Interleukin-22 attenuates allergic airway inflammation in ovalbumin-induced asthma mouse model
Abstract Background Allergic asthma is a chronic airway inflammatory disease with a number of cytokines participating in its pathogenesis and progress. Interleukin (IL)-22, which is derived from lymphocytes, acts on epithelial cells and play a role in the chronic airway inflammation. However, the ac...
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BMC
2021-11-01
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Series: | BMC Pulmonary Medicine |
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Online Access: | https://doi.org/10.1186/s12890-021-01698-x |
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author | Jingru Wang Shengnan Gao Jingyuan Zhang Chunxiao Li Hongwen Li Jiangtao Lin |
author_facet | Jingru Wang Shengnan Gao Jingyuan Zhang Chunxiao Li Hongwen Li Jiangtao Lin |
author_sort | Jingru Wang |
collection | DOAJ |
description | Abstract Background Allergic asthma is a chronic airway inflammatory disease with a number of cytokines participating in its pathogenesis and progress. Interleukin (IL)-22, which is derived from lymphocytes, acts on epithelial cells and play a role in the chronic airway inflammation. However, the actual role of IL-22 in allergic asthma is still unclear. Therefore, we explored the effect of IL-22 on allergic airway inflammation and airway hyperresponsiveness (AHR) in an ovalbumin (OVA)-induced asthma mouse model. Methods To evaluate the effect of IL-22 in an allergic asthma model, BALB/c mice were sensitized and challenged with OVA; then the recombinant mouse IL-22 was administered intranasally 24 h prior to each challenge. The IL-22 levels in lung homogenates and bronchoalveolar lavage fluid (BALF) were measured by enzyme linked immunosorbent assay, respectively. AHR was evaluated through indicators including airways resistance (Rrs), elastance (Ers) and compliance (Crs); the inflammatory cell infiltration was assessed by quantification of differential cells counts in BALF and lung tissues stained by hematoxylin and eosin (H&E); IL-22 specific receptors were determined by immunohistochemistry staining. Results The concentration of IL-22 was significantly elevated in the OVA-induced mice compared with the control mice in lung homogenates and BALF. In the OVA-induced mouse model, IL-22 administration could significantly attenuate AHR, including Rrs, Ers and Crs, decrease the proportion of eosinophils in BALF and reduce inflammatory cell infiltration around bronchi and their concomitant vessels, compared with the OVA-induced group. In addition, the expression of IL-22RA1 and IL-10RB in the lung tissues of OVA-induced mice was significantly increased compared with the control mice, while it was dramatically decreased after the treatment with IL-22, but not completely attenuated in the IL-22-treated mice when compared with the control mice. Conclusion Interleukin-22 could play a protective role in an OVA-induced asthma model, by suppressing the inflammatory cell infiltration around bronchi and their concomitant vessels and airway hyperresponsiveness, which might associate with the expression of its heterodimer receptors. Thus, IL-22 administration might be an effective strategy to attenuate allergic airway inflammation. |
first_indexed | 2024-12-18T02:06:32Z |
format | Article |
id | doaj.art-1c0695ce253e49dc835abd7d52faa60a |
institution | Directory Open Access Journal |
issn | 1471-2466 |
language | English |
last_indexed | 2024-12-18T02:06:32Z |
publishDate | 2021-11-01 |
publisher | BMC |
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series | BMC Pulmonary Medicine |
spelling | doaj.art-1c0695ce253e49dc835abd7d52faa60a2022-12-21T21:24:34ZengBMCBMC Pulmonary Medicine1471-24662021-11-0121111010.1186/s12890-021-01698-xInterleukin-22 attenuates allergic airway inflammation in ovalbumin-induced asthma mouse modelJingru Wang0Shengnan Gao1Jingyuan Zhang2Chunxiao Li3Hongwen Li4Jiangtao Lin5Peking University China-Japan Friendship School of Clinical MedicineDepartment of Pulmonary and Critical Care Medicine, China-Japan Friendship HospitalDepartment of Pulmonary and Critical Care Medicine, China-Japan Friendship HospitalPeking University China-Japan Friendship School of Clinical MedicinePeking University China-Japan Friendship School of Clinical MedicinePeking University China-Japan Friendship School of Clinical MedicineAbstract Background Allergic asthma is a chronic airway inflammatory disease with a number of cytokines participating in its pathogenesis and progress. Interleukin (IL)-22, which is derived from lymphocytes, acts on epithelial cells and play a role in the chronic airway inflammation. However, the actual role of IL-22 in allergic asthma is still unclear. Therefore, we explored the effect of IL-22 on allergic airway inflammation and airway hyperresponsiveness (AHR) in an ovalbumin (OVA)-induced asthma mouse model. Methods To evaluate the effect of IL-22 in an allergic asthma model, BALB/c mice were sensitized and challenged with OVA; then the recombinant mouse IL-22 was administered intranasally 24 h prior to each challenge. The IL-22 levels in lung homogenates and bronchoalveolar lavage fluid (BALF) were measured by enzyme linked immunosorbent assay, respectively. AHR was evaluated through indicators including airways resistance (Rrs), elastance (Ers) and compliance (Crs); the inflammatory cell infiltration was assessed by quantification of differential cells counts in BALF and lung tissues stained by hematoxylin and eosin (H&E); IL-22 specific receptors were determined by immunohistochemistry staining. Results The concentration of IL-22 was significantly elevated in the OVA-induced mice compared with the control mice in lung homogenates and BALF. In the OVA-induced mouse model, IL-22 administration could significantly attenuate AHR, including Rrs, Ers and Crs, decrease the proportion of eosinophils in BALF and reduce inflammatory cell infiltration around bronchi and their concomitant vessels, compared with the OVA-induced group. In addition, the expression of IL-22RA1 and IL-10RB in the lung tissues of OVA-induced mice was significantly increased compared with the control mice, while it was dramatically decreased after the treatment with IL-22, but not completely attenuated in the IL-22-treated mice when compared with the control mice. Conclusion Interleukin-22 could play a protective role in an OVA-induced asthma model, by suppressing the inflammatory cell infiltration around bronchi and their concomitant vessels and airway hyperresponsiveness, which might associate with the expression of its heterodimer receptors. Thus, IL-22 administration might be an effective strategy to attenuate allergic airway inflammation.https://doi.org/10.1186/s12890-021-01698-xAllergic asthmaCytokinesInterleukin-22Animal modelOvalbumin sensitization |
spellingShingle | Jingru Wang Shengnan Gao Jingyuan Zhang Chunxiao Li Hongwen Li Jiangtao Lin Interleukin-22 attenuates allergic airway inflammation in ovalbumin-induced asthma mouse model BMC Pulmonary Medicine Allergic asthma Cytokines Interleukin-22 Animal model Ovalbumin sensitization |
title | Interleukin-22 attenuates allergic airway inflammation in ovalbumin-induced asthma mouse model |
title_full | Interleukin-22 attenuates allergic airway inflammation in ovalbumin-induced asthma mouse model |
title_fullStr | Interleukin-22 attenuates allergic airway inflammation in ovalbumin-induced asthma mouse model |
title_full_unstemmed | Interleukin-22 attenuates allergic airway inflammation in ovalbumin-induced asthma mouse model |
title_short | Interleukin-22 attenuates allergic airway inflammation in ovalbumin-induced asthma mouse model |
title_sort | interleukin 22 attenuates allergic airway inflammation in ovalbumin induced asthma mouse model |
topic | Allergic asthma Cytokines Interleukin-22 Animal model Ovalbumin sensitization |
url | https://doi.org/10.1186/s12890-021-01698-x |
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