Gill Muhammad Arslan, Rafique Muhammad Wasim, Manan Talha, Slaeem Sidrah, Römling Ute, Matin Abdul, Ahmad Irfan
Institute of Biomedical and Allied Health Sciences, University of Health Sciences, Lahore, Pakistan.
Department of Microbiology, University of Health Sciences, Lahore, Pakistan.
Parasitol Res. 2018 Jul;117(7):2283-2289. doi: 10.1007/s00436-018-5917-4. Epub 2018 May 24.
Pathogenic bacteria share their natural habitat with many other organisms such as animals, plants, insects, parasites and amoeba. Interactions between these organisms influence not only the life style of the host organisms, but also modulate bacterial physiology. Adaptation can include biofilm formation, capsule formation, and production of virulence factors. Although biofilm formation is a dominant mode of bacterial life in environmental settings, its role in host-pathogen interactions is not extensively studied. In this work, we investigated the role of molecular pathways involved in rdar biofilm formation in the interaction of Salmonella typhimurium with the Acanthamoeba castellanii genotype T4. Genes coding for the rdar biofilm activator CsgD, the cellulose synthase BcsA, and curli fimbriae subunits CsgBA were deleted from the genome of S. typhimurium. Assessment of interactions of wild-type and mutant strains of S. typhimurium with A. castellanii revealed that deletion of the cellulose synthase BcsA promoted association and uptake by A. castellanii, whereas the interactions with csgD and csgBA mutants were not changed. Our findings suggest that cellulose synthase BcsA inhibits the capabilities of S. typhimurium to associate with and invade into A. castellanii.
致病细菌与其许多其他生物（如动物、植物、昆虫、寄生虫和变形虫）共享其自然栖息地。这些生物之间的相互作用不仅影响宿主生物的生活方式，还调节细菌的生理机能。适应过程可包括生物膜形成、荚膜形成以及毒力因子的产生。尽管生物膜形成是细菌在环境中主要的生存方式，但其在宿主 - 病原体相互作用中的作用尚未得到广泛研究。在这项研究中，我们调查了参与鼠伤寒沙门氏菌与卡氏棘阿米巴基因型T4相互作用的rdar生物膜形成相关分子途径的作用。编码rdar生物膜激活剂CsgD、纤维素合酶BcsA和卷曲菌毛亚基CsgBA的基因从鼠伤寒沙门氏菌基因组中被删除。对鼠伤寒沙门氏菌野生型和突变株与卡氏棘阿米巴相互作用的评估表明，纤维素合酶BcsA的缺失促进了卡氏棘阿米巴对其的黏附与摄取，而与csgD和csgBA突变株的相互作用则没有改变。我们的研究结果表明，纤维素合酶BcsA抑制了鼠伤寒沙门氏菌与卡氏棘阿米巴黏附及侵入的能力。
