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Increased MCP-1 and MIP-1β in bronchoalveolar lavage fluid of chronic bronchitics

Authors


  • The study was supported by grants: “Ricerca Corrente” from the Ministry of Health and “Ricerca Sanitaria Finalizzata” from Regione Piemonte, Torino, Italy.

A. Capelli
Divisione di Pneumologia
Centro Medico di Riabilitazione
Veruno (Novara)
Italy
Fax: 390 322830294

Abstract

CC-chemokines are chemotactic factors expressed in a wide range of cell types and tissues. The aim of this study was to evaluate the involvement of CC-chemokines in the airways inflammation of patients affected by chronic bronchitis.

The study evaluated, with an immunoassay, the concentrations of monocyte chemotactic protein-1 (MCP-1), macrophage inflammatory protein-1α (MIP-1α) and macrophage inflammatory protein-1β (MIP-1β), in the bronchoalveolar lavage fluid (BALF) of 12 smokers affected by chronic bronchitis and 14 smoking, 15 nonsmoking and six exsmoking healthy subjects.

MCP-1 was significantly increased in patients with chronic bronchitis ((mean±sd) 10.75±4.04 pg·mL-1) and in the smoker control group (12.39±5.87 pg·mL-1) compared with healthy exsmokers: (7.12±1.60 pg·mL-1, p=0.035 and p=0.045, respectively) and nonsmokers (6.41±3.87 pg·mL-1, p=0.003 and p=0.006, respectively). MIP-1α concentrations were undetectable. A significant difference was observed in MIP-1-β levels in BALF of chronic bronchitics (8.11±5.97 pg·mL-1) compared to smoker (3.57±2.90 pg·mL-1, p=0.018), exsmoker (3.43±0.68 pg·mL-1, p=0.025) and nonsmoker (3.39±3.73 pg·mL-1, p=0.008) control groups. A negative correlation was observed between MIP-1β levels and forced expiratory volume in one second values (ρ= -0.64, p=0.035) in chronic bronchitics.

An increase of monocyte chemotactic protein-1 is related to smoking habit and seems consistent with a lung inflammatory reaction. On the contrary, an increase in macrophage inflammatory protein-1β levels is restricted to smokers developing chronic obstructive pulmonary disease. These data suggest a role of CC-chemokines in the pathogenesis of chronic bronchitis.

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