title: Distinct alleles of mannose-binding lectin (MBL) and surfactant proteins A (SP-A) in patients with chronic cavitary pulmonary aspergillosis and allergic bronchopulmonary aspergillosis.
abstract: BACKGROUND
  Distinct host immune status predisposes to different forms of pulmonary aspergillosis.
  
  
  METHODS
  Patients with chronic cavitary pulmonary aspergillosis (CCPA; n=15) or allergic bronchopulmonary aspergillosis (ABPA; n=7) of Caucasian origin were screened for single nucleotide polymorphisms (SNPs) in the collagen region of surfactant proteins A1 (SP-A1) and A2 (SP-A2) and mannose binding lectin (MBL).
  
  
  RESULTS
  The T allele at T1492C and G allele at G1649C of SP-A2 were observed at slightly higher frequencies in ABPA patients (86% and 93%) than in controls (63% and 83%), and the C alleles at position 1492 and 1649 were found in higher frequencies in CCPA patients (33% and 25%) than in ABPA patients (14% and 7%) (all p>0.05). However, the CC genotype at position 1649 of SP-A2 was significantly associated with CCPA (chi(2)=7.94; p(corr)< or =0.05). Similarly, ABPA patients showed a higher frequency of the TT genotype (71%) at 1492 of SP-A2 than controls (43%) and CCPA patients (41%) (p>0.05). In the case of MBL, the T allele (OR=3.1, range 1.2-8.9; p< or =0.02) and CT genotype (chi(2)=6.54; p(corr)< or =0.05) at position 868 (codon 52) were significantly associated with CCPA, but not with ABPA. Further analysis of genotype combinations at position 1649 of SP-A2 and at 868 of MBL between patient groups showed that both CC/CC and CC/CT SP-A2/MBL were found only in CCPA patients, while GG/CT SP-A2/MBL was significantly higher in CCPA patients in comparison to ABPA patients (p< or =0.05). SNPs analysed in SP-A1 did not differ between cases and controls.
  
  
  CONCLUSIONS
  Distinct alleles, genotypes and genotype combinations of SP-A2 and MBL may contribute to differential susceptibility of the host to CCPA or ABPA.
authors.affiliation: Molecular Biochemistry and Diagnostics, Institute of Genomics and Integrative Biology, Delhi, India.
authors.forename: Mudit
authors.initials: M
authors.lastname: Vaid
authors.forename: Savneet
authors.initials: S
authors.lastname: Kaur
authors.forename: Helen
authors.initials: H
authors.lastname: Sambatakou
authors.forename: Taruna
authors.initials: T
authors.lastname: Madan
authors.forename: David W
authors.initials: DW
authors.lastname: Denning
authors.forename: P Usha
authors.initials: PU
authors.lastname: Sarma
mesh_terms: D000483:Alleles; D001229:Aspergillosis, Allergic Bronchopulmonary / Q000209:etiology / Q000235:genetics*; D016022:Case-Control Studies; D002908:Chronic Disease; D005787:Gene Frequency; D020022:Genetic Predisposition to Disease; D005820:Genetic Testing; D005838:Genotype; D006801:Humans; D037241:Mannose-Binding Lectins / Q000235:genetics*; D020641:Polymorphism, Single Nucleotide; D037662:Pulmonary Surfactant-Associated Protein A / Q000235:genetics*
chemical_list: D037241:Mannose-Binding Lectins; D037662:Pulmonary Surfactant-Associated Protein A