Maruo K, Akaike T, Ono T, Maeda H
Department of Dermatology, Kumamoto University School of Medicine, Japan.
Infect Immun. 1998 Feb;66(2):866-9. doi: 10.1128/IAI.66.2.866-869.1998.
Involvement of bradykinin generation in bacterial invasion was examined by using a gram-negative bacillus, Vibrio vulnificus, which is known to invade the blood circulatory system and cause septicemia. V. vulnificus was injected intraperitoneally (i.p.) into mice with or without bradykinin or a bradykinin (B2 receptor) antagonist. Dissemination of V. vulnificus from peritoneal septic foci to the circulating blood was assessed by counting of viable bacteria in venous blood by use of the colony-forming assay. Intravascular dissemination of V. vulnificus in mice was significantly potentiated by simultaneous injection with bradykinin but was markedly reduced by coadministration with the B2 antagonist D-Arg,[Hyp3, Thi(5,8), D-Phe7]-bradykinin. Furthermore, V. vulnificus lethality was significantly increased when bradykinin was administered simultaneously with the bacillus, whereas it was definitely suppressed by treatment with D-Arg,[Hyp3, Thi(5,8), D-Phe7]-bradykinin. Similarly, ovomacroglobulin, a potent inhibitor of the V. vulnificus protease, showed a strong suppressive effect on the V. vulnificus septicemia. We also confirmed appreciable bradykinin production in the primary septic foci in the mouse peritoneal cavity after i.p. inoculation with V. vulnificus. It is thus concluded that bradykinin generation in infectious foci is critically involved in facilitation of intravascular dissemination of V. vulnificus.
利用革兰氏阴性杆菌创伤弧菌（已知其可侵入血液循环系统并导致败血症），研究缓激肽生成在细菌侵袭中的作用。将创伤弧菌腹腔注射到注射或未注射缓激肽或缓激肽（B2受体）拮抗剂的小鼠体内。通过使用菌落形成试验对静脉血中的活菌进行计数，评估创伤弧菌从腹膜感染灶向循环血液中的扩散情况。与缓激肽同时注射可显著增强创伤弧菌在小鼠体内的血管内扩散，但与B2拮抗剂D-Arg，[Hyp3，Thi(5,8)，D-Phe7]-缓激肽共同给药则可显著降低扩散。此外，当缓激肽与该细菌同时给药时，创伤弧菌的致死率显著增加，而用D-Arg，[Hyp3，Thi(5,8)，D-Phe7]-缓激肽治疗则可明显抑制致死率。同样，卵巨球蛋白是创伤弧菌蛋白酶的有效抑制剂，对创伤弧菌败血症有很强的抑制作用。我们还证实，腹腔接种创伤弧菌后，小鼠腹腔原发性感染灶中有明显的缓激肽产生。因此得出结论，感染灶中缓激肽的生成在促进创伤弧菌的血管内扩散中起关键作用。
