Fcγ receptor IIA genotype and susceptibility to P. aeruginosa infection in patients with cystic fibrosis

It has been suggested that genes other than CFTR could modulate the severity of lung disease in cystic fibrosis (CF). Neutrophil Fcγ receptor II (FcγRII) is involved in host defense against microorganisms and in inflammatory response. We evaluated the association between genetic variability of this gene and both airway infection with Pseudomonas aeruginosa and severity of lung disease in patients with CF. We studied 167 Italian unrelated patients with CF and 50 control subjects. The distribution of FcγRIIA genotypes in CF patients was compared with that in control subjects and the different genotypes were related with the presence or absence of P. aeruginosa infection and markers of disease severity in CF patients. The distribution of FcγRIIA genotypes was not significantly different between CF patients and controls. We observed that in CF patients with the same CFTR genotype (ΔF508/ΔF508), those carrying the R allele of FcγRIIA had an increased risk of acquiring chronic P. aeruginosa infection (P=0.042, R.R.: 4.38; 95% CI: 1.17 ÷ 22.4). Moreover, the frequency of R/R genotype in patients with chronic P. aeruginosa infection seems to be higher than that of control subjects and patients without chronic infection. The observation that CF patients carrying the R allele of FcγRIIA are at higher risk of acquiring chronic P. aeruginosa infection suggests that the FcγRII loci genetic variation is contributing to this infection susceptibility.