2.50
Hdl Handle:
http://hdl.handle.net/10755/165845
Category:
Abstract
Type:
Presentation
Title:
Stress-induced airway cytokine responses: Implications in asthma
Author(s):
Kang, Duck-Hee
Author Details:
Duck-Hee Kang, University of Alabama at Birmingham School of Nursing, Birmingham, Alabama, USA, email: kangd@uab.edu
Abstract:
Despite the advances in asthma management, the prevalence and severity of asthma are rising. Although causes for this rise are not clear, psychosocial factors, such as stress, are thought to play a role in the exacerbation of asthma. However, the precise mechanisms by which stress modulates asthma symptoms are poorly understood. Asthma is a chronic inflammatory airway disease with a predominant Th2 cytokine profile -- increased interleukin (IL)-4 and IL-5. On the other hand, stress is known to alter cytokine responses. These findings collectively suggest that cytokine mechanisms, particularly dysregulated Th1 (IL-2 and gamma-interferon [IFN-(]) and Th2 cytokine profiles, are a potential mechanism for stress-associated exacerbation of asthma. Thus, specific aims of this study were to (1) examine effects of stress on Th1 and Th2 airway cytokine responses and their ratios; and (2) compare cytokine responses between acute single and chronic repeated stress and between asthma and non-asthmatic mice. Because of difficulty in obtaining airway samples, we conducted this descriptive comparative study using a well-established murine model of allergic asthma. Male BALB/c mice (N=70) were divided into seven groups: G1-control; G2-antigen challenged; G3-sensitized and antigen challenged (asthma model); G4-antigen and acute single tress; G5-asthma and acute single stress; G6-antigen and repeated stress for 4 days; and G7-asthma and repeated stress for 4 days. Using ovalbumin intraperitoneal injections and aerosols, mice were sensitized and antigen challenged with or without the exposure to open-field rotation stress. Bronchoalveolar lavage fluid was obtained and batch-assayed with ELISA for Th1and Th2 cytokine responses. Results indicated that non-asthmatic mice with acute or chronic stress showed significantly lower IL-4 but higher IL-2:IL-4 and IFN-(:IL-4 responses than non-stressed, non-asthmatic mice. Asthmatic mice with acute stress showed significantly higher IL-4 and IL-2:IL-5 but lower IFN-( and IFN-(:IL-5 responses than asthmatic mice without stress. Asthmatic mice with chronic stress showed significantly lower IFN-(, IL-4 and IL-5 but higher IL-2:IL-5, IFN-(:IL-4 and IFN-(:IL-5 responses than asthmatic mice without stress. Lastly, asthmatic mice showed significantly higher IL-4 but lower IL-2, IL-2:IL-4 and IL-2:IL-5 responses than non-asthmatic control mice. These findings indicate that acute novel stress induces significant airway cytokine changes toward a predominant Th2 pattern in asthmatic mice but a predominant Th1 pattern in non-asthmatic mice, supporting a Th2 cytokine mechanism in stress-induced exacerbation of asthma. Further, such cytokine profiles were most distinctive following acute stress as compared to chronic stress.
Repository Posting Date:
27-Oct-2011
Date of Publication:
27-Oct-2011
Conference Host:
Southern Nursing Research Society
Note:
This is an abstract-only submission. If the author has submitted a full-text item based on this abstract, you may find it by browsing the Virginia Henderson Global Nursing e-Repository by author. If author contact information is available in this abstract, please feel free to contact him or her with your queries regarding this submission. Alternatively, please contact the conference host, journal, or publisher (according to the circumstance) for further details regarding this item. If a citation is listed in this record, the item has been published and is available via open-access avenues or a journal/database subscription. Contact your library for assistance in obtaining the as-published article.

Full metadata record

DC FieldValue Language
dc.type.categoryAbstracten_US
dc.typePresentationen_GB
dc.titleStress-induced airway cytokine responses: Implications in asthmaen_GB
dc.contributor.authorKang, Duck-Heeen_US
dc.author.detailsDuck-Hee Kang, University of Alabama at Birmingham School of Nursing, Birmingham, Alabama, USA, email: kangd@uab.eduen_US
dc.identifier.urihttp://hdl.handle.net/10755/165845-
dc.description.abstractDespite the advances in asthma management, the prevalence and severity of asthma are rising. Although causes for this rise are not clear, psychosocial factors, such as stress, are thought to play a role in the exacerbation of asthma. However, the precise mechanisms by which stress modulates asthma symptoms are poorly understood. Asthma is a chronic inflammatory airway disease with a predominant Th2 cytokine profile -- increased interleukin (IL)-4 and IL-5. On the other hand, stress is known to alter cytokine responses. These findings collectively suggest that cytokine mechanisms, particularly dysregulated Th1 (IL-2 and gamma-interferon [IFN-(]) and Th2 cytokine profiles, are a potential mechanism for stress-associated exacerbation of asthma. Thus, specific aims of this study were to (1) examine effects of stress on Th1 and Th2 airway cytokine responses and their ratios; and (2) compare cytokine responses between acute single and chronic repeated stress and between asthma and non-asthmatic mice. Because of difficulty in obtaining airway samples, we conducted this descriptive comparative study using a well-established murine model of allergic asthma. Male BALB/c mice (N=70) were divided into seven groups: G1-control; G2-antigen challenged; G3-sensitized and antigen challenged (asthma model); G4-antigen and acute single tress; G5-asthma and acute single stress; G6-antigen and repeated stress for 4 days; and G7-asthma and repeated stress for 4 days. Using ovalbumin intraperitoneal injections and aerosols, mice were sensitized and antigen challenged with or without the exposure to open-field rotation stress. Bronchoalveolar lavage fluid was obtained and batch-assayed with ELISA for Th1and Th2 cytokine responses. Results indicated that non-asthmatic mice with acute or chronic stress showed significantly lower IL-4 but higher IL-2:IL-4 and IFN-(:IL-4 responses than non-stressed, non-asthmatic mice. Asthmatic mice with acute stress showed significantly higher IL-4 and IL-2:IL-5 but lower IFN-( and IFN-(:IL-5 responses than asthmatic mice without stress. Asthmatic mice with chronic stress showed significantly lower IFN-(, IL-4 and IL-5 but higher IL-2:IL-5, IFN-(:IL-4 and IFN-(:IL-5 responses than asthmatic mice without stress. Lastly, asthmatic mice showed significantly higher IL-4 but lower IL-2, IL-2:IL-4 and IL-2:IL-5 responses than non-asthmatic control mice. These findings indicate that acute novel stress induces significant airway cytokine changes toward a predominant Th2 pattern in asthmatic mice but a predominant Th1 pattern in non-asthmatic mice, supporting a Th2 cytokine mechanism in stress-induced exacerbation of asthma. Further, such cytokine profiles were most distinctive following acute stress as compared to chronic stress.en_GB
dc.date.available2011-10-27T14:34:54Z-
dc.date.issued2011-10-27en_GB
dc.date.accessioned2011-10-27T14:34:54Z-
dc.conference.hostSouthern Nursing Research Societyen_US
dc.description.noteThis is an abstract-only submission. If the author has submitted a full-text item based on this abstract, you may find it by browsing the Virginia Henderson Global Nursing e-Repository by author. If author contact information is available in this abstract, please feel free to contact him or her with your queries regarding this submission. Alternatively, please contact the conference host, journal, or publisher (according to the circumstance) for further details regarding this item. If a citation is listed in this record, the item has been published and is available via open-access avenues or a journal/database subscription. Contact your library for assistance in obtaining the as-published article.-
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