Coe N E, Frank D E, Wood R L, Roth J A
Physiopathology Research Unit, US Department of Agriculture, Ames, IA 50010.
Vet Immunol Immunopathol. 1992 Jun;33(1-2):37-50. doi: 10.1016/0165-2427(92)90033-m.
Salmonella typhimurium infection in swine causes an enterocolitis followed by a persistent carrier state, but little is known about the mechanisms that allow this organism to colonize and persist in host tissues. Neutrophils provide a first line of defense against invading pathogens such as Salmonella typhimurium. The purpose of this study was to evaluate porcine neutrophil function after in vivo exposure to Salmonella and to determine if the immunomodulator, bacillus Calmette Guerin (BCG), exerts any effect on neutrophil function or on the colonization and persistence of S. typhimurium in the pig. Compared to negative controls, neutrophils from pigs exposed to S. typhimurium exhibited significantly decreased iodination, cytochrome-C reduction, antibody-dependent cell-mediated cytotoxicity, random migration, and chemotaxis (P less than or equal to 0.05). Neutrophil bactericidal activity against S. typhimurium was significantly enhanced. Most of the significant differences were noted in the first two days after exposure to Salmonella. Often the functional alterations were biphasic, peaking again 7-10 days after exposure. BCG alone significantly depressed random migration and cytochrome-C reduction in unstimulated neutrophils. The clinical course, colonization pattern, and persistence of Salmonella were similar between pigs receiving BCG and untreated pigs. These data suggest that S. typhimurium infection causes a depression in oxidative metabolism and motility, yet an increase in overall bactericidal activity against S. typhimurium in circulating porcine neutrophils. It also appears that BCG treatment, as reported here, does not enhance resistance of pigs to S. typhimurium colonization or reduce the number of persistent organisms in the porcine ileum.
猪感染鼠伤寒沙门氏菌会引发小肠结肠炎,随后进入持续携带状态,但对于该菌在宿主组织中定殖和持续存在的机制,人们了解甚少。中性粒细胞是抵御鼠伤寒沙门氏菌等入侵病原体的第一道防线。本研究的目的是评估猪体内暴露于沙门氏菌后中性粒细胞的功能,并确定免疫调节剂卡介苗(BCG)是否对中性粒细胞功能或鼠伤寒沙门氏菌在猪体内的定殖和持续存在有任何影响。与阴性对照组相比,暴露于鼠伤寒沙门氏菌的猪的中性粒细胞在碘化、细胞色素C还原、抗体依赖性细胞介导的细胞毒性、随机迁移和趋化性方面均显著降低(P≤0.05)。对鼠伤寒沙门氏菌的中性粒细胞杀菌活性显著增强。大多数显著差异在暴露于沙门氏菌后的前两天被观察到。功能改变通常呈双相性,在暴露后7 - 10天再次达到峰值。单独使用卡介苗会显著降低未刺激的中性粒细胞的随机迁移和细胞色素C还原。接受卡介苗的猪和未治疗的猪在沙门氏菌的临床病程、定殖模式和持续存在情况方面相似。这些数据表明,鼠伤寒沙门氏菌感染会导致循环猪中性粒细胞的氧化代谢和运动性降低,但对鼠伤寒沙门氏菌的总体杀菌活性增加。此外,如本研究所示,卡介苗治疗似乎并未增强猪对鼠伤寒沙门氏菌定殖的抵抗力,也未减少猪回肠中持续存在的细菌数量。