A fibronectin-binding protein (FbpA) of Weissella cibaria inhibits colonization and infection of Staphylococcus aureus in mammary glands
A fibronectin-binding protein (FbpA) of Weissella cibaria inhibits colonization and infection of Staphylococcus aureus in mammary glands
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DOI：
10.1111/cmi.12731
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发表时间：
2017-08-01
影响因子：
3.4
通讯作者：
Zhao, Xin
中科院分区：
文献类型：
--
作者：
Wang, Liangliang;Si, Wei;Zhao, Xin
金黄色葡萄球菌(S.aureus)是人类和动物感染的常见原因。众所周知，益生菌可以抑制病原体在宿主组织上的定植。然而，由于复杂的宿主-微生物和微生物-微生物相互作用，抑制作用的机制仍然不清楚。在这里，我们表明，金黄色葡萄球菌感染乳腺的能力在魏氏杆菌(W.cibaria)存在的情况下降低与其对乳腺上皮细胞的粘附性差有关。这种抑制作用至少部分归因于乳酸菌上的纤维连接蛋白结合蛋白(FbpA)。3株含有fbpA基因的炭疽菌比其他3株不含fbpA基因的乳酸菌具有更强的抑制能力。炭疽菌分离株LW1的fbpA缺失突变体LW1fbpA失去了减少金黄色葡萄球菌与乳腺上皮细胞黏附的抑制活性，并不能减少金黄色葡萄球菌在乳腺中的定植。FbpA在LW1fbpA表面的表达逆转了其抑制活性。此外，加入纯化的FbpA可抑制金黄色葡萄球菌生物被膜的形成。我们的结果表明，金黄色葡萄球菌FbpA通过干扰纤维连接蛋白结合蛋白介导的金黄色葡萄球菌侵袭途径，抑制金黄色葡萄球菌生物膜的形成，从而抑制金黄色葡萄球菌的定植和感染。
Staphylococcus aureus (S.aureus) is a frequent cause of infections in both humans and animals. Probiotics are known to inhibit colonization of pathogens on host tissues. However, mechanisms for the inhibition are still elusive due to complex host-microbe and microbe-microbe interactions. Here, we show that reduced abilities of S.aureus to infect mammary glands in the presence of Weissella cibaria (W.cibaria) were correlated with its poor adherence to mammary epithelial cells. Such inhibition by W.cibaria isolates was at least partially attributed to a fibronectin-binding protein (FbpA) on this lactic acid bacterium. Three W.cibaria isolates containing fbpA had higher inhibitory abilities than other three LAB isolates without the gene. The fbpA-deficient mutant of W.cibaria isolate LW1, LW1fbpA, lost the inhibitory activity to reduce the adhesion of S.aureus to mammary epithelial cells and was less able to reduce the colonization of S.aureus in mammary glands. Expression of FbpA to the surface of LW1fbpA reversed its inhibitory activities. Furthermore, addition of purified FbpA inhibited S.aureus biofilm formation. Our results suggest that W.cibaria FbpA hinders S.aureus colonization and infection through interfering with the S.aureus invasion pathway mediated by fibronectin-binding proteins and inhibiting biofilm formation of S.aureus.