A murine model of stress controllability attenuates Th2-dominant airway inflammatory responses

Deshmukh, Aniket; Kim, Byung-Jin; Gonzales, Xavier; Caffrey, James; Vishwanatha, Jamboor; Jones, Harlan P.

doi:10.1016/j.jneuroim.2010.03.010

« Previous Next »Journal of Neuroimmunology
Volume 225, Issue 1 , Pages 13-21, 25 August 2010

A murine model of stress controllability attenuates Th2-dominant airway inflammatory responses

Aniket Deshmukh
- Department of Molecular Biology and Immunology, University of North Texas Health Science Center, Fort Worth, Texas 3500 Camp Bowie Boulevard, Fort Worth, Texas 76107, United States
Byung-Jin Kim
- Department of Molecular Biology and Immunology, University of North Texas Health Science Center, Fort Worth, Texas 3500 Camp Bowie Boulevard, Fort Worth, Texas 76107, United States
Xavier Gonzales
- Department of Molecular Biology and Immunology, University of North Texas Health Science Center, Fort Worth, Texas 3500 Camp Bowie Boulevard, Fort Worth, Texas 76107, United States
James Caffrey
- Department of Integrative Physiology, University of North Texas Health Science Center, Fort Worth, Texas 3500 Camp Bowie Boulevard, Fort Worth, Texas 76107, United States
Jamboor Vishwanatha
- Department of Molecular Biology and Immunology, University of North Texas Health Science Center, Fort Worth, Texas 3500 Camp Bowie Boulevard, Fort Worth, Texas 76107, United States
Harlan P. Jones
- Department of Molecular Biology and Immunology, University of North Texas Health Science Center, Fort Worth, Texas 3500 Camp Bowie Boulevard, Fort Worth, Texas 76107, United States
- Corresponding author. Tel.: +817 735 2448; fax: +817 735 2133.

Received 22 September 2009; received in revised form 8 March 2010; accepted 15 March 2010. published online 13 May 2010.

Abstract

Epidemiological and experimental studies suggest a positive correlation between chronic respiratory inflammatory disease and the ability to cope with adverse stress. Interactions between neuroendocrine and immune systems are believed to provide insight toward the biological mechanisms of action. The utility of an experimental murine model was employed to investigate the immunological consequences of stress-controllability and ovalbumin-induced airway inflammation. Pre-conditioned uncontrollable stress exacerbated OVA-induced lung histopathological changes that were typical of Th2-predominant inflammatory response along respiratory tissues. Importantly, mice given the ability to exert control over aversive stress attenuated inflammatory responses and reduced lung pathology. This model represents a means of investigating the neuro-immune axis in defining mechanisms of stress and respiratory disease.

Keywords: Stress, Controllability, Asthma, Immunity