Immunoparalysis in patients with acute respiratory distress syndrome
© BioMed Central Ltd 2008
Published: 13 March 2008
Dysregulation of innate immunity may contribute to both the initiation and progression of acute respiratory distress syndrome (ARDS) . The deactivation of alveolar macrophages (AMs), which is expressed by reduced HLA-DR surface molecules, was associated with higher mortality rate in patients with acute lung injury . Our aim was to investigate the immune status in the lungs and systemically in early ARDS, by evaluating the AM and peripheral blood monocyte (PBM) HLA-DR expression.
Forty-one mechanically ventilated patients, 34 with early ARDS and seven without lung disease (control), were studied. On the third day after the onset of ARDS, all patients underwent fiberoptic bronchoscopy. Bronchoalveolar lavage fluid was obtained, and, besides the cell differential analysis, evaluation of AM HLA-DR expression was performed. At the same time, peripheral blood samples were obtained for evaluation of HLA-DR expression on PBMs. The three-step immunoperoxidase method was applied using the streptavidin–biotin complex Kit and the monoclonal mouse anti-human HLA-DR antigen. Levels of HLA-DR expression were determined from the percentages of cells with positive cytoplasmic staining to the total number of cells.
Patients were characterized as having direct ARDS (group A, 17 patients) and indirect ARDS (group B, 17 patients), respectively. In both groups, percentages of polymorphonuclear cells and lymphocytes were higher, while AM percentages were lower in comparison with the control group. HLA-DR expressions on AMs in both ARDS groups were lower than in controls (19.9 ± 11.4% (group A), 32.1 ± 10.4% (group B) vs 56.4 ± 10.5% (control), respectively; P < 0.05). AM HLA-DR expression in group A was lower than in group B (P < 0.05). PBM HLA-DR expressions in both ARDS groups were lower than in controls (38.06 ± 15.7% (group A), 27.5 ± 12.6% (group B) vs 54.1 ± 15.4% (control), respectively; P < 0.05). PBM HLA-DR expression in group B was lower than in group A (P = 0.01).
In early ARDS, HLA-DR expressions on AMs as well as on PBMs were low. In direct ARDS, however, local immunoparalysis was more profound, while more intense peripheral monocyte deactivation was observed in the indirect syndrome. The understanding of the immune dysfunction in ARDS may allow the assessment of novel treatments in an attempt to modify lung injury.
This article is published under license to BioMed Central Ltd.