Stenotrophomonas indicatrix and the Role of the Microbiome in C. elegans Innate Immune Response
Open Access DepositedGFP expression, we tested whether JUb19 also requires ZIP-1. We found that ZIP-1 is only needed during the early phase of IPR reporter expression induction by JUb19, suggesting that additional transcription factors regulate pals-5p
GFP expression. When investigating how JUb19 induces IPR reporter expression, we found that JUb19 colonizes the intestinal lumen in adult animals without invading host cells, making it the first microbe known to activate pals-5p
The microbiome plays a crucial role in shaping host immunity, but the mechanisms by which specific bacteria modulate innate immune pathways remain poorly understood. Caenorhabditis elegans, a bacterivore with a well-defined microbiome, provides an ideal model for dissecting the role of the microbiome in modulating host-pathogen defense mechanisms. One such defense mechanism in C. elegans is the Intracellular Pathogen Response (IPR), a transcriptional immune response activated upon infection by obligate intracellular pathogens such as the fugal parasite Nematocida parisii and Orsay virus. The IPR coordinates the upregulation of multiple genes, including pals-5, whose promoter region was used to create a fluorescent transcriptional reporter for IPR activation. We screened 12 representative microbiome species for their ability to induce pals-5p
GFP expression, and we found that Stenotrophomonas indicatrix (JUb19) promotes IPR reporter expression in multiple tissues, including the intestine, epidermis, neurons, and somatic gonad. Because all previously described IPR triggers depend on the bZIP transcription factor ZIP-1 for pals-5p
GFP expression extracellularly. Interestingly, while heat-killed JUb19 fails to induce reporter expression, mechanically disrupted and chemically inactivated JUb19 retains this ability. This suggests that IPR activation is triggered by a molecular component of JUb19 that is sensitive to heat. Our preliminary results indicate that this component may be bacterial RNA specific to JUb19. Our transcriptomic analyses demonstrate that JUb19 induces the expression of a small subset of IPR genes, as well as genes with lysosome-associated functions. Importantly, these transcriptional changes are sufficient to protect the host against both viral and fungal pathogens based on our infection assay results. However, JUb19 also causes fitness disadvantages, including developmental delay, shorter lifespan, and reduced brood size. Together, our study identifies JUb19 as a component of the C. elegans natural microbiome that induces a novel transcriptional response, promoting innate immunity against obligate intracellular pathogens.
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