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Original Research |

Cysteinyl Leukotriene 1 Receptor Expression Associated With Bronchial Inflammation in Severe Exacerbations of COPDCysteinyl Leukotriene 1 Receptor in COPD Exacerbations

Jie Zhu, MD, PhD; Venkata Bandi, MD, FCCP; Shengyang Qiu, MD; David J. Figueroa, PhD; Jilly F. Evans, PhD; Neil Barnes, MD; Kay K. Guntupalli, FCCP; Peter K. Jeffery, DSc
Author and Funding Information

From the Lung Pathology Unit, Department of Respiratory Medicine (Drs Zhu, Qiu, and Jeffery), Imperial College London, London, England; Department of Medicine (Drs Bandi and Guntupalli), Baylor College of Medicine, Ben Taub General Hospital, Houston, TX; Department of Pharmacology (Drs Figueroa and Evans), Merck & Co Inc, West Point, PA; and Department of Respiratory Medicine (Dr Barnes), Barts and The London Hospital, London, England.

Correspondence to: Peter K. Jeffery, DSc, Lung Pathology, Imperial College London, Royal Brompton Hospital, Sydney St, London, SW3 6NP, England; e-mail: p.jeffery@imperial.ac.uk


Funding/Support: This work was supported by research grants from the National Institutes of Health [Grant NO1 AI065298], Merck Sharp & Dohme Limited UK, and by departmental funds.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2012;142(2):347-357. doi:10.1378/chest.11-1581
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Background:  Cysteinyl leukotriene 1 (CysLT1) receptor expression is known to be increased in the airway mucosa of patients with asthma, especially during exacerbations; however, nothing is known of its expression in COPD.

Methods:  We applied immunohistochemistry and in situ hybridization to endobronchial biopsies to determine inflammatory cell CysLT1 receptor protein and mRNA expression in the following: (1) 15 nonsmoker control subjects (NSC), (2) 16 smokers with moderate to severe COPD in its stable phase (S-COPD), and (3) 15 smokers with COPD hospitalized for a severe exacerbation (SE-COPD).

Results:  The total number of bronchial mucosal inflammatory cells (CD45+) and those expressing CysLT1 receptor protein were significantly greater in SE-COPD (CysLT1 receptor protein: median [range] = 139 [31-634]) as compared with S-COPD (32 [6-114]) or NSC (16 [4-66]) (P < .001 for both). CysLT1 receptor gene expression showed similar differences. A greater proportion of CD451 cells expressed CysLT1 receptor protein in SE-COPD (median [range] = 22% [8-81]) compared with S-COPD (10% [4-32]) (P < .03) or NSC (7% [1-19]) (P < .002). In SE-COPD, the relative frequencies of CysLT1 receptor-expressing cells were as follows: tryptase1 mast cells > CD681 monocytes/macrophage > neutrophils > CD201 B lymphocytes = EG21 eosinophils. Moreover, there were positive correlations between the numbers of cells expressing CysLT1 receptor protein and the numbers of CD451 cells (r = 0.78; P < .003) and tryptase1 mast cells (r = 0.62; P < .02).

Conclusions:  Bronchial mucosal CysLT1 receptor-positive inflammatory cells are present in the bronchial mucosa in COPD in greatest number in those experiencing a severe exacerbation.

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