Clostridium difficile in one of the most commonly reported nosocomial pathogens worldwide. Beyond antibiotic use, little is known about the host, microbiota, and environmental factors that contribute to susceptibility to and severity of C. difficile infection (CDI). We recently observed that in a mouse model of CDI, excess dietary zinc (Zn) alters the gut microbiota and decreases resistance to CDI. Moreover, we determined that high levels of Zn exacerbate C. difficile-associated disease and calprotectin-mediated Zn limitation is an essential host response to infection. In this addendum, we discuss how these findings add to our understanding of CDI and consider the potential implications of excess metal intake on the microbiota and infection.
Keywords: Animal models of GI infection or GI-diseases with microbial components; Antibiotics in treatment of GI diseases; Clostridium; Defining/profiling gut microbiome; Host-pathogen interactions; Mechanisms of pathogenesis of gut microbes; Role of commensal flora in GI diseases; Role of gut microbiome in GI disease; calprotectin; diet; microbiome; zinc.