Drosophila immune response: From systemic antimicrobial peptide production in fat body cells to local defense in the intestinal tract

Charroux, Bernard; Royet, Julien

doi:10.4161/fly.4.1.10810

Cited by 114 publications

(105 citation statements)

References 69 publications

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“…The systemic immune response in Drosophila induced the synthesis of several families of AMPs by cells in the fat body, but AMP induction in the epidermis and epithelia of gut is regulated by the immune deficiency pathway for local immune challenges (44). In our study, we found that S. aureus challenge could induce the expression of the same kinds of AMPs in hemocytes, intestine and gill.…”

Section: Discussionsupporting

confidence: 50%

β-Arrestins Negatively Regulate the Toll Pathway in Shrimp by Preventing Dorsal Translocation and Inhibiting Dorsal Transcriptional Activity

Sun

Lan

Shi

et al. 2016

Journal of Biological Chemistry

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The Toll signaling pathway plays an important role in the innate immunity of Drosophila melanogaster and mammals. The activation and termination of Toll signaling are finely regulated in these animals. Although the primary components of the Toll pathway were identified in shrimp, the functions and regulation of the pathway are seldom studied. We first demonstrated that the Toll signaling pathway plays a central role in host defense against Staphylococcus aureus by regulating expression of antimicrobial peptides in shrimp. We then found that ␤-arrestins negatively regulate Toll signaling in two different ways. ␤-Arrestins interact with the C-terminal PEST domain of Cactus through the arrestin-N domain, and Cactus interacts with the RHD domain of Dorsal via the ankyrin repeats domain, forming a heterotrimeric complex of ␤-arrestin⅐Cactus⅐ Dorsal, with Cactus as the bridge. This complex prevents Cactus phosphorylation and degradation, as well as Dorsal translocation into the nucleus, thus inhibiting activation of the Toll signaling pathway. ␤-Arrestins also interact with non-phosphorylated ERK (extracellular signal-regulated protein kinase) through the arrestin-C domain to inhibit ERK phosphorylation, which affects Dorsal translocation into the nucleus and phosphorylation of Dorsal at Ser 276 that impairs Dorsal transcriptional activity. Our study suggests that ␤-arrestins negatively regulate the Toll signaling pathway by preventing Dorsal translocation and inhibiting Dorsal phosphorylation and transcriptional activity.

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Section: Discussionsupporting

confidence: 50%

β-Arrestins Negatively Regulate the Toll Pathway in Shrimp by Preventing Dorsal Translocation and Inhibiting Dorsal Transcriptional Activity

Sun

Lan

Shi

et al. 2016

Journal of Biological Chemistry

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“…The mosquito immune response involves both cellular and humoral components. The cellular component includes phagocytosis and encapsulation of invading organisms by haemocytes and pericardial cells, while the humoral component includes secretion of inducible antimicrobial peptides [29,31], pattern recognition receptor proteins [32] and activation of the phenoloxidase (PO) cascade, which promotes melanization of the invading parasites and wound healing [33]. The production of oxygen and nitrogen free radicals also occurs in response to infection [34].…”

Section: Introductionmentioning

confidence: 99%

Highly specific host-pathogen interactions influence Metarhizium brunneum blastospore virulence against Culex quinquefasciatus larvae

et al. 2018

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Entomopathogenic fungi are potential biological control agents of mosquitoes. Our group observed that not all mosquitoes were equally susceptible to fungal infection and observed significant differences in virulence of different spore types. Conidiospores and blastospores were tested against Culex quinquefasciatus larvae. Blastospores are normally considered more virulent than conidia as they form germ tubes and penetrate the host integument more rapidly than conidia. However, when tested against Cx. quinquefasciatus, blastospores were less virulent than conidia. This host-fungus interaction was studied by optical, electron and atomic force microscopy (AFM). Furthermore, host immune responses and specific gene expression were investigated. Metarhizium brunneum (formerly M. anisopliae) ARSEF 4556 blastospores did not readily adhere to Culex larval integument and the main route of infection was through the gut. Adhesion forces between blastospores and Culex cuticle were significantly lower than for other insects. Larvae challenged with blastospores showed enhanced immune responses, with increased levels of phenoloxidase, glutathione-S-transferase, esterase, superoxide dismutase and lipid peroxidase activity. Interestingly, M. brunneum pathogenicity/stress-related genes were all down-regulated in blastospores exposed to Culex. Conversely, when conidia were exposed to Culex, the pathogenicity genes involved in adhesion or cuticle degradation were up-regulated. Delayed host mortality following blastospore infection of Culex was probably due to lower adhesion rates of blastospores to the cuticle and enhanced host immune responses deployed to counter infection. The results here show that subtle differences in host-pathogen interactions can be responsible for significant changes in virulence when comparing mosquito species, having important consequences for biological control strategies and the understanding of pathogenicity processes.

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“…When the insect takes an infectious blood meal, the initial host encounters with pathogens occur locally, usually at an epithelial surface (1)(2)(3). Although studies have successfully infected a range of vectors by directly injecting arboviruses into the thoracic cavity, oral challenge often does not result in productive infection (3)(4)(5). This distinguishing characteristic has led to the description of a midgut barrier, whereby it is thought that the arbovirus is unable to establish a productive infection in the midgut cells due to restriction by local defenses.…”

mentioning

confidence: 99%

ERK signaling couples nutrient status to antiviral defense in the insect gut

Hopkins

Sabin

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

127

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A unique facet of arthropod-borne virus (arbovirus) infection is that the pathogens are orally acquired by an insect vector during the taking of a blood meal, which directly links nutrient acquisition and pathogen challenge. We show that the nutrient responsive ERK pathway is both induced by and restricts disparate arboviruses in Drosophila intestines, providing insight into the molecular determinants of the antiviral "midgut barrier." Wild-type flies are refractory to oral infection by arboviruses, including Sindbis virus and vesicular stomatitis virus, but this innate restriction can be overcome chemically by oral administration of an ERK pathway inhibitor or genetically via the specific loss of ERK in Drosophila intestinal epithelial cells. In addition, we found that vertebrate insulin, which activates ERK in the mosquito gut during a blood meal, restricts viral infection in Drosophila cells and against viral invasion of the insect gut epithelium. We find that ERK's antiviral signaling activity is likely conserved in Aedes mosquitoes, because genetic or pharmacologic manipulation of the ERK pathway affects viral infection of mosquito cells. These studies demonstrate that ERK signaling has a broadly antiviral role in insects and suggest that insects take advantage of cross-species signals in the meal to trigger antiviral immunity.innate immunity | enterocytes

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Drosophila immune response: From systemic antimicrobial peptide production in fat body cells to local defense in the intestinal tract

Cited by 114 publications

References 69 publications

β-Arrestins Negatively Regulate the Toll Pathway in Shrimp by Preventing Dorsal Translocation and Inhibiting Dorsal Transcriptional Activity

β-Arrestins Negatively Regulate the Toll Pathway in Shrimp by Preventing Dorsal Translocation and Inhibiting Dorsal Transcriptional Activity

Highly specific host-pathogen interactions influence Metarhizium brunneum blastospore virulence against Culex quinquefasciatus larvae

ERK signaling couples nutrient status to antiviral defense in the insect gut

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