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Published ahead of print on March 5, 2003, doi:10.1164/rccm.200205-487OC

Am. J. Respir. Crit. Care Med., Volume 167, Number 12, June 2003, 1695-1703

A more recent version of this article appeared on June 15, 2003
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Submitted on May 30, 2002
Accepted on March 4, 2003

Expression of Macrophage Inflammatory Protein (MIP)-3{beta}/CCL19 in pulmonary sarcoidosis

Agata Gibejova1, Frantisek Mrazek1, Daniela Subrtova1, Veronika Sekerova1, Jaroslava Szotkowska1, Vitezslav Kolek2, Roland M du Bois3, and Martin Petrek1*

1 Immunology, Palacky University, Olomouc, Czech Republic, 2 Respiratory Medicine, Palacky University, Olomouc, Czech Republic, 3 Interstitial Lung Disease Unit, Royal Brompton Hospital, London, United Kingdom

* To whom correspondence should be addressed. E-mail: petrekm{at}fnol.cz.

In this study, mRNA expression for novel T-lymphocyte chemoattractants, Leukotactin-1, Macrophage inflammatory protein (MIP)-3{alpha} and MIP-3{beta}, was investigated in bronchoalveolar lavage fluid (BALF) cells from patients with sarcoidosis, a T-cell-mediated disease with typical CD4+ lymphocyte alveolitis. Of these three chemokines, only MIP-3{beta} mRNA was upregulated in sarcoidosis and, therefore, protein levels of this chemokine, its pharmacological regulation and association with disease clinical course were explored. MIP-3{beta} protein concentrations were elevated in BALF from sarcoid patients compared to control subjects (p=0.001), and in patients with CXR-Stage-II chemokine protein levels were increased compared to Stage-I (p=0.003). MIP-3{beta} protein was associated predominantly with alveolar macrophages and correlated with BALF lymphocytes and T-cell subsets. mRNA expression for the MIP-3{beta} receptor, CC chemokine receptor (CCR)7, was increased in sarcoidosis and correlated with MIP-3{beta} protein levels. MIP-3{beta} mRNA and protein expression in BALF cells was suppressed by Dexamethasone and Cyclosporine A in vitro. In conclusion, MIP-3{beta} is implicated in T-lymphocyte recruitment in sarcoidosis, is associated with disease progression and downregulated by drugs used for sarcoidosis treatment. This novel chemokine, therefore, represents a candidate for studies of sarcoidosis pathobiological mechanisms.
Key words: chemokine, Lkn-1, MIP-3alpha, CCR7, alveolar macrophages, Dexamethasone, Cyclosporine A




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