Clostridium difficile is a Gram-positive spore-forming bacterium. Gut colonization is associated with a wide spectrum of gastrointestinal diseases, ranging from mild to severe, acute to persistent. Bacterial survival and multiplication are essential processes dependent in the maintenance of homeostasis, which is, in turn, inherently dependent on the integrity of the cell wall. Bacteria present different mechanisms to maintain cell wall integrity, particularly, to protect it from direct contact with the external environment, such as phosphate polymers, capsule, outer membrane and S-layer. The S-layer is an evolutionary conserved macromolecule present in almost all bacterial types, however its role(s) remain(s) to be clarified. The S-layer is ubiquitous in C. difficile strains and is comprised of a conserved and a variable region that confers strain specificity and faces the external environment. In C. difficile FM2.5 strain, the absence of S-layer resulted in impaired pathogenicity. Gut colonization of FM2.5 infected mice was significantly lower than mice infected with the wild-type strain R20291. In addition, FM2.5 showed compromised toxin activity and in vitromotility. Accordingly, FM2.5 failed to cause disease in mice and trigger a strong inflammatory response, contrary to mice infected with R20291. Reversion of the S-layer gene restored motility, toxin activity and the abilities to colonize and cause disease. It appears that the S-layer plays a crucial role in various bacterial processes, hence FM2.5 loss of virulence may be due both to the absence of S-layer at the cell surface and its role in other processes that aid to bacterial virulence.


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