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Association of polymorphisms in the collagen region ofSP-A2with increased levels of total IgE antibodies and eosinophilia in patients with allergic bronchopulmonary aspergillosis

Journal of Allergy and Clinical Immunology
DOI: 10.1067/mai.2003.1395
  • Sp-A1
  • Sp-A2
  • Collagen
  • Abpa
  • Single Nucleotide Polymorphism
  • Association
  • Ige
  • Eosinophilia
  • Biology
  • Medicine


Abstract Background: Studies from our group have shown a protective role of pulmonary surfactant protein A (SP-A) against lung allergy and infections caused by Aspergillus fumigatus . Objective: Present study investigated the association of polymorphisms in the collagen region of SP-A1 and SP-A2 (genes encoding SP-A) with allergic bronchopulmonary aspergillosis (ABPA) and its clinical markers. Methods: Genomic DNA was extracted from blood samples of patients with ABPA and age-matched, unrelated control subjects. The polymorphisms were detected by means of PCR amplification and sequencing of the collagen region of SP-A1 and SP-A2 . Results: Two exonic (SP-A2 G1649C and SP-A2 A1660G, 10 patients and 11 control subjects) and 2 intronic (SP-A2 T1492C, 8 patients and 8 control subjects; SP-A1 C1416T, 5 patients and 7 control subjects) polymorphisms in the collagen region of SP-A2 and SP-A1 showed significant association with patients with ABPA. A significantly higher frequency of the AGA allele (A1660G) of SP-A2 was observed in patients with ABPA in comparison with control subjects (P = .0156, odds ratio [OR] = 4.78, 95% CI = 1.23 < OR < 18.52). This polymorphism, when existing along with a nonredundant polymorphism, SP-A2 G1649C (Ala91Pro) resulted in a stronger association with ABPA (A1660G and G1649C: P = .0079, OR = 10.4, 95% CI = 1.62 < OR < 66.90). Patients with ABPA with GCT and AGG alleles showed significantly high levels of total IgE and percentage eosinophilia versus patients with ABPA with CCT and AGA alleles. Conclusion: The results indicated that SP-A2 G1649C and SP-A2 A1660G, polymorphisms in the collagen region of SP-A2 , might be one of the contributing factors to genetic predisposition and severity of clinical markers of ABPA. (J Allergy Clin Immunol 2003;111:1001-7.)

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