Increased leukotriene B4 and interleukin-6 in exhaled breath condensate in cystic fibrosis

被引:104
作者
Carpagnano, GE
Barnes, PJ
Geddes, DM
Hodson, ME
Kharitonov, SA
机构
[1] Univ London Imperial Coll Sci Technol & Med, Fac Med, Natl Heart & Lung Inst, Dept Thorac Med, London SW3 6LY, England
[2] Univ Bari, Inst Resp Dis, Bari, Italy
关键词
leukotriene B-4; interleukin-6; cystic fibrosis; exhaled breath condensate; airway inflammation;
D O I
10.1164/rccm.200203-179OC
中图分类号
R4 [临床医学];
学科分类号
1002 ; 100602 ;
摘要
Chronic neutrophilic airway inflammation is an important feature of cystic fibrosis (CF). Noninvasive inflammatory markers may be useful in monitoring CF. Leukotriene B-4 (LTB4) and interleukin (IL)-6 are inflammatory mediators that are increased in chronic neutrophilic inflammation. The aim of this study was to assess whether LTB4 and IL-6 were increased in exhaled breath condensate of CF patients and whether they could be used to monitor inflammation. Twenty patients with CF (13 males, age of 28 +/- 9 years) were recruited together with 15 age-matched healthy subjects (8 males, age 35 +/- 7 years). LTB4 and IL-6 levels were markedly elevated in patients with acute exacerbations (28.8 +/- 4.3 and 8.7 +/- 0.4 pg/ml) compared with control subjects (6.8 +/- 0.7 and 2.6 +/- 0.1 pg/ml, p < 0.0001). We also observed a decrease of exhaled LTB4 and IL-6 concentrations after antibiotic treatment in six patients who were followed until clinically stable (31.1 +/- 4.4 and 9.5 +/- 0.4 pg/ml vs. 18.8 +/- 0.8 and 6.4 +/- 0.2 pg/ml, respectively) and an increase in 15 CF patients infected with Pseudomonas aeruginosa (34.3 +/- 5.0 and 9.3 +/- 0.3 pg/m) compared with those infected with other bacteria (18.3 +/- 0.7 and 6.9 +/- 0.5 pg/ml). These findings suggest that LTB4 and IL-6 levels are increased in exhaled breath condensate of patients with CF during exacerbation and could be used to monitor airway inflammation in these patients.
引用
收藏
页码:1109 / 1112
页数:4
相关论文
共 33 条
[1]   Increase in exhaled carbon monoxide during exacerbations of cystic fibrosis [J].
Antuni, JD ;
Kharitonov, SA ;
Hughes, D ;
Hodson, ME ;
Barnes, PJ .
THORAX, 2000, 55 (02) :138-142
[2]   Increased nitrotyrosine in exhaled breath condensate in cystic fibrosis [J].
Balint, B ;
Kharitonov, SA ;
Hanazawa, T ;
Donnelly, LE ;
Shah, PL ;
Hodson, ME ;
Barnes, PJ .
EUROPEAN RESPIRATORY JOURNAL, 2001, 17 (06) :1201-1207
[3]  
BERGER M, 1991, CLIN REV ALLERG, V9, P119
[4]  
Bland JM, 1996, BRIT MED J, V313, P744
[5]   PATHOLOGICAL REGULATION OF ARACHIDONIC-ACID RELEASE IN CYSTIC-FIBROSIS - THE PUTATIVE BASIC DEFECT [J].
CARLSTEDTDUKE, J ;
BRONNEGARD, M ;
STRANDVIK, B .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1986, 83 (23) :9202-9206
[6]   Porins of Pseudomonas aeruginosa induce release of tumor necrosis factor alpha and interleukin-6 by human leukocytes [J].
Cusumano, V ;
Tufano, MA ;
Mancuso, G ;
Carbone, M ;
Rossano, F ;
Fera, MT ;
Ciliberti, FA ;
Ruocco, E ;
Merendino, RA ;
Teti, G .
INFECTION AND IMMUNITY, 1997, 65 (05) :1683-1687
[7]   PROMINENT NEUTROPHILIC INFLAMMATION IN SPUTUM FROM SUBJECTS WITH ASTHMA EXACERBATION [J].
FAHY, JV ;
KIM, KW ;
LIU, J ;
BOUSHEY, HA .
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, 1995, 95 (04) :843-852
[8]  
Grasemann H, 1997, PEDIATR PULM, V24, P173, DOI 10.1002/(SICI)1099-0496(199709)24:3<173::AID-PPUL2>3.0.CO
[9]  
2-O
[10]  
Heuertz RM, 1996, J IMMUNOL, V156, P3412