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Lack of an antibacterial response defect in Drosophila Toll-9 mutant.

Narbonne-Reveau K, Charroux B, Royet J - PLoS ONE (2011)

Bottom Line: These results have led to the idea that Toll-9 could be a constitutively active receptor that maintain significant levels of antimicrobial molecules and therefore provide constant basal protection against micro-organisms.To test theses hypotheses, we generated and analyzed phenotypes associated with a complete loss-of-function allele of Toll-9.Our results suggest that Toll-9 is neither required to maintain a basal anti-microbial response nor to mount an efficient immune response to bacterial infection.

View Article: PubMed Central - PubMed

Affiliation: Institut de Biologie du Développement de Marseille-Luminy, CNRS UMR 6216/Aix-Marseille II University, Campus de Luminy, Marseille, France.

ABSTRACT
Toll and Toll-like receptors represent families of receptors involved in mediating innate immunity response in insects and mammals. Although Drosophila proteome contains multiple Toll paralogs, Toll-1 is, so far, the only receptor to which an immune role has been attributed. In contrast, every single mammalian TLR is a key membrane receptor upstream of the vertebrate immune signaling cascades. The prevailing view is that TLR-mediated immunity is ancient. Structural analysis reveals that Drosophila Toll-9 is the most closely related to vertebrate TLRs and utilizes similar signaling components as Toll-1. This suggests that Toll-9 could be an ancestor of TLR-like receptors and could have immune function. Consistently, it has been reported that over-expression of Toll-9 in immune tissues is sufficient to induce the expression of some antimicrobial peptides in flies. These results have led to the idea that Toll-9 could be a constitutively active receptor that maintain significant levels of antimicrobial molecules and therefore provide constant basal protection against micro-organisms. To test theses hypotheses, we generated and analyzed phenotypes associated with a complete loss-of-function allele of Toll-9. Our results suggest that Toll-9 is neither required to maintain a basal anti-microbial response nor to mount an efficient immune response to bacterial infection.

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Related in: MedlinePlus

Gut epithelium renewal is not affected in Toll-9−/− mutants.Immunostaining with antibodies against GFP (white, A–D; green, A”–D”) and Delta (white, A'–D'; red, A” –D”). DNA is shown in blue (A”–D”). Esg-GFP positive cells correspond to ISCs or young enteroblasts, whereas Dl stains only ISCs in unchallenged adult guts (A, B). 20 hours after Ecc15 oral infection, Esg-GFP positive cell and Dl positive cell numbers strongly increase (C–D), corresponding to an increased epithelium renewal, observed both in the control and in Toll-9−/− guts.
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pone-0017470-g008: Gut epithelium renewal is not affected in Toll-9−/− mutants.Immunostaining with antibodies against GFP (white, A–D; green, A”–D”) and Delta (white, A'–D'; red, A” –D”). DNA is shown in blue (A”–D”). Esg-GFP positive cells correspond to ISCs or young enteroblasts, whereas Dl stains only ISCs in unchallenged adult guts (A, B). 20 hours after Ecc15 oral infection, Esg-GFP positive cell and Dl positive cell numbers strongly increase (C–D), corresponding to an increased epithelium renewal, observed both in the control and in Toll-9−/− guts.

Mentions: Recent studies have revealed that bacterial infection can trigger a gut immune response that involves the production of Reactive Oxygen Species and antimicrobial peptides [52]–[55]. Associated with this mechanism of defense, the gut epithelium triggers the proliferation and differentiation of intestinal stem cells (ISCs, stained with Delta (Dl) and Escargot (Esg), [52]. Upon stimulation, the ISCs give rise to two intestinal cell types: enterocytes (young enterocytes still express Esg) and enteroendocrine cells [56]. It has been shown that oral infection with some bacteria species can stimulate epithelium renewal by inducing ISCs proliferation and therefore production of enterocytes [52], [53]. We then tested whether the gut homeostasis was modified in a Toll-9−/− mutant. As shown in Figure 8, the numbers of ISCs (Esg-positive and Dl-positive cells) and young enterocytes (Esg-positive and Dl-negative cells) were similar in unaffected Toll-9−/− mutants and in control guts (Figure 8A–A” and B–B”). Upon infection, the epithelium renewal occurred normally in a Toll-9−/− mutant midguts (Figure 8C–C” and D–D”). These results indicate that neither the basal gut renewal in non-infected guts nor the epithelium renewal triggered by bacterial infection is dependent on Toll-9 function.


Lack of an antibacterial response defect in Drosophila Toll-9 mutant.

Narbonne-Reveau K, Charroux B, Royet J - PLoS ONE (2011)

Gut epithelium renewal is not affected in Toll-9−/− mutants.Immunostaining with antibodies against GFP (white, A–D; green, A”–D”) and Delta (white, A'–D'; red, A” –D”). DNA is shown in blue (A”–D”). Esg-GFP positive cells correspond to ISCs or young enteroblasts, whereas Dl stains only ISCs in unchallenged adult guts (A, B). 20 hours after Ecc15 oral infection, Esg-GFP positive cell and Dl positive cell numbers strongly increase (C–D), corresponding to an increased epithelium renewal, observed both in the control and in Toll-9−/− guts.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3046252&req=5

pone-0017470-g008: Gut epithelium renewal is not affected in Toll-9−/− mutants.Immunostaining with antibodies against GFP (white, A–D; green, A”–D”) and Delta (white, A'–D'; red, A” –D”). DNA is shown in blue (A”–D”). Esg-GFP positive cells correspond to ISCs or young enteroblasts, whereas Dl stains only ISCs in unchallenged adult guts (A, B). 20 hours after Ecc15 oral infection, Esg-GFP positive cell and Dl positive cell numbers strongly increase (C–D), corresponding to an increased epithelium renewal, observed both in the control and in Toll-9−/− guts.
Mentions: Recent studies have revealed that bacterial infection can trigger a gut immune response that involves the production of Reactive Oxygen Species and antimicrobial peptides [52]–[55]. Associated with this mechanism of defense, the gut epithelium triggers the proliferation and differentiation of intestinal stem cells (ISCs, stained with Delta (Dl) and Escargot (Esg), [52]. Upon stimulation, the ISCs give rise to two intestinal cell types: enterocytes (young enterocytes still express Esg) and enteroendocrine cells [56]. It has been shown that oral infection with some bacteria species can stimulate epithelium renewal by inducing ISCs proliferation and therefore production of enterocytes [52], [53]. We then tested whether the gut homeostasis was modified in a Toll-9−/− mutant. As shown in Figure 8, the numbers of ISCs (Esg-positive and Dl-positive cells) and young enterocytes (Esg-positive and Dl-negative cells) were similar in unaffected Toll-9−/− mutants and in control guts (Figure 8A–A” and B–B”). Upon infection, the epithelium renewal occurred normally in a Toll-9−/− mutant midguts (Figure 8C–C” and D–D”). These results indicate that neither the basal gut renewal in non-infected guts nor the epithelium renewal triggered by bacterial infection is dependent on Toll-9 function.

Bottom Line: These results have led to the idea that Toll-9 could be a constitutively active receptor that maintain significant levels of antimicrobial molecules and therefore provide constant basal protection against micro-organisms.To test theses hypotheses, we generated and analyzed phenotypes associated with a complete loss-of-function allele of Toll-9.Our results suggest that Toll-9 is neither required to maintain a basal anti-microbial response nor to mount an efficient immune response to bacterial infection.

View Article: PubMed Central - PubMed

Affiliation: Institut de Biologie du Développement de Marseille-Luminy, CNRS UMR 6216/Aix-Marseille II University, Campus de Luminy, Marseille, France.

ABSTRACT
Toll and Toll-like receptors represent families of receptors involved in mediating innate immunity response in insects and mammals. Although Drosophila proteome contains multiple Toll paralogs, Toll-1 is, so far, the only receptor to which an immune role has been attributed. In contrast, every single mammalian TLR is a key membrane receptor upstream of the vertebrate immune signaling cascades. The prevailing view is that TLR-mediated immunity is ancient. Structural analysis reveals that Drosophila Toll-9 is the most closely related to vertebrate TLRs and utilizes similar signaling components as Toll-1. This suggests that Toll-9 could be an ancestor of TLR-like receptors and could have immune function. Consistently, it has been reported that over-expression of Toll-9 in immune tissues is sufficient to induce the expression of some antimicrobial peptides in flies. These results have led to the idea that Toll-9 could be a constitutively active receptor that maintain significant levels of antimicrobial molecules and therefore provide constant basal protection against micro-organisms. To test theses hypotheses, we generated and analyzed phenotypes associated with a complete loss-of-function allele of Toll-9. Our results suggest that Toll-9 is neither required to maintain a basal anti-microbial response nor to mount an efficient immune response to bacterial infection.

Show MeSH
Related in: MedlinePlus