Abstract
The nematode Caenorhabditis elegans relies on its innate immune defenses to counter infection. In this review, we focus on its response to infection by bacterial and fungal pathogens. We describe the different families of effector proteins that contribute to host defense, as well as the signal transduction pathways that regulate their expression. We discuss what is known of the activation of innate immunity in C. elegans, via pathogen recognition or sensing the damage provoked by infection. Damage causes a stress response; we review the role of stress signaling in host defense to infection. We examine examples of inter-tissue communication in innate immunity and end with a survey of post-transcriptional regulation of innate immune responses.
Highlights
The maintenance of cellular and organismal homeostasis in the face of changes in the environment is essential for survival
In the three well-characterized systems of infection of C. elegans described below evolutionarily conserved mitogen-activated protein kinase (MAPK) pathways have been found to have a central role in resistance to microbial pathogens (Figure 2)
Mutation in pmk-1 suppressed the requirement for XBP-1 during development in the presence of P. aeruginosa. This apparently paradoxical finding was proposed to result from a decrease in immune effector synthesis lessening the secretory load on the endoplasmic reticulum (ER) and thereby increasing host fitness in the absence of XBP-1 function, so permitting survival (Ewbank and Pujol, 2010; Richardson et al, 2010; Richardson et al, 2011). These data point to an ancient, essential role for XBP-1 and the Unfolded Protein Response (UPR) in maintaining ER homeostasis in response to the endogenous ER stress generated by the innate immune response to infection by pathogenic bacteria
Summary
The maintenance of cellular and organismal homeostasis in the face of changes in the environment is essential for survival. Additional putative antimicrobial proteins and peptides have been shown to promote resistance to pathogens, including clec-70 and clec-71 (to S. aureus) (Irazoqui et al, 2010), spp-12 (to B. thuringiensis) (Hoeckendorf et al, 2012), and the nlp-29 and cnc-2 clusters of AMP genes (to the fungus D. coniospora) (Pujol et al, 2008b; Zugasti and Ewbank, 2009). In C. elegans, insulin and TGFβ pathways are best understood in terms of their roles in the neuroendocrine regulation of host defenses in a cell non-autonomous fashion (Zugasti and Ewbank, 2009; Kawli et al, 2010) This is discussed further, Inter-tissue signaling in innate immunity. Ascarosides, including dauer pheromone, and other uncharacterized small molecules, influence multiple aspects of nematode development, behavior, and physiology, as well as nematode interactions with microbes (Kaplan et al, 2009; Yamada et al, 2010; Artyukhin et al, 2013; Ludewig et al, 2013; Ludewig and Schroeder, 2013; Olofsson, 2014)
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