'Re-Wilding' an Animal Model With Microbiota Shifts Immunity and Stress Gene Expression During Infection

Area of Science:

• Microbiology and Immunology
• Host-Pathogen Interactions
• Nematode Biology

Background:

• Emerging infectious diseases are increasing due to human activities promoting novel host-pathogen interactions.
• Host-associated microbial communities (microbiota) can significantly influence infection outcomes.
• The nematode Caenorhabditis elegans serves as a model organism to study host-microbe-pathogen dynamics.

Purpose of the Study:

• To investigate the molecular mechanisms underlying increased mortality in C. elegans co-infected with Staphylococcus aureus and its native microbiota.
• To understand how the host microbiota modulates host responses to a common pathogen.

Main Methods:

• Transcriptomic analysis (RNA sequencing) was performed on C. elegans under three conditions: native microbiota alone, S. aureus infection alone, and co-colonization with both microbiota and S. aureus.
• Gene expression patterns, particularly focusing on collagen and immunity genes, were analyzed in relation to host mortality.

Main Results:

• C. elegans infected with both S. aureus and its native microbiota exhibited higher mortality rates compared to infection with S. aureus alone.
• Transcriptomic analysis revealed altered expression of collagen genes correlating with increased mortality in co-colonized hosts, suggesting impaired host resistance.
• Microbiota-colonized hosts showed upregulated immunity genes and variable stress response gene expression during S. aureus infection.

Conclusions:

• The native microbiota of C. elegans can exacerbate the negative effects of S. aureus infection by altering host molecular responses.
• Commensal microbes can induce costly molecular changes in the host, compromising its ability to cope with emerging pathogens.
• Understanding these complex ecological interactions is crucial for predicting and managing severe infection outcomes.