AI Article Synopsis
- Innate immunity is a set of ancient defense mechanisms in animals and plants that protect against infections.
- Research using the nematode C. elegans shows that infection by the bacterium Serratia marcescens triggers a significant increase in gene expression, particularly in genes linked to immune responses.
- Findings indicate that certain immune-related genes are regulated by the DBL-1/TGFbeta pathway, with mutants showing higher infection susceptibility while overexpressing lysozymes enhances resistance, highlighting new insights into innate immunity evolution.
Article Abstract
The term innate immunity refers to a number of evolutionary ancient mechanisms that serve to defend animals and plants against infection. Genetically tractable model organisms, especially Drosophila, have contributed greatly to advances in our understanding of mammalian innate immunity. Essentially, nothing is known about immune responses in the nematode Caenorhabditis elegans. Using high-density cDNA microarrays, we show here that infection of C. elegans by the Gram-negative bacterium Serratia marcescens provokes a marked upregulation of the expression of many genes. Among the most robustly induced are genes encoding lectins and lysozymes, known to be involved in immune responses in other organisms. Certain infection-inducible genes are under the control of the DBL-1/TGFbeta pathway. We found that dbl-1 mutants exhibit increased susceptibility to infection. Conversely, overexpression of the lysozyme gene lys-1 augments the resistance of C. elegans to S. marcescens. These results constitute the first demonstration of inducible antibacterial defenses in C. elegans and open new avenues for the investigation of evolutionary conserved mechanisms of innate immunity.
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| http://dx.doi.org/10.1016/s0960-9822(02)00928-4 | DOI Listing |
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