IL‐31 transgenic mice show reduced allergen‐induced lung inflammation
Interleukin‐31 (IL‐31) is a Th2 cell–derived cytokine that has been closely linked to pruritic skin inflammation. More recently, enhanced IL‐31 serum levels have also been observed in patients with allergic rhinitis and allergic asthma. Therefore, the main aim of this study was to unravel the contri...
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Published in | European journal of immunology Vol. 51; no. 1; pp. 191 - 196 |
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Main Authors | , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
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01.01.2021
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ISSN | 0014-2980 1521-4141 1521-4141 |
DOI | 10.1002/eji.202048547 |
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Abstract | Interleukin‐31 (IL‐31) is a Th2 cell–derived cytokine that has been closely linked to pruritic skin inflammation. More recently, enhanced IL‐31 serum levels have also been observed in patients with allergic rhinitis and allergic asthma. Therefore, the main aim of this study was to unravel the contribution of IL‐31 to allergen‐induced lung inflammation. We analyzed lung inflammation in response to the timothy grass (Phleum pratense) pollen allergen Phl p 5 in C57BL/6 wild‐type (wt) mice, IL‐31 transgenic (IL‐31tg) mice, and IL‐31 receptor alpha‐deficient animals (IL‐31RA−/−). IL‐31 and IL‐31RA levels were monitored by qRT‐PCR. Cellular infiltrate in bronchoalveolar lavage fluid (BALF) and lung tissue inflammation, mucus production as well as epithelial thickness were measured by flow cytometry and histomorphology. While allergen challenge induced IL‐31RA expression in lung tissue of wt and IL‐31tg mice, high IL‐31 expression was exclusively observed in lung tissue of IL‐31tg mice. Upon Phl p 5 challenge, IL‐31tg mice showed reduced numbers of leukocytes and eosinophils in BALF and lung tissue as well as diminished mucin expression and less pronounced epithelial thickening compared to IL‐31RA−/− or wt animals. These findings suggest that the IL‐31/IL‐31RA axis may regulate local, allergen‐induced inflammation in the lungs.
This study describes a role for IL‐31 signaling in the context of allergen‐induced lung inflammation. Mice overexpressing IL‐31 develop less severe lung inflammation upon allergen exposure, characterized by decreased leukocyte infiltration, mucus production and epithelial thickening. Thus, our data indicate that IL‐31 signaling regulates allergen‐induced lung inflammation. |
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AbstractList | Interleukin‐31 (IL‐31) is a Th2 cell–derived cytokine that has been closely linked to pruritic skin inflammation. More recently, enhanced IL‐31 serum levels have also been observed in patients with allergic rhinitis and allergic asthma. Therefore, the main aim of this study was to unravel the contribution of IL‐31 to allergen‐induced lung inflammation. We analyzed lung inflammation in response to the timothy grass (
Phleum pratense
) pollen allergen Phl p 5 in C57BL/6 wild‐type (wt) mice, IL‐31 transgenic (IL‐31tg) mice, and IL‐31 receptor alpha‐deficient animals (IL‐31RA
−/−
). IL‐31 and IL‐31RA levels were monitored by qRT‐PCR. Cellular infiltrate in bronchoalveolar lavage fluid (BALF) and lung tissue inflammation, mucus production as well as epithelial thickness were measured by flow cytometry and histomorphology. While allergen challenge induced IL‐31RA expression in lung tissue of wt and IL‐31tg mice, high IL‐31 expression was exclusively observed in lung tissue of IL‐31tg mice. Upon Phl p 5 challenge, IL‐31tg mice showed reduced numbers of leukocytes and eosinophils in BALF and lung tissue as well as diminished mucin expression and less pronounced epithelial thickening compared to IL‐31RA
−/−
or wt animals. These findings suggest that the IL‐31/IL‐31RA axis may regulate local, allergen‐induced inflammation in the lungs. Interleukin‐31 (IL‐31) is a Th2 cell–derived cytokine that has been closely linked to pruritic skin inflammation. More recently, enhanced IL‐31 serum levels have also been observed in patients with allergic rhinitis and allergic asthma. Therefore, the main aim of this study was to unravel the contribution of IL‐31 to allergen‐induced lung inflammation. We analyzed lung inflammation in response to the timothy grass (Phleum pratense) pollen allergen Phl p 5 in C57BL/6 wild‐type (wt) mice, IL‐31 transgenic (IL‐31tg) mice, and IL‐31 receptor alpha‐deficient animals (IL‐31RA−/−). IL‐31 and IL‐31RA levels were monitored by qRT‐PCR. Cellular infiltrate in bronchoalveolar lavage fluid (BALF) and lung tissue inflammation, mucus production as well as epithelial thickness were measured by flow cytometry and histomorphology. While allergen challenge induced IL‐31RA expression in lung tissue of wt and IL‐31tg mice, high IL‐31 expression was exclusively observed in lung tissue of IL‐31tg mice. Upon Phl p 5 challenge, IL‐31tg mice showed reduced numbers of leukocytes and eosinophils in BALF and lung tissue as well as diminished mucin expression and less pronounced epithelial thickening compared to IL‐31RA−/− or wt animals. These findings suggest that the IL‐31/IL‐31RA axis may regulate local, allergen‐induced inflammation in the lungs. Interleukin‐31 (IL‐31) is a Th2 cell–derived cytokine that has been closely linked to pruritic skin inflammation. More recently, enhanced IL‐31 serum levels have also been observed in patients with allergic rhinitis and allergic asthma. Therefore, the main aim of this study was to unravel the contribution of IL‐31 to allergen‐induced lung inflammation. We analyzed lung inflammation in response to the timothy grass (Phleum pratense) pollen allergen Phl p 5 in C57BL/6 wild‐type (wt) mice, IL‐31 transgenic (IL‐31tg) mice, and IL‐31 receptor alpha‐deficient animals (IL‐31RA−/−). IL‐31 and IL‐31RA levels were monitored by qRT‐PCR. Cellular infiltrate in bronchoalveolar lavage fluid (BALF) and lung tissue inflammation, mucus production as well as epithelial thickness were measured by flow cytometry and histomorphology. While allergen challenge induced IL‐31RA expression in lung tissue of wt and IL‐31tg mice, high IL‐31 expression was exclusively observed in lung tissue of IL‐31tg mice. Upon Phl p 5 challenge, IL‐31tg mice showed reduced numbers of leukocytes and eosinophils in BALF and lung tissue as well as diminished mucin expression and less pronounced epithelial thickening compared to IL‐31RA−/− or wt animals. These findings suggest that the IL‐31/IL‐31RA axis may regulate local, allergen‐induced inflammation in the lungs. This study describes a role for IL‐31 signaling in the context of allergen‐induced lung inflammation. Mice overexpressing IL‐31 develop less severe lung inflammation upon allergen exposure, characterized by decreased leukocyte infiltration, mucus production and epithelial thickening. Thus, our data indicate that IL‐31 signaling regulates allergen‐induced lung inflammation. Interleukin‐31 (IL‐31) is a Th2 cell–derived cytokine that has been closely linked to pruritic skin inflammation. More recently, enhanced IL‐31 serum levels have also been observed in patients with allergic rhinitis and allergic asthma. Therefore, the main aim of this study was to unravel the contribution of IL‐31 to allergen‐induced lung inflammation. We analyzed lung inflammation in response to the timothy grass (Phleum pratense) pollen allergen Phl p 5 in C57BL/6 wild‐type (wt) mice, IL‐31 transgenic (IL‐31tg) mice, and IL‐31 receptor alpha‐deficient animals (IL‐31RA−/−). IL‐31 and IL‐31RA levels were monitored by qRT‐PCR. Cellular infiltrate in bronchoalveolar lavage fluid (BALF) and lung tissue inflammation, mucus production as well as epithelial thickness were measured by flow cytometry and histomorphology. While allergen challenge induced IL‐31RA expression in lung tissue of wt and IL‐31tg mice, high IL‐31 expression was exclusively observed in lung tissue of IL‐31tg mice. Upon Phl p 5 challenge, IL‐31tg mice showed reduced numbers of leukocytes and eosinophils in BALF and lung tissue as well as diminished mucin expression and less pronounced epithelial thickening compared to IL‐31RA−/− or wt animals. These findings suggest that the IL‐31/IL‐31RA axis may regulate local, allergen‐induced inflammation in the lungs. This study describes a role for IL‐31 signaling in the context of allergen‐induced lung inflammation. Mice overexpressing IL‐31 develop less severe lung inflammation upon allergen exposure, characterized by decreased leukocyte infiltration, mucus production and epithelial thickening. Thus, our data indicate that IL‐31 signaling regulates allergen‐induced lung inflammation. Interleukin-31 (IL-31) is a Th2 cell-derived cytokine that has been closely linked to pruritic skin inflammation. More recently, enhanced IL-31 serum levels have also been observed in patients with allergic rhinitis and allergic asthma. Therefore, the main aim of this study was to unravel the contribution of IL-31 to allergen-induced lung inflammation. We analyzed lung inflammation in response to the timothy grass (Phleum pratense) pollen allergen Phl p 5 in C57BL/6 wild-type (wt) mice, IL-31 transgenic (IL-31tg) mice, and IL-31 receptor alpha-deficient animals (IL-31RA ). IL-31 and IL-31RA levels were monitored by qRT-PCR. Cellular infiltrate in bronchoalveolar lavage fluid (BALF) and lung tissue inflammation, mucus production as well as epithelial thickness were measured by flow cytometry and histomorphology. While allergen challenge induced IL-31RA expression in lung tissue of wt and IL-31tg mice, high IL-31 expression was exclusively observed in lung tissue of IL-31tg mice. Upon Phl p 5 challenge, IL-31tg mice showed reduced numbers of leukocytes and eosinophils in BALF and lung tissue as well as diminished mucin expression and less pronounced epithelial thickening compared to IL-31RA or wt animals. These findings suggest that the IL-31/IL-31RA axis may regulate local, allergen-induced inflammation in the lungs. Interleukin-31 (IL-31) is a Th2 cell-derived cytokine that has been closely linked to pruritic skin inflammation. More recently, enhanced IL-31 serum levels have also been observed in patients with allergic rhinitis and allergic asthma. Therefore, the main aim of this study was to unravel the contribution of IL-31 to allergen-induced lung inflammation. We analyzed lung inflammation in response to the timothy grass (Phleum pratense) pollen allergen Phl p 5 in C57BL/6 wild-type (wt) mice, IL-31 transgenic (IL-31tg) mice, and IL-31 receptor alpha-deficient animals (IL-31RA-/- ). IL-31 and IL-31RA levels were monitored by qRT-PCR. Cellular infiltrate in bronchoalveolar lavage fluid (BALF) and lung tissue inflammation, mucus production as well as epithelial thickness were measured by flow cytometry and histomorphology. While allergen challenge induced IL-31RA expression in lung tissue of wt and IL-31tg mice, high IL-31 expression was exclusively observed in lung tissue of IL-31tg mice. Upon Phl p 5 challenge, IL-31tg mice showed reduced numbers of leukocytes and eosinophils in BALF and lung tissue as well as diminished mucin expression and less pronounced epithelial thickening compared to IL-31RA-/- or wt animals. These findings suggest that the IL-31/IL-31RA axis may regulate local, allergen-induced inflammation in the lungs.Interleukin-31 (IL-31) is a Th2 cell-derived cytokine that has been closely linked to pruritic skin inflammation. More recently, enhanced IL-31 serum levels have also been observed in patients with allergic rhinitis and allergic asthma. Therefore, the main aim of this study was to unravel the contribution of IL-31 to allergen-induced lung inflammation. We analyzed lung inflammation in response to the timothy grass (Phleum pratense) pollen allergen Phl p 5 in C57BL/6 wild-type (wt) mice, IL-31 transgenic (IL-31tg) mice, and IL-31 receptor alpha-deficient animals (IL-31RA-/- ). IL-31 and IL-31RA levels were monitored by qRT-PCR. Cellular infiltrate in bronchoalveolar lavage fluid (BALF) and lung tissue inflammation, mucus production as well as epithelial thickness were measured by flow cytometry and histomorphology. While allergen challenge induced IL-31RA expression in lung tissue of wt and IL-31tg mice, high IL-31 expression was exclusively observed in lung tissue of IL-31tg mice. Upon Phl p 5 challenge, IL-31tg mice showed reduced numbers of leukocytes and eosinophils in BALF and lung tissue as well as diminished mucin expression and less pronounced epithelial thickening compared to IL-31RA-/- or wt animals. These findings suggest that the IL-31/IL-31RA axis may regulate local, allergen-induced inflammation in the lungs. |
Author | Korotchenko, Evgeniia Sarajlic, Muamera Strandt, Helen Suchanek, Patrick Weiss, Richard Schwarz, Harald Neuper, Theresa Dillon, Stacey R. Hammerl, Peter Stoecklinger, Angelika Bauer, Renate Horejs‐Hoeck, Jutta Neureiter, Daniel |
AuthorAffiliation | 1 Department of Biosciences University of Salzburg Salzburg Austria 3 ZymoGenetics, Inc. Bristol‐Myers Squibb East Syracuse NY USA 2 Institute of Pathology Paracelsus Medical University/Salzburger Landeskliniken (SALK) Salzburg Austria |
AuthorAffiliation_xml | – name: 1 Department of Biosciences University of Salzburg Salzburg Austria – name: 2 Institute of Pathology Paracelsus Medical University/Salzburger Landeskliniken (SALK) Salzburg Austria – name: 3 ZymoGenetics, Inc. Bristol‐Myers Squibb East Syracuse NY USA |
Author_xml | – sequence: 1 givenname: Theresa surname: Neuper fullname: Neuper, Theresa organization: University of Salzburg – sequence: 2 givenname: Daniel surname: Neureiter fullname: Neureiter, Daniel organization: Paracelsus Medical University/Salzburger Landeskliniken (SALK) – sequence: 3 givenname: Muamera surname: Sarajlic fullname: Sarajlic, Muamera organization: University of Salzburg – sequence: 4 givenname: Helen surname: Strandt fullname: Strandt, Helen organization: University of Salzburg – sequence: 5 givenname: Renate surname: Bauer fullname: Bauer, Renate organization: University of Salzburg – sequence: 6 givenname: Harald surname: Schwarz fullname: Schwarz, Harald organization: University of Salzburg – sequence: 7 givenname: Patrick surname: Suchanek fullname: Suchanek, Patrick organization: University of Salzburg – sequence: 8 givenname: Evgeniia surname: Korotchenko fullname: Korotchenko, Evgeniia organization: University of Salzburg – sequence: 9 givenname: Stacey R. surname: Dillon fullname: Dillon, Stacey R. organization: Bristol‐Myers Squibb – sequence: 10 givenname: Peter surname: Hammerl fullname: Hammerl, Peter organization: University of Salzburg – sequence: 11 givenname: Angelika surname: Stoecklinger fullname: Stoecklinger, Angelika organization: University of Salzburg – sequence: 12 givenname: Richard orcidid: 0000-0003-3185-7253 surname: Weiss fullname: Weiss, Richard organization: University of Salzburg – sequence: 13 givenname: Jutta orcidid: 0000-0002-0984-204X surname: Horejs‐Hoeck fullname: Horejs‐Hoeck, Jutta email: jutta.horejs_hoeck@sbg.ac.at organization: University of Salzburg |
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Keywords | Lung inflammation Grass pollen allergen IL-31RA expression Leukocyte infiltration IL-31 |
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Snippet | Interleukin‐31 (IL‐31) is a Th2 cell–derived cytokine that has been closely linked to pruritic skin inflammation. More recently, enhanced IL‐31 serum levels... Interleukin-31 (IL-31) is a Th2 cell-derived cytokine that has been closely linked to pruritic skin inflammation. More recently, enhanced IL-31 serum levels... |
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SubjectTerms | Allergens Allergens - adverse effects Allergens - immunology Allergic rhinitis Allergies Allergy and inflammation Alveoli Animals Asthma Asthma - etiology Asthma - immunology Asthma - prevention & control Bronchoalveolar Lavage Fluid - immunology Bronchus Disease Models, Animal Eosinophils - immunology Female Flow cytometry Grass pollen allergen Helper cells IL‐31 IL‐31RA expression Inflammation Interleukins - genetics Interleukins - immunology Leukocyte infiltration Leukocytes (eosinophilic) Leukocytes - immunology Lung - immunology Lung - pathology Lung inflammation Lungs Lymphocytes T Mice Mice, Inbred C57BL Mice, Knockout Mice, Transgenic Mucin Phleum - adverse effects Phleum - immunology Plant Proteins - adverse effects Plant Proteins - immunology Pneumonia - etiology Pneumonia - immunology Pneumonia - prevention & control Pollen - adverse effects Pollen - immunology Receptors, Interleukin - deficiency Receptors, Interleukin - genetics Receptors, Interleukin - immunology Serum levels Short Communication|Basic Transgenic mice |
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Title | IL‐31 transgenic mice show reduced allergen‐induced lung inflammation |
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