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Interleukin-25 Mediated Induction of Angiogenin-4 Is Interleukin-13 Dependent.

Noor Z, Burgess SL, Watanabe K, Petri WA - PLoS ONE (2016)

Bottom Line: The intestinal surface is directly exposed to both commensal microorganisms as well as pathogens with a single layer of epithelium separating luminal microorganisms from internal tissues.Here we show that IL-13 downstream of IL-25 is required to induce angiogenin-4.IL-25 mediated induction of angiogenin-4 is furthermore not dependent on IL-22 or IL-17.

View Article: PubMed Central - PubMed

Affiliation: Division of Infectious Diseases and International Health, Department of Medicine, University of Virginia Health System, Charlottesville, Virginia, United States of America.

ABSTRACT
The intestinal surface is directly exposed to both commensal microorganisms as well as pathogens with a single layer of epithelium separating luminal microorganisms from internal tissues. Antimicrobial peptides play a crucial role in allowing epithelial cells to contain in the lumen beneficial and pathogenic microorganisms. The commensal dependent, epithelial produced, Th2 cytokine IL-25 can induce IL-13 and potentially the antimicrobial peptide angiogenin-4. Here we show that IL-13 downstream of IL-25 is required to induce angiogenin-4. IL-25 mediated induction of angiogenin-4 is furthermore not dependent on IL-22 or IL-17.

No MeSH data available.


Depletion of IL-13 abrogates rIL-25 induction of angiogenin-4.CBA/J mice were treated with 0.5 micrograms of recombinant IL-25 each day for a total 6 doses. Control mice received PBS. Recombinant IL-25 treated mice received 200μg anti-IL-13 antibody or isotype control on day 3 and on day 5. Angiogenin-4 relative expression was measured from cecal tissue, n = 5–8 (A). Histological scoring (1 to 5; low to high) for Angiogenin-4 in cecum from mice treated with PBS or rIL-25 with isotype control or rIL-25 with anti-IL-13 (B). Representative IHC staining for angiogenin-4 in samples of cecum tissue from PBS treated (C) or rIL-25 with isotype control (D) or rIL-25 with anti-IL-13 treated mice (E).
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pone.0153572.g005: Depletion of IL-13 abrogates rIL-25 induction of angiogenin-4.CBA/J mice were treated with 0.5 micrograms of recombinant IL-25 each day for a total 6 doses. Control mice received PBS. Recombinant IL-25 treated mice received 200μg anti-IL-13 antibody or isotype control on day 3 and on day 5. Angiogenin-4 relative expression was measured from cecal tissue, n = 5–8 (A). Histological scoring (1 to 5; low to high) for Angiogenin-4 in cecum from mice treated with PBS or rIL-25 with isotype control or rIL-25 with anti-IL-13 (B). Representative IHC staining for angiogenin-4 in samples of cecum tissue from PBS treated (C) or rIL-25 with isotype control (D) or rIL-25 with anti-IL-13 treated mice (E).

Mentions: IL-25 is known to induce Th2 cytokines, including IL-13. Therefore, the role of IL-13 in the ability of IL-25 to induce angiogenin-4 was examined. CBA/J mice were treated with rIL-25 (closed square, n = 8) and control mice received PBS (closed circle, n = 7). IL-13 relative expression was measured from mouse cecal tissue. We found that there was significantly higher expression of IL-13 in rIL-25 treated mice than that in control mice (Fig 3). Previous studies have shown that IL-13 can induce Paneth cell degranulation and trigger the release of the antimicrobial peptide angiogenin-4. We confirmed that IL-13 induced angiogenin-4 expression (Fig 4A) in cecal epithelial cells (Fig 4B–4D). IL-25 mediated angiogenin-4 expression was abrogated when IL-13 was depleted by neutralizing antibodies (Fig 5A). This result was confirmed via immunohistochemistry of angiogenin-4 as before (Fig 5B–5E). These results indicated that IL-25 induced angiogenin-4 expression was mediated via the IL-25 downstream pathway cytokine IL-13.


Interleukin-25 Mediated Induction of Angiogenin-4 Is Interleukin-13 Dependent.

Noor Z, Burgess SL, Watanabe K, Petri WA - PLoS ONE (2016)

Depletion of IL-13 abrogates rIL-25 induction of angiogenin-4.CBA/J mice were treated with 0.5 micrograms of recombinant IL-25 each day for a total 6 doses. Control mice received PBS. Recombinant IL-25 treated mice received 200μg anti-IL-13 antibody or isotype control on day 3 and on day 5. Angiogenin-4 relative expression was measured from cecal tissue, n = 5–8 (A). Histological scoring (1 to 5; low to high) for Angiogenin-4 in cecum from mice treated with PBS or rIL-25 with isotype control or rIL-25 with anti-IL-13 (B). Representative IHC staining for angiogenin-4 in samples of cecum tissue from PBS treated (C) or rIL-25 with isotype control (D) or rIL-25 with anti-IL-13 treated mice (E).
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Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4835063&req=5

pone.0153572.g005: Depletion of IL-13 abrogates rIL-25 induction of angiogenin-4.CBA/J mice were treated with 0.5 micrograms of recombinant IL-25 each day for a total 6 doses. Control mice received PBS. Recombinant IL-25 treated mice received 200μg anti-IL-13 antibody or isotype control on day 3 and on day 5. Angiogenin-4 relative expression was measured from cecal tissue, n = 5–8 (A). Histological scoring (1 to 5; low to high) for Angiogenin-4 in cecum from mice treated with PBS or rIL-25 with isotype control or rIL-25 with anti-IL-13 (B). Representative IHC staining for angiogenin-4 in samples of cecum tissue from PBS treated (C) or rIL-25 with isotype control (D) or rIL-25 with anti-IL-13 treated mice (E).
Mentions: IL-25 is known to induce Th2 cytokines, including IL-13. Therefore, the role of IL-13 in the ability of IL-25 to induce angiogenin-4 was examined. CBA/J mice were treated with rIL-25 (closed square, n = 8) and control mice received PBS (closed circle, n = 7). IL-13 relative expression was measured from mouse cecal tissue. We found that there was significantly higher expression of IL-13 in rIL-25 treated mice than that in control mice (Fig 3). Previous studies have shown that IL-13 can induce Paneth cell degranulation and trigger the release of the antimicrobial peptide angiogenin-4. We confirmed that IL-13 induced angiogenin-4 expression (Fig 4A) in cecal epithelial cells (Fig 4B–4D). IL-25 mediated angiogenin-4 expression was abrogated when IL-13 was depleted by neutralizing antibodies (Fig 5A). This result was confirmed via immunohistochemistry of angiogenin-4 as before (Fig 5B–5E). These results indicated that IL-25 induced angiogenin-4 expression was mediated via the IL-25 downstream pathway cytokine IL-13.

Bottom Line: The intestinal surface is directly exposed to both commensal microorganisms as well as pathogens with a single layer of epithelium separating luminal microorganisms from internal tissues.Here we show that IL-13 downstream of IL-25 is required to induce angiogenin-4.IL-25 mediated induction of angiogenin-4 is furthermore not dependent on IL-22 or IL-17.

View Article: PubMed Central - PubMed

Affiliation: Division of Infectious Diseases and International Health, Department of Medicine, University of Virginia Health System, Charlottesville, Virginia, United States of America.

ABSTRACT
The intestinal surface is directly exposed to both commensal microorganisms as well as pathogens with a single layer of epithelium separating luminal microorganisms from internal tissues. Antimicrobial peptides play a crucial role in allowing epithelial cells to contain in the lumen beneficial and pathogenic microorganisms. The commensal dependent, epithelial produced, Th2 cytokine IL-25 can induce IL-13 and potentially the antimicrobial peptide angiogenin-4. Here we show that IL-13 downstream of IL-25 is required to induce angiogenin-4. IL-25 mediated induction of angiogenin-4 is furthermore not dependent on IL-22 or IL-17.

No MeSH data available.