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 inEuropean journal of immunology Vol. 51; no. 1; pp. 191 - 196
Main Authors Neuper, Theresa, Neureiter, Daniel, Sarajlic, Muamera, Strandt, Helen, Bauer, Renate, Schwarz, Harald, Suchanek, Patrick, Korotchenko, Evgeniia, Dillon, Stacey R., Hammerl, Peter, Stoecklinger, Angelika, Weiss, Richard, Horejs‐Hoeck, Jutta
Format Journal Article
LanguageEnglish
Published Germany Wiley Subscription Services, Inc 01.01.2021
John Wiley and Sons Inc
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Online AccessGet full text
ISSN0014-2980
1521-4141
1521-4141
DOI10.1002/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.
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
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Issue 1
Keywords Lung inflammation
Grass pollen allergen
IL-31RA expression
Leukocyte infiltration
IL-31
Language English
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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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StartPage 191
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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