Department of Biochemistry and Molecular Biology, Faculty of Veterinary Medicine, Wroclaw University of Environmental and Life Sciences, Wroclaw, Poland.
Department of Biochemistry and Molecular Biology, Faculty of Veterinary Medicine, Wroclaw University of Environmental and Life Sciences, Wroclaw, Poland.
Poult Sci. 2023 Aug;102(8):102833. doi: 10.1016/j.psj.2023.102833. Epub 2023 Jun 3.
Significant differences in pathogenicity between Salmonella Enteritidis and Salmonella Gallinarum exist despite the fact that S. Gallinarum is a direct descendant of S. Enteritidis. It was hypothesized that such various properties may be in part the result of differences in structure and functions of type 1 fimbriae (T1Fs). In S. Enteritidis, T1Fs bind to oligomannosidic structures carried by host cell glycoproteins and are called mannose-sensitive T1Fs (MST1F). In S. Gallinarum, T1Fs lost ability to bind such carbohydrate chains, and were named mannose-resistant MRT1Fs (MRT1F). Therefore, the present study was undertaken to evaluate the role of MST1Fs and MRT1Fs in the adhesion, invasion, intracellular survival and cytotoxicity of S. Enteritidis and S. Gallinarum toward chicken intestinal CHIC8-E11cells and macrophage-like HD11 cells. Using mutant strains: S. Enteritidis fimH::kan and S. Gallinarum fimH::kan devoid of T1Fs and in vitro assays the following observations were made. MST1Fs have a significant impact on the chicken cell invasion by S. Enteritidis as MST1F-mediated adhesion facilitates direct and stable contact of bacteria with host cells, in contrast to MRT1Fs expressed by S. Gallinarum. MST1Fs as well as MRT1Fs did not affected intracellular viability of S. Enteritidis and S. Gallinarum. However, absolute numbers of intracellular viable wild-type S. Enteritidis were significantly higher than S. Enteritidis fimH::kan mutant and wild-type S. Gallinarum and S. Gallinarum fimH::kan mutant. These differences, reflecting the numbers of adherent and invading bacteria, underline the importance of MST1Fs in the pathogenicity of S. Enteritidis infections. The cytotoxicity of wild-type S. Enteritidis and its mutant devoid of MST1Fs to HD11 cells was essentially the same, despite the fact that the number of viable intracellular bacteria was significantly lower in the mutated strain. Using HD11 cells with similar number of intracellular wild-type S. Enteritidis and S. Enteritidis fimH::kan mutant, it was found that the lack of MST1Fs did not affect directly the cytotoxicity, suggesting that the increase in cytotoxicity of S. Enteritidis devoid of MST1Fs may be associated with crosstalk between T1Fs and other virulence factors.
尽管肠炎沙门氏菌是鸡白痢沙门氏菌的直接后裔，但它们在致病性方面存在显著差异。据推测，这些不同的特性可能部分是由于 1 型菌毛（T1F）结构和功能的差异所致。在肠炎沙门氏菌中，T1F 与宿主细胞糖蛋白携带的寡甘露糖结构结合，称为甘露糖敏感 T1F（MST1F）。在鸡白痢沙门氏菌中，T1F 丧失了与这种碳水化合物链结合的能力，被命名为甘露糖抗性 MRT1F（MRT1F）。因此，本研究旨在评估 MST1F 和 MRT1F 在肠炎沙门氏菌和鸡白痢沙门氏菌黏附、侵袭、细胞内存活和细胞毒性方面对鸡肠 CHIC8-E11 细胞和巨噬样 HD11 细胞的作用。使用突变株：缺乏 T1F 的肠炎沙门氏菌 fimH::kan 和鸡白痢沙门氏菌 fimH::kan 以及体外试验，观察到以下结果。MST1F 对肠炎沙门氏菌感染鸡细胞的侵袭有显著影响，因为 MST1F 介导的黏附促进了细菌与宿主细胞的直接和稳定接触，而鸡白痢沙门氏菌表达的 MRT1F 则没有。MST1F 和 MRT1F 均不影响肠炎沙门氏菌和鸡白痢沙门氏菌的细胞内活力。然而，野生型肠炎沙门氏菌的细胞内活菌数量明显高于肠炎沙门氏菌 fimH::kan 突变株和野生型鸡白痢沙门氏菌和鸡白痢沙门氏菌 fimH::kan 突变株。这些差异反映了黏附和侵袭细菌的数量，强调了 MST1F 在肠炎沙门氏菌感染发病机制中的重要性。野生型肠炎沙门氏菌及其缺乏 MST1F 的突变株对 HD11 细胞的细胞毒性基本相同，尽管突变株中细胞内活菌数量明显较低。使用具有相似数量的野生型肠炎沙门氏菌和肠炎沙门氏菌 fimH::kan 突变株的 HD11 细胞，发现缺乏 MST1F 不会直接影响细胞毒性，表明缺乏 MST1F 的肠炎沙门氏菌细胞毒性增加可能与 T1F 和其他毒力因子之间的串扰有关。
