Metabolic and innate immune response pathways are evolutionarily conserved throughout species and are fundamental to survival. As a result, metabolic regulation and immune responses are intimately integrated and the proper function of each is dependent on the other. In recent decades, the prevalence of obesity has reached epidemic proportions in Western societies; moreover, chronic inflammation is now recognized as a central characteristic of obesity and the associated health complications. However, the endogenous and environmental cues that drive inflammation in the context of nutritional surplus and the metabolic pathways that support adequate immune responses are not understood.
We recently reported that the expansion of an aberrant microbiota in inflammasome-deficient mice has profound deleterious effects on fatty liver disease progression and obesity (Henao-Mejia et al., Nature. 2012). Moreover, it is increasingly evident that the interactions between the microbiota and the innate immune system are critical for the development and progression of chronic metabolic diseases.
We seek to further elucidate the specific metabolic and microbial signals that activate the immune system during obesity. Moreover, we think that understanding the complex interactions between microbial-derived metabolites and the immune system will soon change our view of host-commensal interactions.
© 2020 by HENAO-MEJÍA LAB.