Mucin Dynamics in Intestinal Bacterial Infection |
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| Authors: | Sara K Lindén Timothy H J Florin Michael A McGuckin |
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| Institution: | 1. Mucosal Diseases Program, Mater Medical Research Institute, Mater Health Services, South Brisbane, Queensland, Australia.; 2. Mucosal Immunobiology and Vaccine Center, Sahlgrenska Academy, Gothenburg University, Gothenburg, Sweden.; 3. Department of Medicine, University of Queensland, Brisbane, Queensland, Australia.;University of Cambridge, United Kingdom |
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| Abstract: | BackgroundBacterial gastroenteritis causes morbidity and mortality in humans worldwide. Murine Citrobacter rodentium infection is a model for gastroenteritis caused by the human pathogens enteropathogenic Escherichia coli and enterohaemorrhagic E. coli. Mucin glycoproteins are the main component of the first barrier that bacteria encounter in the intestinal tract.Methodology/Principal FindingsUsing Immunohistochemistry, we investigated intestinal expression of mucins (Alcian blue/PAS, Muc1, Muc2, Muc4, Muc5AC, Muc13 and Muc3/17) in healthy and C. rodentium infected mice. The majority of the C. rodentium infected mice developed systemic infection and colitis in the mid and distal colon by day 12. C. rodentium bound to the major secreted mucin, Muc2, in vitro, and high numbers of bacteria were found in secreted MUC2 in infected animals in vivo, indicating that mucins may limit bacterial access to the epithelial surface. In the small intestine, caecum and proximal colon, the mucin expression was similar in infected and non-infected animals. In the distal colonic epithelium, all secreted and cell surface mucins decreased with the exception of the Muc1 cell surface mucin which increased after infection (p<0.05). Similarly, during human infection Salmonella St Paul, Campylobacter jejuni and Clostridium difficile induced MUC1 in the colon.ConclusionMajor changes in both the cell-surface and secreted mucins occur in response to intestinal infection. |
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