Despite these differences in microbiota dynamics in the two organ systems, we see consistent IAV-dependent sensitization of lung and intestinal tissue to bacterial super infection. These changes are transient, independent of the virus subtype and resolve after clearance of viral infection. In contrast, we find substantial elimination of microbiota from small intestine of IAV-infected mice both by culture-dependent and culture-independent techniques. Using a combination of 16S rRNA gene NGS, 16S rRNA gene-specific qPCR, and culture of bacterial content, we demonstrate here surprisingly little effect of IAV infection on lower respiratory tract microbiota abundance and composition. Here, we used a longitudinal approach to study microbiota kinetics after IAV infections and their consequences for the host. ĭespite these rapid advances, there is little information on the impact of acute viral infection on composition, kinetics, and quantity of commensal microbiota in a given host site. Recently, chronic infectious diseases were characterized as a factor, disturbing microbiota balance. Pathological changes in microbiota composition were extensively studied in a number of chronic (inflammatory) diseases, such as asthma, COPD, cystic fibrosis, or IBD (summarized in ). For instance, both local (respiratory) and distal (gut) microbiota impact lung immune responses against IAV infection. These consequences can occur locally and systemically. Consequently, disturbance of microbial balance (dysbiosis) might have substantial consequences, e.g., for host metabolism and adaptive immune responses. Additionally, commensal microbiota were demonstrated to have an important role in the education of regulatory T cells in the intestinal tract.
They occupy ecological niches, thus posing a competitive threshold to invasion of pathogenic bacteria. In the intestine, commensal microbes are essential for the breakdown of nutritional products and key producers of essential vitamins. This is especially true with respect to causality under given pathologic conditions. Despite the vast amount of sequencing data, our understanding of the physiological function of microbiota and their dynamics is still a matter of ongoing research. With the development of culture independent next-generation sequencing (NGS) techniques and the use of axenic animal models, the field of metagenomics research underwent exponential growth. The human body hosts a substantial number of symbiotically living microorganisms on basically all surfaces, including the respiratory and the intestinal tract. However, during a short-time window, specific ecological niches might lose their microbiota shield and remain vulnerable to bacterial invasion. The transiently induced dysbiosis underlines the overall stability of microbial communities to effects of acute infection. The discrepancy of relative 16S rRNA gene next-generation sequencing (NGS) and normalized 16S rRNA gene-specific qPCR stresses the importance of combining qualitative and quantitative approaches to correctly analyze composition of organ associated microbial communities. We show for the first time the consequences of IAV infection for lower respiratory tract and intestinal microbiobiota in a qualitative and quantitative fashion. As a functional consequence of IAV-mediated microbiota depletion, we demonstrated that the small intestine is rendered more susceptible to bacterial pathogen invasion, in a Salmonella typhimurium super infection model. In contrast, in the intestine, IAV induced robust depletion of bacterial content, disruption of mucus layer integrity, and higher levels of antimicrobial peptides in Paneth cells. No quantitative impact on bacterial colonization after IAV infection was detectable, despite a robust antimicrobial host response and increased sensitivity to bacterial super infection. In the lower respiratory tract, we observed only minor qualitative changes in microbiota composition. Using a combination of 16S rRNA gene-specific next generation sequencing and qPCR as well as culturing of bacterial organ content, we found body site-specific and transient microbiota responses. Here, we show dynamic changes in respiratory and intestinal microbiota over the course of a sublethal IAV infection in a mouse model. Influenza A viruses (IAV) are common respiratory pathogens causing acute infections. The impact of viral infections on host microbiota composition and dynamics is poorly understood. Importantly, commensal microbiota provide a shield against invading bacterial pathogens, probably by direct competition. Consequently, disruption of microbiota homeostasis correlates with a variety of pathological states. Microbiota integrity is essential for a growing number of physiological processes.