Nevola J J, Laux D C, Cohen P S
Department of Microbiology, University of Rhode Island, Kingston 02881.
Infect Immun. 1987 Dec;55(12):2884-90. doi: 10.1128/iai.55.12.2884-2890.1987.
The relative abilities of an avirulent Salmonella typhimurium strain with wild-type lipopolysaccharide (LPS) character, SL5319, and a nearly isogenic LPS-deficient mutant, SL5325, to colonize the large intestines of streptomycin-treated CD-1 mice in vivo and to penetrate colonic mucus in vitro were studied. Previously it had been shown that, when fed simultaneously to streptomycin-treated mice (approximately 10(10) CFU each), the S. typhimurium strain with wild-type LPS colonized at 10(8) CFU/g of feces indefinitely, whereas the LPS-deficient mutant dropped within 3 days to a level of only 10(4) CFU/g of feces. In the present investigation, when SL5325 was allowed to colonize for 8 days before feeding mice SL5319 or when it was fed to mice simultaneously with an Escherichia coli strain of human fecal origin (10(10) CFU each), both strains colonized indefinitely at 10(7) CFU/g of feces. Moreover, when the wild-type and LPS-deficient mutant strains were fed to mice simultaneously in low numbers (approximately 10(5) CFU each) the strains survived equally well in the large intestines for 8 days, after which the LPS-deficient mutant was eliminated (less than 10(2) CFU/g of feces), whereas the wild-type colonized at a level of 10(7) CFU/g of feces. In addition although both strains were able to adhere to mucus and epithelial cell preparations in vitro, the wild-type strain was shown to have greater motility and chemotactic activity on CD-1 mouse colonic mucus in vitro and to more rapidly penetrate and form a stable association with immobilized colonic mucosal components in vitro. Based on these data, we suggest that the ability of an S. typhimurium strain to colonize the streptomycin-treated mouse large intestine may, in part, depend on its ability to penetrate deeply into the mucus layer on the intestinal wall and subsequently, through growth, colonize the mucosa.
研究了具有野生型脂多糖（LPS）特性的无毒鼠伤寒沙门氏菌菌株SL5319和近乎同基因的LPS缺陷突变体SL5325在体内定殖于经链霉素处理的CD-1小鼠大肠以及在体外穿透结肠黏液的相对能力。此前已表明，当同时给经链霉素处理的小鼠喂食（每种约10¹⁰CFU）时，具有野生型LPS的鼠伤寒沙门氏菌菌株以10⁸CFU/g粪便的数量无限期定殖，而LPS缺陷突变体在3天内降至仅10⁴CFU/g粪便的水平。在本研究中，当允许SL5325定殖8天后再给小鼠喂食SL5319，或者当它与源自人类粪便的大肠杆菌菌株（每种10¹⁰CFU）同时给小鼠喂食时，两种菌株均以10⁷CFU/g粪便的数量无限期定殖。此外，当野生型和LPS缺陷突变体菌株以少量（每种约10⁵CFU）同时给小鼠喂食时，这些菌株在大肠中存活8天的情况相同，此后LPS缺陷突变体被清除（低于10²CFU/g粪便），而野生型以10⁷CFU/g粪便的水平定殖。另外，尽管两种菌株在体外均能黏附于黏液和上皮细胞制剂，但野生型菌株在体外对CD-1小鼠结肠黏液具有更大的运动性和趋化活性，并且能更快地穿透并与固定的结肠黏膜成分在体外形成稳定的结合。基于这些数据，我们认为鼠伤寒沙门氏菌菌株定殖于经链霉素处理的小鼠大肠的能力可能部分取决于其深入穿透肠壁黏液层并随后通过生长定殖于黏膜的能力。
