Nod1 and Nod2 signaling does not alter the composition of intestinal bacterial communities at homeostasis

• DOI: 10.4161/gmic.24373
• Publication Date: 2013-04-02T22:20:40Z
• Authors: Susan J. Robertson; Jun Yu Zhou; Kaoru Geddes; Stephen J. Rubino; Joon Ho Cho; Stephen E. Girardin; Dana J. Philpott
• Keywords: Dysbiosis; NOD1; Cecum

Patients with inflammatory bowel diseases (IBD) harbour intestinal bacterial communities altered composition compared healthy counterparts; however, it is unknown whether changes in the microbiota are associated genetic susceptibility of individuals for developing disease or instead reflect other environment related to itself. Since deficiencies innate immune receptors Nod1 and Nod2 linked IBD, we tested hypothesis that Nod-signaling alters profiles subsequently community structure. We used qPCR analyze expression patterns selected mediators ileum cecum Nod-deficient mice their Nod-sufficient littermates assessed relative abundance major groups sampled from ileum, colon. The Nod1-deficient exhibited significantly lower Nod2, Muc2, α- β-defensins keratinocyte-derived chemokine (KC), suggesting a weakened epithelial barrier WT littermates; there were no significant differences targeted groups, indicating Nod1-associated alone do not promote dysbiosis. Furthermore, Nod2-deficient did display any markers communities. Shifts observed this study correlated housing conditions independent genotype. These findings emphasize importance using F2 littermate controls minimize environmental sources variation microbial analyses, establish baseline host-microbe homeostasis strengthen models testing factors contributing dysbiosis IBD.