IMMUNOREGULATION BY MACROPHAGES III PROSTAGLANDIN-E SUPPRESSES LYMPHOCYTE-ACTIVATION BUT NOT MACROPHAGE EFFECTOR FUNCTION DURING SALMONELLA-ENTERITIDIS INFECTION
IMMUNOREGULATION BY MACROPHAGES III PROSTAGLANDIN-E SUPPRESSES LYMPHOCYTE-ACTIVATION BUT NOT MACROPHAGE EFFECTOR FUNCTION DURING SALMONELLA-ENTERITIDIS INFECTION
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DOI：
10.1016/0192-0561(84)90029-8
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发表时间：
1984-01-01
期刊：
影响因子：
--
通讯作者：
HOPPER, KE
中科院分区：
文献类型：
--
作者：
CAHILL, J;HOPPER, KE
腹腔巨噬细胞在原发性或继发性感染与S。前列腺素E（PGE）和白细胞介素1（IL 1）的分泌能力，并在体外具有杀菌和杀肿瘤活性的亚群的比例不同。用吲哚美辛和前列腺素E分别在体内和体外研究了炎症反应中前列腺素E对淋巴细胞和巨噬细胞亚群的调节作用。吲哚美辛治疗促进了沙门氏菌的清除，并且在原发性和继发性感染动物中从腹腔中回收的巨噬细胞增加了50-90%。在体外阻断巨噬细胞分泌PGE的能力的同时，吲哚美辛治疗并没有改变它们的杀菌（或杀肿瘤）活性，也没有改变它们对PGE 2的cAMP反应。吲哚美辛在体内和PGE 2在体外的主要作用是对IL 1和IL 2的产生和表达。吲哚美辛处理的小鼠在体外巨噬细胞分泌IL 1大大增强，并在体外被PGE 2抑制。PGE_2还抑制IL-1依赖的T淋巴细胞分化。IL 2分泌和IL 2依赖性胚细胞体外增殖和细胞对PGE 2抑制的敏感性通过该反应序列增加。在原发性或继发性感染期间间隔收获的淋巴细胞群体在体外对PGE 2和IL 2分泌的cAMP反应不同。这可能与具有Lyt 1+标志物的淋巴细胞亚群的比例变化有关。显然，沙门氏菌感染小鼠的腹腔巨噬细胞分泌PGE和IL 1的能力不同。淋巴细胞功能的抑制或增强程度取决于分泌PGE和IL 1的巨噬细胞亚群和对PGE敏感的淋巴细胞亚群的比例。淋巴因子产生的变化可能反过来改变效应巨噬细胞的募集和功能。
Peritoneal macrophages obtained during primary or secondary infection with S. enteritidis differ in the proportions of subpopulations with the capacity to secrete prostaglandin E (PGE) and interleukin 1 (IL1) and have bactericidal and tumoricidal activities in vitro. Using indomethacin in vivo and PGE in vitro the regulation of subpopulations of lymphocytes and macrophages by PGE during the inflammatory reaction was studied. Indomethacin treatment promoted clearance of the Salmonella and a 50-90% increase in macrophages recovered from the peritoneal cavity in both primary and secondary infected animals. While blocking the capacity of macrophages to secrete PGE in vitro the indomethacin treatment did not alter their bactericidal (or tumoricidal) activity nor their cAMP response to PGE2. A major effect of indomethacin in vivo and of PGE2 in vitro was on the production and expression of IL1 and IL2. Secretion of IL1 by macrophages in vitro was greatly enhanced in indomethacin treated mice and was suppressed in vitro by PGE2. PGE2 also inhibited IL1 dependent T-lymphocyte differentiation. IL2 secretion and IL2 dependent blast cell proliferation in vitro and sensitivity of the cells to PGE2 inhibition increased through this sequence of reactions. Lymphocyte populations harvested at intervals during primary or secondary infection differed in their cAMP response to PGE2 and IL2 secretion in vitro. This may be related to changes in the proportions of lymphocyte subsets having Lyt 1+ markers. Evidently, peritoneal macrophages from Salmonella infected mice differ in their capacity to secrete PGE and IL1. The degree of inhibition or enhancement of lymphocyte functions would depend on the proportion of the subpopulations of macrophages secreting PGE and IL1 and of lymphocytes sensitive to PGE. The resulting changes in the production of lymphokines may, in turn, alter the recruitment and function of effector macrophages.