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The mammalian gut is the largest organ of adaptive immune responses with a total surface area of 300 m2 of the gut epithelium. The intestinal mucosa contains at least 80% of the body’s activated B cells [1]. The adaptive immune responses mainly consist of secretory immunoglobulin A (IgA) antibodies produced by B cells which have converted to plasma cells in the gut submucosa [2,3]. The bacteria present in the gut are mainly Proteobacteria, Bacteriodetes, Firmicutis, and Actinobacteria (>90%) [4], mostly located in the colon. The total number of gut bacteria has been estimated to be 1014 [4]. They are either commensal or symbiotic, sometimes pathogenic. Besides bacteria, various viruses, fungi, protozoa and helminths can populate the gut, often as pathogens. A disturbance of the gut microbiota accompanied by illness is defined as dysbiosis [5]. The residual and potentially pathogenic gut microbiomes have attracted much attention recently, since their composition was shown to be temporarily correlated with changes in mucosal and systemic immune responses [6]. Animal models have played a major role in elucidating microbiome-host relationships and in improving a mechanistic understanding of gut microbehost relationship [5]. However, there are still gaps in the knowledge of the molecular mechanisms underlying the interactions of the gut microbiome with host functions such as immune responsiveness, and with enteric and extra-intestinal disease development [6]. Here, new data on the bacterial microbiome will be reviewed, which were obtained with the aim to identify and analyse such causal relationships. Abstract

The Mammalian Gut Microbiome, Immune Responses and Disease: From Observational to Causal Relationships