN adherence, chemotaxis, and SE killing. SE organ invasion was significantly reduced in chicks treated with either ILK alone or DEX + ILK compared to controls. Chicks treated with either DEX alone or DEX + ILK responded with a significant increase in numbers of peripheral blood PMNs as compared to controls, while numbers of PMNs in the peripheral blood from chicks treated with ILK alone were not significantly increased. PMN adherence and percent SE killing by PMNs derived from chicks treated with either ILK alone or DEX + ILK were significantly increased compared to controls. Chemotaxis of PMNs derived from chicks treated with either ILK alone or DEX alone significantly increased 2-fold over control levels. Interestingly, chemotaxis of PMNs derived from chicks that received DEX + ILK was similar to controls. Generally, ILK abated the anti-inflammatory effects of DEX on PMNs in these assays, except for chemotaxis. We interpret these data to suggest that ILK may confer protection to chicks against the early phase of SE organ invasion by inducing an inflammatory response predominated by activated PMNs.

摘要

我们给雏鸡使用抗炎剂量的地塞米松(DEX)和肠炎沙门氏菌(SE)免疫淋巴细胞因子(ILK),随后进行口服SE攻毒,以确定这些处理对SE器官侵袭以及外周血来源的中性粒细胞(PMN)体外功能的影响。观察指标包括抵御SE器官侵袭的保护率、外周血PMN数量以及体外PMN的黏附、趋化和SE杀伤情况。与对照组相比,单独使用ILK或DEX + ILK处理的雏鸡中SE器官侵袭显著减少。与对照组相比,单独使用DEX或DEX + ILK处理的雏鸡外周血PMN数量显著增加,而单独使用ILK处理的雏鸡外周血PMN数量未显著增加。与对照组相比,单独使用ILK或DEX + ILK处理的雏鸡来源的PMN的黏附以及PMN对SE的杀伤率显著增加。单独使用ILK或DEX处理的雏鸡来源的PMN的趋化作用比对照水平显著增加2倍。有趣的是,接受DEX + ILK处理的雏鸡来源的PMN的趋化作用与对照组相似。一般来说,在这些试验中,除趋化作用外,ILK减轻了DEX对PMN的抗炎作用。我们对这些数据的解读是,ILK可能通过诱导以活化的PMN为主导的炎症反应,为雏鸡抵御SE器官侵袭的早期阶段提供保护。

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引用本文的文献

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Neutralization of G-CSF inhibits ILK-induced heterophil influx: granulocyte-colony stimulating factor mediates the Salmonella enteritidis-immune lymphokine potentiation of the acute avian inflammatory response.G-CSF的中和作用抑制了ILK诱导的异嗜性粒细胞流入:粒细胞集落刺激因子介导肠炎沙门氏菌-免疫淋巴因子对急性禽类炎症反应的增强作用。
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