Austin J W, Sanders G, Kay W W, Collinson S K
Bureau of Microbial Hazards, Health Protection Branch, Health Canada, Ottawa, Ont., Canada.
FEMS Microbiol Lett. 1998 May 15;162(2):295-301. doi: 10.1111/j.1574-6968.1998.tb13012.x.
Salmonella enteritidis enteropathogens produce a variety of potentially adherent fimbrial types including SEF14, SEF17, SEF18 and SEF21 (type I). In a simplified, pure culture, biofilm generating system the virulent isolate, S. enteritidis 3b, readily adhered to Teflon (polytetrafluoroethylene) and stainless steel forming thick cell aggregates. The inability of an isogenic SEF17-deficient mutant to form thick biofilms suggested a role for SEF17 in stabilizing cell-cell interactions during biofilm formation. Epifluorescent detection of SEF17 in biofilms confirmed the association of these fimbriae with aggregated cells but not with adherent mutants unable to produce SEF17. The reduced adherence observed with an isogenic SEF14/SEF21-deficient strain implicated the involvement of additional cell surface adherence factors, possibly including SEF21 (type I) fimbriae in the adherence of S. enteritidis to stainless steel or Teflon. The role of SEF17 fimbriae in biofilm formation and the contributions of SEF17 to the persistence of Salmonellae on surfaces and in food are discussed.
肠炎沙门氏菌肠道病原体可产生多种潜在的黏附菌毛类型，包括SEF14、SEF17、SEF18和SEF21（I型）。在一个简化的纯培养生物膜生成系统中，强毒株肠炎沙门氏菌3b很容易黏附在聚四氟乙烯（特氟龙）和不锈钢上，形成厚厚的细胞聚集体。同基因SEF17缺陷型突变体无法形成厚厚的生物膜，这表明SEF17在生物膜形成过程中稳定细胞间相互作用方面发挥作用。对生物膜中SEF17的落射荧光检测证实了这些菌毛与聚集细胞的关联，但与无法产生SEF17的黏附突变体无关。同基因SEF14/SEF21缺陷型菌株观察到的黏附力降低表明，可能还有其他细胞表面黏附因子参与其中，可能包括SEF21（I型）菌毛在肠炎沙门氏菌黏附不锈钢或特氟龙过程中的作用。本文讨论了SEF17菌毛在生物膜形成中的作用以及SEF17对沙门氏菌在表面和食物中持久性的贡献。
