A MAP Kinase pathway in Caenorhabditis elegans is required for defense against infection by opportunistic Proteus species.

Caenorhabditis elegans innate immunity requires a conserved mitogen activated protein kinase (MAPK) pathway that regulates the basal and pathogen-induced expression of immune effectors. Being in the group of opportunistic pathogens, Proteus spp. cause large number of nosocomial infections. Since, Proteus spp. do not cause death in wild type C. elegans, to understand the role and contribution of MAP Kinase pathway, the mutants (sek-1 and pmk-1) of this pathway were employed. Physiological experiments revealed that the Proteus spp. were able to kill MAP Kinase pathway mutant's C. elegans significantly. To understand the involvement of innate immune pathways specific players at the mRNA level, the regulation of few candidate antimicrobial genes were kinetically investigated during Proteus spp. infections. Real-time PCR analysis indicated a regulation of few candidate immune regulatory genes (F08G5.6, lys-7, nlp-29, ATF-7 and daf-16) during the course of Proteus spp. infections. In addition, the lipopolysaccharides (LPS) isolated from Proteus mirabilis upon exposure to mutant C. elegans showed modifications at their functional regions suggesting that the pathogen modifies its internal machinery according to the specific host for effective pathogenesis.