The barrier function of the intestinal mucosa is crucial for the prevention of an invasion of bacteria of the gut microbiota into the human body. Subsequently, an intact barrier is of great importance for the prevention of permanent and chronic inflammation as a reaction to the commensal intestinal flora. The mucosal innate immune system has developed effective defense mechanisms against microbial attacks. Local inflammation that is always present to some limited extent can be regarded as one component of the mucosal defense system. Immediate recognition of bacteria by pattern recognition receptors and lysis of bacteria in (auto)phagosomes are crucial for these functions. It is obvious that the mechanisms initiating or limiting inflammation need to be tightly regulated as they themselves might alter the mechanical barrier function Nod2 variants that have been identified to be a susceptibility factor for Crohn's disease. The Nod2 protein is an intracellular sensor of the bacterial wall product muramyl dipeptide (MDP) and activates the transcription factor NF-kappaB upon MDP binding. A reduced expression of defensins (endogenous antibiotics) has been found in patients with Crohn's disease and ulcerative colitis especially when Nod2 variants are present. We particularly take an interest in manuscripts focusing on recent advances in basic mechanisms of how the bacteria contribute to mucosal inflammation as well as how bacterial induction of mucosal inflammation contributes to human disease. Papers that focus on mechanisms of tolerance induction against the commensal flora would be of great interest. In addition, signal transduction pathways induced in the mucosa by the gut microbiota should be reviewed. Microbial factors regulating experimental and human colitis should be highlighted.

Main topics include, but are not limited to:

• Regulation of colitis by bacterial DNA and bacterial wall components
• Bacteria induced apoptosis of intestinal epithelial
• Autophagy and pattern recognition receptors in mucosal inflammation
• Nod2 and bacterial recognition as a control system for mucosal inflammation
• T-bet, regulatory T-cells, and host-commensal relationships
• How bacterial induction of mucosal inflammation contributes to human disease
• Changes of the mucosa microbiota during chronic inflammation
• Defensins, bacteria, and mucosal defence in inflammatory bowel disease
• Traditional and opportunistic pathogens in inflammatory bowel disease

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