Colonic mucosal immune activation in mice with ovalbumin-induced allergic airway disease: Association between allergic airway disease and irritable bowel syndrome
- Authors
- Kim, S.; Keum, B.; Byun, J.; Kim, B.; Lee, K.; Yeon, J.; Lee, J.; Choi, H.; Kim, E.; Jeen, Y.; Lee, H.; Chun, H.; Kim, T.
- Issue Date
- 1월-2022
- Publisher
- MDPI
- Keywords
- Allergic airway diseases; Irritable bowel syndrome; Mast cells; Salbutamol
- Citation
- International Journal of Molecular Sciences, v.23, no.1
- Indexed
- SCIE
SCOPUS
- Journal Title
- International Journal of Molecular Sciences
- Volume
- 23
- Number
- 1
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/136562
- DOI
- 10.3390/ijms23010181
- ISSN
- 1661-6596
- Abstract
- Recent studies on the pathophysiology of irritable bowel syndrome (IBS) have focused on the role of mast cells (MCs) in intestinal mucosal immunity. A link between allergic airway diseases (AADs) and IBS has been suggested because both diseases have similar pathophysiology. We aimed to investigate whether the induction of AAD in mice could lead to inflammation of the colonic mucosa, similar to IBS. We also evaluated whether this inflammatory response could be suppressed by administering a therapeutic agent. Mice were divided into three groups: control, AAD-induced, and salbutamol-treated. An AAD mouse model was established by intraperitoneal injection and nasal challenge with ovalbumin. Mice with AAD were intranasally administered salbutamol. Analyses of cytokine levels, MC count, and tryptase levels in the intestinal mucosa were performed to compare the changes in inflammatory responses among the three groups. Inflammation was observed in the intestinal mucosa of mice in the AAD group. This inflammation in AAD mice was suppressed after salbutamol treatment. Our study demonstrates that AAD induces an inflammatory response similar to that in IBS, suggesting a possible association between IBS and AADs. In patients with IBS with such allergic components, salbutamol may have the potential to alleviate the inflammatory response. © 2021 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https:// creativecommons.org/licenses/by/ 4.0/).
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