‘Re‐Wilding’ an Animal Model With Microbiota Shifts Immunity and Stress Gene Expression During Infection

This is the authors' abstract. We don't add key points for this paper.

The frequency of emerging disease is growing with ongoing human activity facilitating new host-pathogen interactions. Novel infection outcomes can also be shaped by the host microbiota. Caenorhabditis elegans nematodes experimentally colonised by a wild microbiota community and infected by the widespread animal pathogen, Staphylococcus aureus, have been shown to suffer higher mortality than those infected by the pathogen alone. Understanding the host responses to such microbiota-pathogen ecological interactions is key to pinpointing the mechanism underlying severe infection outcomes. We conducted transcriptomic analyses of C. elegans colonised by its native microbiota, S. aureus and both in combination. Correlations between altered collagen gene expression and heightened mortality in co-colonised hosts suggest the microbiota modified host resistance to infection. Furthermore, microbiota colonised hosts showed increased expression of immunity genes and variable expression of stress response genes during infection. Changes in host immunity and stress response could encompass both causes and effects of severe infection outcomes. 'Re-wilding' this model nematode host with its native microbiota indicated that typically commensal microbes can mediate molecular changes in the host that are costly when challenged by a novel emerging pathogen.