Open AccessInvestigating the humoral immune response in chronic venous leg ulcer patients colonised with Pseudomonas aeruginosa
Author(s) -
Jacobsen Jasper N,
Andersen Anders S,
Sonnested Michael K,
Laursen Inga,
Jorgensen Bo,
Krogfelt Karen A
Publication year - 2011
Publication title -
international wound journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.867
H-Index - 63
eISSN - 1742-481X
pISSN - 1742-4801
DOI - 10.1111/j.1742-481x.2010.00741.x
Subject(s) - pseudomonas aeruginosa , medicine , immune system , immunology , elastase , antibody , pseudomonas exotoxin , humoral immunity , microbiology and biotechnology , mannan binding lectin , lectin , biology , bacteria , biochemistry , genetics , enzyme
The ability to manage the bioburden in chronic wounds is most likely coupled to the humoral immune response of the patient. We analysed markers of systemic immune response in patients with chronic venous leg ulcers (CVLUs) colonised (no‐systemic infection) with the opportunistic pathogen Pseudomonas aeruginosa . Sera from 44 clinically non infected patients with CVLUs were analysed for total IgM and IgG isotype 1–4, complement C3, mannose‐binding lectin (MBL), interleukin (IL)‐6, C‐reactive protein (CRP) and specific anti‐ P. aeruginosa antibodies against exotoxin A, elastase and alkaline phosphatase. Concentrations of IL‐6 versus CRP intercorrelated ( β = 2·43 95% CI (1·34–4·34)), but were independent of P. aeruginosa colonisation. MBL deficiency (MBL < 500 ng/ml) correlated to high serum levels of IgG 1 ( P = 0·038) consistent with a compensatory mechanism, but not related to presence of P. aeruginosa in the ulcers. Twenty‐four patients (54·5%) were culture positive for P. aeruginosa , also conferring significantly high serum levels of complement C3 ( P = 0·014), but only two of these had positive titres for antibodies against exotoxin A. All patient sera were negative for antibodies against elastase and alkaline phosphatase. Fluorescent in situ hybridization analysis on randomly selected culture‐positive patients could not establish unambiguous presence of P. aeruginosa biofilms in the ulcers. A multiple regression model showed P. aeruginosa and systemic CRP as significant factors in deterioration of ulcer healing rate.