Abstract 2563 The Response of Interleukin-12 vs Interleukin-17 Under Stress Controllability in a Murine Model of Airway Inflammation

Airway disease such as allergy and asthma is a leading cause of illness in the U.S. While the pathophysiological characteristics are well-known, the underlying mediators remain less understood. Experimental and anecdotal evidence support the long-standing idea that 'stress' can exacerbate airway hypersensitivity that is linked to neuroendocrine stress responses' (e.g., steroid and catecholamine) effect on cellular immune and inflammatory function. Using a rodent model of aversive stress-induced airway hypersensitivity.

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Publication Details

Journal
Journal of Biological Chemistry
Published
2025-05-01
DOI
https://doi.org/10.1016/j.jbc.2025.109371
Primary Topic
IL-33, ST2, and ILC Pathways
Type
article
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article

Abstract 2563 The Response of Interleukin-12 vs Interleukin-17 Under Stress Controllability in a Murine Model of Airway Inflammation

Harlan P. Jones, Byron Quinn, Maria Brown, Jamie Y. Choe
Journal of Biological Chemistry
IL-33, ST2, and ILC Pathways
article

Abstract 2563 The Response of Interleukin-12 vs Interleukin-17 Under Stress Controllability in a Murine Model of Airway Inflammation

Harlan P. Jones, Byron Quinn, Maria Brown, Jamie Y. Choe
article en

Abstract

Airway disease such as allergy and asthma is a leading cause of illness in the U.S. While the pathophysiological characteristics are well-known, the underlying mediators remain less understood. Experimental and anecdotal evidence support the long-standing idea that 'stress' can exacerbate airway hypersensitivity that is linked to neuroendocrine stress responses' (e.g., steroid and catecholamine) effect on cellular immune and inflammatory function. Using a rodent model of aversive stress-induced airway hypersensitivity.

Journal of Biological ChemistryVol. 301(5)
Langston University (US)
Good health and well-being
Openalex Percentile: Top 85%
IL-33, ST2, and ILC Pathways
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