Characterization of C. elegans innate immunity has largely focused on (1) the isolation of mutants with altered susceptibility to pathogens, (2) the characterization of the transcriptional responses to pathogens in wild type worms, and (3) the characterization of the transcriptional profiles of mutants with altered susceptibility to pathogens under normal growth conditions. We sought to investigate the regulation of host responses to pathogen by examining transcript profiles in mutants with altered susceptibility to pathogens in the context of infection. Towards that end, we established a quantitative RT-PCR assay to measure transcript levels of 146 candidate immunity genes. We examined mutants in the
p38 MAPK, TGF-beta, and insulin signaling pathways on E. coli (OP50) and Pseudomonas aeruginosa (PA14), from which we established transcript profiles for each pathway. Mutants in the
p38 MAPK pathway strongly affect absolute basal (OP50) and induced (PA14) transcript levels, but have little effect on the relative magnitude of response to pathogen (PA14/OP50). Thus while the
p38 MAPK pathway is essential for maintenance of proper expression levels of many immunity genes, the pathway appears to be largely dispensable for the response of immunity genes to PA14 infection. Likewise, while the basal and induced levels of immunity genes are affected in TGF-beta and insulin pathway mutants, neither pathway is required for the increase of immunity gene expression in response to PA14 infection. To assess the generality of these conclusions, we also assessed the response of immunity genes in worms infected by the Gram positive bacterial pathogen Enterococcus faecalis (V583). The transcriptional responses to infection by PA14 or V583 are overlapping but distinct. As with PA14 infection, candidate genes in both the
p38 MAPK and insulin signaling pathways are largely dispensable for the transcriptional response to V583 infection (V583/OP50). Our analysis of transcript profiles in mutants with altered susceptibility to pathogens indicates that the
p38 MAPK, TGF-beta, and insulin signaling pathways affect the expression of immunity genes largely independent of the response to infection by pathogens.