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The mosquito microbiota impacts the physiology of its host and is essential for normal larval development, thereby influencing transmission of vector-borne pathogens. Germ-free mosquitoes generated with current methods show larval stunting and developmental deficits. Therefore, functional studies of the mosquito microbiota have so far mostly been limited to antibiotic treatments of emerging adults. In this study, we developed a novel approach to produce germ-free Aedes aegypti . It is based on reversible colonisation with bacteria genetically modified to allow complete decolonisation at the end of larval development. We show that, unlike germ-free mosquitoes produced using sterile diets, reversibly-colonised mosquitoes showed no developmental retardation and reached the same size as control mosquitoes. This allowed us to study the role of bacteria during larval development by inducing decolonisation at the beginning of the third larval instar. Based on a transcriptome analysis and diet supplementation experiments, we propose that bacteria support larval development by contributing to folate biosynthesis and by enhancing energy storage. Overall, this study provides a new tool to study the microbiota in insects and deepens our knowledge on the metabolic contribution of bacteria to mosquito development.

Infections after surgical interventions are assumed to be caused by contamination. We show by analyzing multicentric data of 6561 patients that surgical infections as well as sepsis had a predominantly enteric microbial signature irrespective of the type of surgery, suggesting failure of intestinal bacterial compartmentalization. In mice, we reveal that hepatic surgery induced dysregulation of intestinal and hepatic type 3 innate lymphoid cells (ILC3s) and intestinal leakage resulting in enteric bacterial translocation via lymphatic vessels. In the absence of hepatic ILC3s, inflammasome activation and the induction of antimicrobial peptide encoding genes, bacteria colonized remote systemic organs and impaired surgical outcomes. Conversely, mammalian-microbial commensalism is required for the education of host immunity to ensure optimal hepatic healing responses. In fact, microbial-derived products were sufficient for the induction of proliferative transcriptional networks in the mouse liver, as illustrated by serum transfer experiments, mass spectrometry and RNA expression analysis, indicating that the balanced exposure of the host to commensals is essential for recovery. This study reveals the intestinal origin of microbes causing complications after surgical interventions and highlights host protective mechanisms of controlled commensalism that prevent infections.