Innate immune response of Aedes aegypti

Lowenberger, Carl

doi:10.1016/s0965-1748(00)00141-7

Cited by 160 publications

(142 citation statements)

References 76 publications

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“…Several innate immune pathways in mosquitoes have been elucidated for defense against bacterial and macroparasite infections (18,(37)(38)(39)(40); however, no antiviral mechanisms or pathways have been described. In vertebrate species, there are innate immune mechanisms that recognize and mount responses to dsRNA, including the interferon and protein kinase R pathways, but neither has been detected in the mosquito.…”

Section: Discussionmentioning

confidence: 99%

RNA interference acts as a natural antiviral response to O'nyong-nyong virus ( Alphavirus ; Togaviridae) infection of Anopheles gambiae

Keene

Foy

Sánchez-Vargas

et al. 2004

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

315

272

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RNA interference (RNAi) is triggered in eukaryotic organisms by double-stranded RNA (dsRNA), and it destroys any mRNA that has sequence identity with the dsRNA trigger. The RNAi pathway in Anopheles gambiae can be silenced by transfecting cells with dsRNA derived from exon sequence of the A. gambiae Argonaute2 (AgAgo2) gene. We hypothesized that RNAi may also act as an antagonist to alphavirus replication in A. gambiae because RNA viruses form dsRNA during replication. Silencing AgAgo2 expression would make A. gambiae mosquitoes more permissive to virus infection. To determine whether RNAi conditions the vector competence of A. gambiae for O'nyong-nyong virus (ONNV), we engineered a genetically modified ONNV that expresses enhanced GFP (eGFP) as a marker. After intrathoracic injection, ONNV-eGFP slowly spread to other A. gambiae tissues over a 9-day incubation period. Mosquitoes were then coinjected with virus and either control ␤-galactosidase dsRNA (ds␤gal; note that ''ds'' is used as a prefix to indicate the dsRNA derived from a given gene throughout) or ONNV dsnsP3. Treatment with dsnsP3 inhibited virus spread significantly, as determined by eGFP expression patterns. ONNVeGFP titers from mosquitoes coinjected with dsnsP3 were significantly lower at 3 and 6 days after injection than in mosquitoes coinjected with ds␤gal. Mosquitoes were then coinjected with ONNV-eGFP and dsAgAgo2. Mosquitoes coinjected with virus and AgAgo2 dsRNA displayed widespread eGFP expression and virus titers 16-fold higher than ds␤gal controls after 3 or 6 days after injection. These observations provide direct evidence that RNAi is an antagonist of ONNV replication in A. gambiae, and they suggest that the innate immune response conditions vector competence.innate immunity ͉ mosquito ͉ vector competence

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Section: Discussionmentioning

confidence: 99%

RNA interference acts as a natural antiviral response to O'nyong-nyong virus ( Alphavirus ; Togaviridae) infection of Anopheles gambiae

Keene

Foy

Sánchez-Vargas

et al. 2004

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

315

272

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“…Induction of expression of immune relevant proteins of G. mellonella by RT PCR Larval RNA was extracted using TRI-reagent at 1,4,8,24 and 48 h post-infection. RNA (2 mg) was treated with DNase I prior to cDNA synthesis using the SuperScript Kit (Invitrogen) with oligo(dT) primers.…”

Section: Insect Larvaementioning

confidence: 99%

“…During an infection, the insect's immune response involves a cellular component where haemocytes recognise and phagocytose microbes, form nodules or encapsulate foreign particles [3]. The humoral element of the immune response consists of proteins involved in clotting such as vitellogenin-like proteins that contain a cysteinerich region which is homologous to the mammalian clottable proteins of the Von Willebrand factor involved in blood clotting [2], and antimicrobial peptides (AMPs) such as defensins, which have been highly conserved through evolution [4]. AMPs are released from a range of organs and cells [5,6] into the haemolymph of the insect where they diffuse to the site of infection and attack components of the bacterial or fungal cell wall [7].…”

Section: Introductionmentioning

confidence: 99%

Pre-exposure to yeast protects larvae of Galleria mellonella from a subsequent lethal infection by Candida albicans and is mediated by the increased expression of antimicrobial peptides

Bergin

Murphy

Keenan

et al. 2006

Microbes and Infection

132

130

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Pre-exposure of the larvae of Galleria mellonella to Candida albicans or Saccharomyces cerevisiae protects against a subsequent infection with 10 6 C. albicans cells. This protection can also be induced by exposing larvae to glucan or laminarin prior to the administration of the potentially lethal inoculum. Analysis of the expression of genes coding for galiomicin, a defensin in G. mellonella, a cysteine-rich antifungal peptide gallerimycin, an iron-binding protein transferrin and an inducible metalloproteinase inhibitor (IMPI) from G. mellonella demonstrated increased expression, which is at its highest after 24 h of the initial inoculum. Examination of the expression of proteins in the insect haemolymph using 2D electrophoresis and MALDI TOF analysis revealed an increased expression of a number of proteins associated with the insect immune response to infection 24 h after the initial exposure. This study demonstrates that the larvae of G. mellonella can withstand a lethal inoculum of C. albicans if pre-exposed to a non-lethal dose of yeast or polysaccharide 24 h previously which is mediated by increased expression of a number of antimicrobial peptides and the appearance of a number of peptides in the challenged larvae.

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“…Several defensins have been isolated, and surprisingly, defensins from closely related species show less homology than defensins from species of different phyla (10). Many invertebrate (11) and fungal (12) defensins have a cysteine-stabilized ␣-helix/␤-sheet structure similar to the structure of ␤-defensins from vertebrates.…”

mentioning

confidence: 99%

“…The cDNA clone encoded a putative defensin-like peptide that was named eurocin. The gene encodes 90 amino acids (signal peptide (amino acids (aa) [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20], propeptide (aa , and defensin peptide (aa 49 -90)). The mature peptide consists of 42 amino acids ( Fig.…”

mentioning

confidence: 99%

Eurocin, a New Fungal Defensin

Oeemig

Lynggaard

Knudsen

et al. 2012

Journal of Biological Chemistry

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Background: Antimicrobial peptides are new antibiotics avoiding resistance problems. Results: Eurocin is a new antimicrobial peptide featuring a cysteine-stabilized ␣␤-fold. Eurocin binds the cell wall precursor lipid II but does not disrupt cell membranes. Conclusion: Eurocin acts by inhibiting cell wall synthesis. Its structure is typical for invertebrate defensins. Significance: Knowing the mode of action and structure is a prerequisite for pharmaceutical application of an antibiotic.

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Innate immune response of Aedes aegypti

Cited by 160 publications

References 76 publications

RNA interference acts as a natural antiviral response to O'nyong-nyong virus ( Alphavirus ; Togaviridae) infection of Anopheles gambiae

RNA interference acts as a natural antiviral response to O'nyong-nyong virus ( Alphavirus ; Togaviridae) infection of Anopheles gambiae

Pre-exposure to yeast protects larvae of Galleria mellonella from a subsequent lethal infection by Candida albicans and is mediated by the increased expression of antimicrobial peptides

Eurocin, a New Fungal Defensin

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