PSEUDOMONAS SIDEROPHORE PYOCHELIN ENHANCES NEUTROPHIL-MEDIATED ENDOTHELIAL-CELL INJURY
PSEUDOMONAS SIDEROPHORE PYOCHELIN ENHANCES NEUTROPHIL-MEDIATED ENDOTHELIAL-CELL INJURY
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DOI：
10.1152/ajplung.1994.266.2.l192
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发表时间：
1994-02-01
影响因子：
--
通讯作者：
COX, CD
中科院分区：
文献类型：
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作者：
BRITIGAN, BE;RASMUSSEN, GT;COX, CD
绿脓杆菌 (Pyochelin) 是铜绿假单胞菌 (Pseudomonas aeruginosa) 分泌的一种铁载体，它以某种形式结合铁，可催化中性粒细胞衍生的超氧化物 (O-2(-).) 和过氧化氢 (H2O2) 形成羟基自由基 (.OH)。 铁氧螯合素 (Ferripyochelin) 会因暴露于 H2O2（一种黄嘌呤/黄嘌呤）而诱导浓度依赖性的内皮细胞损伤（Cr-51 释放）增加。氧化酶 O-2(-)./H2O2 生成系统，或刺激的中性粒细胞。这个过程取决于铁的存在。使用自旋捕获证实了 OH 的形成。尽管中性粒细胞 O-2(-) 略有增加 (13%)。观察到铁蛋白存在下的产生，但这似乎不能解释观察到的内皮细胞损伤的程度。抗氧化剂二甲硫脲和过氧化氢酶可减轻内皮细胞损伤，而二甲亚砜和超氧化物歧化酶则没有效果。 Fe-次氮基三乙酸和 Fe-EDTA 也是 OH 催化剂，不会增加因暴露于上述氧化剂系统而导致的内皮细胞损伤。与内皮细胞的结果相反，由黄嘌呤和黄嘌呤氧化酶的反应产生的O-2(-)./H2O2对铜绿假单胞菌的杀伤作用并没有被铁铁螯素增加。这些数据与假单胞菌和吞噬细胞衍生的分泌产物的相互作用可能通过引起.OH的产生而导致铜绿假单胞菌感染部位的局部组织损伤的可能性一致。
Pyochelin, a siderophore secreted by Pseudomonas aeruginosa, binds iron in a form which can catalyze the formation of hydroxyl radical (.OH) from neutrophil-derived superoxide (O-2(-).) and hydrogen peroxide (H2O2) Ferripyochelin induced a concentration-dependent increase in endothelial cell injury (Cr-51 release) resulting from exposure to H2O2, a xanthine/xanthine oxidase O-2(-)./H2O2 generating system, or stimulated neutrophils. This process was dependent on the presence of iron. Formation of OH was confirmed using spin trapping. Although a slight (13%) increase in neutrophil O-2(-). production in the presence of ferripyochelin was observed, this did not appear to account for the extent of endothelial cell injury observed. The antioxidants dimethylthiourea and catalase decreased endothelial cell injury, whereas dimethyl sulfoxide and superoxide dismutase were without effect. Fe-nitrilotriacetic acid and Fe-EDTA, which are also OH catalysts, did not augment endothelial cell injury resulting from exposure to the above oxidant systems. In contrast to results with the endothelial cells, killing of P. aeruginosa by O-2(-)./H2O2 derived from the reaction of xanthine and xanthine oxidase was not increased by ferripyochelin. These data are consistent with the possibility that the interaction of Pseudomonas- and phagocyte-derived secretory products could contribute to local tissue injury at sites of P. aeruginosa infection by causing the generation of .OH.