IGG SUBCLASS RESPONSES TO PSEUDOMONAS-AERUGINOSA A-TYPE AND B-TYPE FLAGELLINS IN PATIENTS WITH CYSTIC-FIBROSIS - A PROSPECTIVE-STUDY

Citation
J. Lagace et al., IGG SUBCLASS RESPONSES TO PSEUDOMONAS-AERUGINOSA A-TYPE AND B-TYPE FLAGELLINS IN PATIENTS WITH CYSTIC-FIBROSIS - A PROSPECTIVE-STUDY, Journal of Medical Microbiology, 43(4), 1995, pp. 270-276
Citations number
32
Categorie Soggetti
Microbiology
ISSN journal
00222615
Volume
43
Issue
4
Year of publication
1995
Pages
270 - 276
Database
ISI
SICI code
0022-2615(1995)43:4<270:ISRTPA>2.0.ZU;2-5
Abstract
Sera from 20 cystic fibrosis patients, whose lungs were colonised by P seudomonas aeruginosa, were examined in a 3-5-year prospective study f or any relationship between IgG subclass antibody levels to P. aerugin osa a- and b-type flagellins and pulmonary function (FEV, and radiolog ical score). Patients were divided into two groups according to their pulmonary status: group 1 comprised 11 patients with poor pulmonary st atus; group 2 comprised nine patients with relatively good pulmonary s tatus. High concentrations of IgG1, IgG2 and IgG3 antibodies to flagel lins, particularly to the b-type, were found in most patients. IgG4 re activity was observed in only a few patients. Comparison of the two gr oups of patients showed that those with poor pulmonary status (group 1 ) had a significantly higher concentration (p < 0.05) of IgG3 for two of the three periods studied and of IgG2 for the last period studied. Moreover, IgG3 and IgG1 reactivities to b-type flagellin and IgG3 to a -type flagellin were also increased significantly (p < 0.05) in group 1 patients between the first and the last period studied. These patien ts also showed a significant (p < 0.05) time-dependent increase in IgG 3 and IgG1 antibody concentrations. These data demonstrate that cystic fibrosis patients with poorer pulmonary status have higher IgG3 level s to flagellin than other cystic fibrosis patients. High concentration s of strong opsonic IgG3 and, to a lesser degree, of IgG1 antibodies m ay increase pulmonary inflammation and induce heightened pulmonary det erioration.