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首页> 外文期刊>Infection and immunity >Propionate induces polymorphonuclear leukocyte activation and inhibits formylmethionyl-leucyl-phenylalanine-stimulated activation.
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Propionate induces polymorphonuclear leukocyte activation and inhibits formylmethionyl-leucyl-phenylalanine-stimulated activation.

机译：丙酸酯诱导多形核白细胞活化，并抑制甲酰基甲硫酰基-亮氨酰-苯丙氨酸刺激的活化。

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Short-chain carboxylic acids (SCCA) are metabolic by-products of bacterial pathogens which can alter cytoplasmic pH and inhibit a variety of polymorphonuclear leukocyte (PMN) motile functions. Since cytoskeletal F-actin alterations are central to PMN mobility, in this study we examined the effects of SCCA on cytoskeletal F-actin. Initially, we tested nine SCCA (formate, acetate, propionate, butyrate, valerate, caproate, lactate, succinate, and isobutyrate). We document here that while eight altered cytoplasmic pH, only six altered cytoskeletal F-actin. We then selected one SCCA that altered both F-actin and cytoplasmic pH (propionate) and one SCCA that altered only cytoplasmic pH (lactate) for further study. Propionate, but not lactate, caused an irregular cell shape and F-actin distribution. Furthermore, propionate, but not lactate, inhibited formylmethionyl-leucyl-phenylalanine (fMLP)-stimulated PMN polarization, F-actin localization, and cytoplasmic pH oscillation. Propionate-induced changes in cytoskeletal F-actin and cytoplasmic acidification were not affected by the fMLP receptor antagonist N-t-BOC-1-methionyl-1-leucyl-1-phenylalanine; however, alkalinization was affected. Pertussis toxin treatment completely inhibited propionate-induced changes in F-actin but had no effect on propionate-induced cytoplasmic pH oscillation. These results indicate that propionate (i) bypasses the fMLP receptor and G protein(s) to induce cytoplasmic pH oscillation, (ii) operates through G protein(s) to induce actin oscillation, cell shape changes (to irregular), and F-actin localization, and (iii) inhibits fMLP-stimulated cytoplasmic pH and actin oscillation, PMN polarization, and F-actin localization.
机译：短链羧酸（SCCA）是细菌病原体的代谢副产物，可以改变细胞质pH值并抑制多种多形核白细胞（PMN）运动功能。由于细胞骨架F-肌动蛋白改变是PMN迁移的关键，因此在这项研究中，我们研究了SCCA对细胞骨架F-肌动蛋白的影响。最初，我们测试了九种SCCA（甲酸酯，乙酸酯，丙酸酯，丁酸酯，戊酸酯，己酸酯，乳酸酯，琥珀酸酯和异丁酸酯）。我们在这里记录，虽然八个改变了细胞质的pH，但只有六个改变了细胞骨架的F-肌动蛋白。然后，我们选择了一种同时改变F-肌动蛋白和细胞质pH值（丙酸）的SCCA和另一种仅改变细胞质pH值（乳酸盐）的SCCA进行进一步研究。丙酸而不是乳酸引起不规则的细胞形状和F-肌动蛋白分布。此外，丙酸而不是乳酸盐抑制甲酰基甲硫酰基-亮氨酰-苯丙氨酸（fMLP）刺激的PMN极化，F-肌动蛋白定位和细胞质pH振荡。丙酸诱导的细胞骨架肌动蛋白变化和细胞质酸化不受fMLP受体拮抗剂N-t-BOC-1-甲硫酰基-1-亮氨酰-1-苯基丙氨酸的影响。但是，碱化受到影响。百日咳毒素处理完全抑制了丙酸酯诱导的F-肌动蛋白变化，但对丙酸酯诱导的细胞质pH振荡没有影响。这些结果表明，丙酸酯（i）绕过fMLP受体和G蛋白诱导细胞质pH振荡，（ii）通过G蛋白起作用以诱导肌动蛋白振荡，细胞形状变化（变为不规则）和F-肌动蛋白定位，和（iii）抑制fMLP刺激的细胞质pH和肌动蛋白振荡，PMN极化和F-肌动蛋白定位。

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