Why do people develop chronic inflammatory illnesses, such as inflammatory bowel disease and auto-immunity, when they are adults? Is the trigger a recent exposure or may the seeds of the problem have formed much earlier in life? What is the role of genetic susceptibility in such processes?
In this issue of Mucosal Immunology, Goethel et al. (Mucosal Immunol. 1, 2019) developed an experimental system in mice to provide at least partial answers to these important questions, in a model relevant to inflammatory bowel disease (IBD). To examine the role of host genotype, they compared wild type C57BL/6 mice with their congenic NOD2 knockouts, focusing on an important innate immunity gene related to detection of bacterial derived ligands and regulation of inflammatory immune responses (Gut Microbes 4:222–231, 2013). To examine the role of the microbiota, mice were exposed, or not, to amoxicillin, an antibiotic with broad-spectrum activity against the normal constituents of the mammalian intestinal microbiome. Further, to examine developmental phenomena related to host age, mice were exposed either during early life or as adults.
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The authors declare no competing interests.
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