The <i>Drosophila</i> Imd Signaling Pathway

Myllymäki, Henna; Valanne, Susanna; Rämet, Mika

doi:10.4049/jimmunol.1303309

Cited by 459 publications

(376 citation statements)

References 126 publications

(140 reference statements)

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“…Similarly, another level of regulation in the gut is due to the expression of the transcription factor Caudal, which blocks the expression of some Imd pathway target genes in the posterior midgut [35], the region of the gut with the highest density of bacteria in Drosophila [42]. In the systemic immune response of Drosophila, mechanisms such as ubiquitination/deubiquitination and sumoylation have also been shown to regulate various components of the Imd pathway (reviewed in [95]). However, it is not yet known whether these mechanisms regulate Imd in the gut.…”

Section: Amps and Gut Immune Responsesmentioning

confidence: 99%

Friend, foe or food? Recognition and the role of antimicrobial peptides in gut immunity and Drosophila –microbe interactions

Broderick

2016

Phil. Trans. R. Soc. B

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One contribution of 13 to a theme issue 'Evolutionary ecology of arthropod antimicrobial peptides'. Drosophila melanogaster lives, breeds and feeds on fermenting fruit, an environment that supports a high density, and often a diversity, of microorganisms. This association with such dense microbe-rich environments has been proposed as a reason that D. melanogaster evolved a diverse and potent antimicrobial peptide (AMP) response to microorganisms, especially to combat potential pathogens that might occupy this niche. Yet, like most animals, D. melanogaster also lives in close association with the beneficial microbes that comprise its microbiota, or microbiome, and recent studies have shown that antimicrobial peptides (AMPs) of the epithelial immune response play an important role in dictating these interactions and controlling the host response to gut microbiota. Moreover, D. melanogaster also eats microbes for food, consuming fermentative microbes of decaying plant material and their by-products as both larvae and adults. The processes of nutrient acquisition and host defence are remarkably similar and use shared functions for microbe detection and response, an observation that has led to the proposal that the digestive and immune systems have a common evolutionary origin. In this manner, D. melanogaster provides a powerful model to understand how, and whether, hosts differentiate between the microbes they encounter across this spectrum of associations.This article is part of the themed issue 'Evolutionary ecology of arthropod antimicrobial peptides'.

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Section: Amps and Gut Immune Responsesmentioning

confidence: 99%

Friend, foe or food? Recognition and the role of antimicrobial peptides in gut immunity and Drosophila –microbe interactions

Broderick

2016

Phil. Trans. R. Soc. B

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“…Humoral immune responses in Drosophila against Gram-negative bacteria are induced through the recognition of invaders by peptidoglycan recognition proteins (PGRPs) and the subsequent activation of the Imd pathway leading to the production of antimicrobial peptides such as diptericin and attacin (59,60,(63)(64)(65)(66). First, we determined the level of mRNA of these peptides in flies infected with Dhfq and the parental strain, but found no significant difference between flies infected with the two E. coli strains (Fig.…”

Section: Hfq-mediated Persistent Infection Of E Coli In Drosophilamentioning

confidence: 99%

Inhibition of Phagocytic Killing of Escherichia coli in Drosophila Hemocytes by RNA Chaperone Hfq

Shiratsuchi

Nitta

Kuroda

et al. 2016

The Journal of Immunology

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An RNA chaperone of Escherichia coli, called host factor required for phage Qβ RNA replication (Hfq), forms a complex with small noncoding RNAs to facilitate their binding to target mRNA for the alteration of translation efficiency and stability. Although the role of Hfq in the virulence and drug resistance of bacteria has been suggested, how this RNA chaperone controls the infectious state remains unknown. In the present study, we addressed this issue using Drosophila melanogaster as a host for bacterial infection. In an assay for abdominal infection using adult flies, an E. coli strain with mutation in hfq was eliminated earlier, whereas flies survived longer compared with infection with a parental strain. The same was true with flies deficient in humoral responses, but the mutant phenotypes were not observed when a fly line with impaired hemocyte phagocytosis was infected. The results from an assay for phagocytosis in vitro revealed that Hfq inhibits the killing of E. coli by Drosophila phagocytes after engulfment. Furthermore, Hfq seemed to exert this action partly through enhancing the expression of σ38, a stress-responsive σ factor that was previously shown to be involved in the inhibition of phagocytic killing of E. coli, by a posttranscriptional mechanism. Our study indicates that the RNA chaperone Hfq contributes to the persistent infection of E. coli by maintaining the expression of bacterial genes, including one coding for σ38, that help bacteria evade host immunity.

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“…[17,[95][96][97][98][99][100][101][102] Altogether, these regulatory components downregulate the IMD cascade following immune stimuli, allowing a balanced AMP response to be re-established once the infection is cleared. [103,104] Another layer of control is provided by the functional compartmentalization of the Drosophila gut. [15,23,105] Although the IMD pathway responds to the endogenous microbes all along the gut, the expression of NF-kB-dependent AMPs and immunosuppressor genes follows different patterns.…”

Section: Amp Productionmentioning

confidence: 99%