Add like
Add dislike
Add to saved papers

Upregulation of ICAM-1 and IL-1β protein expression promotes lung injury in chronic obstructive pulmonary disease.

Chronic obstructive pulmonary disease (COPD) is a devastating lung disorder characterized by sustained airway flow restriction that is not fully reversible. The precise pathogenic mechanisms are unknown, but it is clear that cigarette smoking and chronic inflammatory stimulation are the major causes of COPD. Lung inflammation associated with COPD involves multiple cytokines, aggregation, and activation of neutrophils in the airway and lung tissue, and release of proteases and oxygen free radicals. In this study, a rat model of COPD was established by daily cigarette smoke exposure plus endotoxin treatment (the experimental group). Respiratory curves were recorded by the BL-420 biological signal collecting and processing system. Furthermore, the contents of inflammatory mediators, intercellular adhesion molecular (ICAM)-1 and interleukin (IL)-1β, in bronchoalveolar lavage fluid (BALF) were determined by enzyme linked immunosorbent assay for experimental, smoke-exposed only (control), and untreated (blank) rat groups. Protein expression levels of ICAM-1 and IL-1β in the lung tissue were also compared among groups by the immunohistochemical streptavidin-peroxidase method. The COPD model rats exhibited severe dyspnea and lung inflammation as evidenced by significantly prolonged expiratory duration, higher respiratory rate, elevated ICAM-1 and IL-1β in BALF, and higher ICAM-1 and IL-1β protein expression in lung tissue compared to control and blank group rats. Chronic cigarette smoke exposure plus endotoxin is a feasible and reliable model of COPD that recapitulates many clinical signs and pathogenic responses. ICAM-1 and IL-1β upregulation are possible early contributors to COPD-associated inflammatory lung injury.

Full text links

We have located links that may give you full text access.
Can't access the paper?
Try logging in through your university/institutional subscription. For a smoother one-click institutional access experience, please use our mobile app.

For the best experience, use the Read mobile app

Mobile app image

Get seemless 1-tap access through your institution/university

For the best experience, use the Read mobile app

All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.

By using this service, you agree to our terms of use and privacy policy.

Your Privacy Choices Toggle icon

You can now claim free CME credits for this literature searchClaim now

Get seemless 1-tap access through your institution/university

For the best experience, use the Read mobile app