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Published ahead of print on May 28, 2003, doi:10.1164/rccm.200302-221OC
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American Journal of Respiratory and Critical Care Medicine Vol 168. pp. 330-334, (2003)
© 2003 American Thoracic Society

Complement Receptor 1 Gene Polymorphisms Are Associated with Idiopathic Pulmonary Fibrosis

Michele Zorzetto, Ilaria Ferrarotti, Rocco Trisolini, Luigi Lazzari Agli, Roberta Scabini, Monique Novo, Annalisa De Silvestri, Marco Patelli, Miryam Martinetti, MariaClara Cuccia, Venerino Poletti, Ernesto Pozzi and Maurizio Luisetti

Laboratorio di Biochimica e Genetica, Clinica Malattie Apparato Respiratorio; Servizio di Immunoematologia e Trasfusione e Centro di Immunologia dei Trapianti; Servizio di Patologia Neonatale, Dipartimento di Genetica e Microbiologia, IRCCS Policlinico San Matteo and Università degli Studi, Pavia; Unità Operativa di Endoscopia Toracica, Dipartimento di Scienze Oncologiche, Ospedale Maggiore, Bologna; Dipartimento di Malattie dell'Apparato Respiratorio e del Torace, Ospedale G.B. Morgagni, Forlì, Italy

Correspondence and requests for reprints should be addressed to Maurizio Luisetti, M.D., Laboratorio di Biochimica e Genetica, Clinica di Malattie dell'Apparato Respiratorio, IRCCS Policlinico San Matteo, Via Taramelli 5, 27100 Pavia, Italy. E-mail: m.luisetti{at}smatteo.pv.it

Idiopathic pulmonary fibrosis (IPF) is a chronic, fibrotic disorder underlain by aberrant wound healing of repeated lung injury. Environmental triggers and genetic background are likely to act as modifiers of the fibrotic response. Erythrocyte complement receptor 1 is a membrane protein mediating the transport of immune complexes to phagocytes. Three gene polymorphisms are related to the erythrocyte surface density of complement receptor 1 molecules, which in turn are related to the rate of immune complexes' clearance. There is evidence of association between sarcoidosis and the complement receptor 1 gene. We wondered whether IPF is associated with the complement receptor 1 gene alleles coding for a reduced molecule/erythrocyte ratio. We studied 74 patients and 166 control subjects. Three polymorphic sites of the gene, A3650G exon 22, HindIII RFLP intron 27, and C5507G exon 33, were analyzed and found to be in linkage disequilibrium. The GG genotype for the C5507G exon 33 polymorphism was significantly more common in patients with IPF than in control subjects (odds ratio = 6.232, 95% confidence interval = 2.198–18.419, p = 0.00023). The significant difference was found in both sexes. These findings agree with speculations on the role of the complement receptor 1 gene in idiopathic pulmonary fibrosis.

Key Words: polymerase chain reaction • gene sequencing • candidate gene • association study • immune complexes




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