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Published ahead of print on August 14, 2008, doi:10.1164/rccm.200804-646OC

Am. J. Respir. Crit. Care Med., Volume 178, Number 9, November 2008, 894-901

A more recent version of this article appeared on November 1, 2008
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Submitted on April 30, 2008
Accepted on August 14, 2008

IL-32, A Novel Proinflammatory Cytokine in Chronic Obstructive Pulmonary Disease

Fiorella Calabrese1, Simonetta Baraldo2, Erica Bazzan2, Francesca Lunardi1, Federico Rea2, Piero Maestrelli3, Graziella Turato2, Kim Lokar-Oliani2, Alberto Papi4, Renzo Zuin2, Paolo Sfriso5, Elisabetta Balestro2, Charles A Dinarello6, and Marina Saetta2*

1 Department of Medical Diagnostic Sciences and Special Therapies, University of Padova, Padova, Italy, 2 Department of Cardiac, Thoracic and Vascular Sciences, University of Padova and Padova City Hosptial, Padova, Italy, 3 Department of Environmental Medicine and Public Health, University of Padova, Padova, Italy, 4 Department of Clinical and Experimental Medicine, University of Ferrara, Ferrara, Italy, 5 Department of Clinical and Experimental Medicine, University of Padova, Padova, Italy, 6 University of Colorado Health Sciences Center, Denver, CO, USA

* To whom correspondence should be addressed. E-mail: marina.saetta{at}unipd.it.

Rationale: COPD is a chronic inflammatory disorder of the lung; yet the mechanisms that regulate this immune-inflammatory response are not fully understood. Objectives: We investigated whether IL-32, a newly discovered cytokine, was related to markers of inflammation and clinical progression in COPD. Methods: Using immunohistochemistry, expression of IL-32 was examined in surgically resected specimens from 40 smokers with COPD (FEV1=39±4 % predicted), 11 smokers with normal lung function and 9 non-smoking controls. IL-32 was quantified in alveolar macrophages, alveolar walls, bronchioles and arterioles, and confirmed by molecular analysis. The levels of IL-32 were correlated with the cellular infiltrates, markers of inflammation and clinical data. Measurements and Main Results: Macrophage staining for IL-32 was increased in smokers with COPD compared with control smokers and non-smokers (p=0.0014 and p<0.0001) and similar differences were observed in alveolar walls (p=0.0004 and p=0.0005) and bronchiolar epithelium (p=0.004 and p=0.0009). This increase was also detected at mRNA level (p=0.007 vs control smokers and p=0.029 vs non-smokers) and was mainly due to non-{alpha} isoforms. Moreover, IL-32 expression was positively correlated with TNF{alpha} (p=0.004, rs=0.70), CD8+cells (p=0.02, rs=0.46), phospho p38MAPK (p<0.01, rs=0.60) and negatively with FEV1 values (p=0.004, rs=-0.53). Conclusions: This is the first study to demonstrate increased expression of IL-32 in lung tissue of patients with COPD, where it was co-localized with TNF{alpha} and correlated with the degree of airflow obstruction. These results suggest that IL-32 is implicated in the characteristic immune response of COPD, with a possible impact on disease progression.
Key words: inflammatory cytokines, immune response, airflow limitation, cigarette smoking




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