IL-16 in the airways of lung allograft recipients with acute rejection or obliterative bronchiolitis

被引:17
作者
Laan, M [1 ]
Lindén, A [1 ]
Riise, GC [1 ]
机构
[1] Gothenburg Univ, Lung Pharmacol Grp, Dept Resp Med & Allergol, S-41346 Gothenburg, Sweden
关键词
acute rejection; IL-16; lung allograft; lymphocyte; obliterative bronchiolitis;
D O I
10.1046/j.1365-2249.2003.02196.x
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Acute rejection (AR) is the principal risk factor for obliterative bronchiolitis (OB), the major complication of lung transplantation. It is known that activated CD4(+) T lymphocytes are involved in the development of AR and that interleukin (IL)-16 can inhibit the activity of CD4(+) T lymphocytes. In this study, we evaluated whether the concentration of IL-16 in the airways is altered in AR or OB and, if so, how this IL-16 concentration relates to the number or activity of airway lymphocytes. The concentration of IL-16 protein was measured in bronchoalveolar lavage (BAL) fluid at three time-points in lung allograft recipients with either AR or OB and in matched controls using ELISA. The concentration of soluble IL-2 receptor (R) protein was measured in BAL fluid using ELISA as well, as an indicator of lymphocyte activity. The percentage of airway lymphocytes was evaluated by performing BAL differential cell counts. Lung allograft recipients with AR displayed lower IL-16 concentrations compared with matched control patients and this IL-16 concentration correlated negatively with the sIL-2R concentration, but it did not correlate with the percentage of lymphocytes in BAL fluid. In contrast, in BAL fluid from lung allograft recipients with OB, the IL-16 concentration was not altered compared with matched control patients and it did not correlate with the percentage of lymphocytes or with the sIL-2R concentration. These data are compatible with an increase in IL-16 playing a protective role against AR but not against OB and, hypothetically, this type of protective effect could be exerted via a down-regulation of the activity of T lymphocytes.
引用
收藏
页码:290 / 296
页数:7
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