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Title: The fatty acid oleate is required for innate immune activation and pathogen defense in Caenorhabditis elegans}
Article:
Abstract:
Fatty acids affect a number of physiological processes, in addition to forming the building blocks of membranes and body fat stores. In this study, we uncover a role for the monounsaturated fatty acid oleate in the innate immune response of the nematode Caenorhabditis elegans. From an RNAi screen for regulators of innate immune defense genes, we identified the two stearoyl-coenzyme A desaturases that synthesize oleate in C. elegans. We show that the synthesis of oleate is necessary for the pathogen-mediated induction of immune defense genes. Accordingly, C. elegans deficient in oleate production are hypersusceptible to infection with diverse human pathogens, which can be rescued by the addition of exogenous oleate. However, oleate is not sufficient to drive protective immune activation. Together, these data add to the known health-promoting effects of monounsaturated fatty acids, and suggest an ancient link between nutrient stores, metabolism, and host susceptibility to bacterial infection.
Introduction:
Fatty acids are the key structural components of phospholipids and triglycerides, and thereby affect nearly every facet of eukaryotic physiology. In addition to forming the building blocks of membranes and functioning as a currency of energy storage, fatty acid molecules promote health in a diverse number of ways. For example, fatty acids act as soluble signals for intracellular communication, affect membrane fluidity, and have been directly linked to lifespan regulation[1–3]. Conversely, excess stores of fatty acids in triglycerides lead to atherosclerosis and type 2 diabetes[4]. Thus, it is important to understand how individual fatty acids affect key physiological processes within a cell. The nematode Caenorhabditis elegans is a valuable model for studying the roles of fatty acids in metazoan biology[5–10]. Through the sequential action of conserved elongase( elo) and desaturase( fat) genes, nematodes can synthesize the full range of fatty acid molecules found in plants and animals[5–9]. Thus, C. elegans does not have a dietary requirement for specific fatty acids, unlike mammals. In nematodes, as in mammals, the majority of fatty acid molecules are synthesized from stearic acid, a saturated, 18-carbon molecule, which is progressively desaturated and elongated to a variety of monounsaturated( MUFA) and polyunsaturated( PUFA) fatty acids( Fig 1A)[5–9]. The contribution of individual fatty acids to specific biological processes can be characterized using genetic approaches in C. elegans at the level of an entire organism. Nematodes rely on inducible host defense mechanisms to provide protection from ingested pathogens[11–14]. Because worms normally eat bacteria for food, their evolution has been shaped by interactions with both pathogenic and nonpathogenic microorganisms. The immune effectors in C. elegans include a suite of secreted proteins, including lysozymes, proteins with CUB-like domains, and ShK toxins, some of which are required for host defense during bacterial infection[15–18]. C. elegans with mutations that abrogate the induction of these immune effectors during infection are hypersusceptible to killing by bacterial pathogens[15, 19, 20]. In this study, we define a requirement for the MUFA oleate in innate immune activation and pathogen defense in C. elegans. Previously, Nandakumar et al. showed that two polyunsaturated fatty acids, γ-linolenic acid( GLA) and stearidonic acid( SDA), are required for the basal expression of innate immune effectors[17]. Here, we show that oleate is necessary for innate immune activation and resistance to bacterial infection in a manner distinct from the effects of GLA and SDA. Because oleate is among the most abundant fatty acids in cells, our data suggest an ancient link between cellular energy stores and immune activation.
Discussion:
This study defines a role for the MUFA oleate in C. elegans innate immune activation. We show that animals deficient in oleate production were hypersusceptible to killing by the bacterial pathogens P. aeruginosa, E. faecalis, and S. marcescens in a manner dependent on oleate. Oleate is among the most abundant fatty acids in cells. Thus, these data may explain how a metazoan animal limits the induction of protective immune defenses to times when the host has accumulated sufficient energy reserves to survive challenge from bacterial pathogens. Nandakumar et al. previously identified two fatty acids, GLA and SDA, which are synthesized by the enzyme fat-3 and are required for the basal expression of immune effectors[17]. Our data indicate that oleate and these PUFAs affect immune effector expression and pathogen resistance by different mechanisms. C. elegans with a loss-of-function mutation in fat-2, the enzyme that catalyzes the first step in PUFA synthesis, induced innate immune effector genes normally and were not more susceptible to P. aeruginosa pathogenesis. It is also important to note that knockdown of fat-3 did not affect the R24-mediated induction of 16 fat-6-dependent innate immune effectors. In addition, exogenous supplementation of PUFAs to fat-6( RNAi) animals did not restore immune effector expression, whereas the addition of oleate fully complemented the induction defect of these animals. Also of note, the effect of fat-3( wa22) on susceptibility to bacterial infection was independent of oleate. Han et al. recently found that oleate is sufficient to extend the lifespan of nematodes that were grown under standard laboratory conditions[1]. Interestingly, we found that treatment with oleate is not sufficient to provide protection during bacterial infection, but is required for proper immune gene transcription. Specifically, oleate is important for the pathogen-mediated induction of immune effectors that are downstream of the p38 MAPK PMK-1 pathway and for genes that are regulated by the bZIP transcription factor ZIP-2, which functions independently of the canonical PMK-1 pathway to mediate an early transcriptional response to P. aeruginosa infection[31]. Consistent with these data, RNAi mediated knockdown of tir-1, a component of the p38 MAPK PMK-1 signaling cassette, as well as zip-2, enhanced the susceptibility of fat-6( tm331);fat-7( wa36) animals to P. aeruginosa infection. Thus, oleate has diverse, health-promoting effects on lifespan and pathogen resistance in C. elegans. In plants, oleate is also required for the proper expression of immune defense genes and resistance to pathogen infection, suggesting that the role for oleate in immune activation may be strongly conserved[34, 35]. However, the mechanism by which oleate regulates immune defenses is not known in either C. elegans or plants. Our supplementation studies indicate that oleate treatment itself does not activate immune gene transcription. Thus, oleate is unlikely to be a signal of immune activation in C. elegans, but rather functions as a licensing factor for the elaboration of anti-pathogen responses. Disruption of oleate biosynthesis alters membrane fluidity, which has pleiotropic consequences on membrane-bound organelles, including activating stress pathways associated with endoplasmic reticulum dysfunction[3]. Indeed, alterations of membrane fluidity have been linked to activation of G protein-coupled receptors[36, 37]. Thus, changing the oleate content in C. elegans may modulate the ability of the host to mount protective defense responses, either directly or by disrupting lipid-protein interactions that are essential for immune pathway activation. Our findings present a previously unappreciated link between a highly abundant fatty acid and immune activation, which may represent an ancient connection between body energy stores and susceptibility to bacterial infection.
The evolution of multicellular organisms has been shaped by their interactions with pathogenic microorganisms . The microscopic nematode C . elegans eats bacteria for food and has evolved inducible immune defenses toward ingested pathogens that are coordinated within intestinal epithelial cells . C . elegans , therefore , presents a genetic system to characterize the requirements for the activation of innate immune defenses . Here , we show that the monounsaturated fatty acid oleate is necessary for the induction of innate immune defenses and for protection against bacterial pathogens , which defines a new link between metabolism and the regulation of anti-pathogen responses in a metazoan host .