The gut microbiota confers resistance against Salmonella Typhimurium in the German cockroach vector via key indicator species, contributing to variation in infection outcome

The microbiome is increasingly appreciated as a foundation for systemic organismal health. The German cockroach (Blattella germanica) is no exception, with a vastly expanded and more complex microbiome than the average insect. With the potential for these ubiquitous synanthropic pests to harbor and spread human pathogens, it is essential to better understand the roles their microbiota play in acquisition, maintenance, and transmission of human disease elements. Towards this end, we conducted various experiments to investigate the impact of the German cockroach microbiome on Salmonella Typhimurium infection outcome. We found that the German cockroach microbiota is protective against infection with Salmonella. This is evident from gnotobiotic infection experiments where individuals lacking a microbiota had significantly higher rates and levels of infection than colony controls. Interestingly, this dynamic is not wholly resultant from direct commensal competition, as in-vitro growth assays revealed no significant differences between levels of Salmonella grown in cockroach feces-rich media and those grown in feces-rich media filtered for microbes. However, we found significantly increased antimicrobial peptide (AMP) gut expression in infected controls vs. gnotobiotics. Furthermore, relative abundances of German cockroach microbial constituents are not sufficient indicators of Salmonella infection outcome. Rather, key indicator species are significantly associated with a particular infection outcome. Therefore, immune modulation or priming by specific microbiota elements may contribute to differences in Salmonella susceptibility between control cockroaches and gnotobiotics as well as variation in overall control colony susceptibility. These findings demand further investigation into the German cockroach microbiome and its effects on vector potential.