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Journal of critical care · Feb 2013
Expression of acute-phase cytokines, surfactant proteins, and epithelial apoptosis in small airways of human acute respiratory distress syndrome.
- Ruy Camargo Pires-Neto, Maina Maria Barbosa Morales, Tatiana Lancas, Nicole Inforsato, Maria Irma Seixas Duarte, AmatoMarcelo Britto PassosMB, Carlos Roberto Ribeiro de Carvalho, Luiz Fernando Ferraz da Silva, Thais Mauad, and Marisa Dolhnikoff.
- Department of Pathology, Experimental Air Pollution Laboratory-LIM05, Sao Paulo University Medical School, 01246903 Sao Paulo, Brazil. ruy@usp.br
- J Crit Care. 2013 Feb 1; 28 (1): 111.e9-111.e15.
PurposeRecent studies suggest a role for distal airway injury in acute respiratory distress syndrome (ARDS). The epithelium lining the small airways secretes a large number of molecules such as surfactant components and inflammatory mediators. There is little information on how these small airway secretory functions are altered in ARDS.Materials And MethodsWe studied the lungs of 31 patients with ARDS (Pao(2)/fraction of inspired oxygen ≤200, 45 ± 14 years, 16 men) and 11 controls (52 ± 16 years, 7 men) submitted to autopsy and quantified the expression of interleukin (IL) 6, IL-8, surfactant proteins (SP) A and SP-B in the epithelium of small airways using immunohistochemistry and image analysis. In addition, an index of airway epithelial apoptosis was determined by the terminal deoxynucleotidyl transferase-mediated deoxyuridine-triphosphatase nick-end labeling assay, caspase 3, and Fas/Fas ligand expression. The density of inflammatory cells expressing IL-6 and IL-8 within the small airway walls was also quantified.ResultsAcute respiratory distress syndrome airways showed an increase in the epithelial expression of IL-8 (P = .006) and an increased density of inflammatory cells expressing IL-6 (P = .004) and IL-8 (P < .001) compared with controls. There were no differences in SP-A and SP-B epithelium expression or in epithelial apoptosis index between ARDS and controls.ConclusionDistal airways are involved in ARDS lung inflammation and show a high expression of proinflammatory interleukins in both airway epithelial and inflammatory cells. Apoptosis may not be a major mechanism of airway epithelial cell death in ARDS.Copyright © 2013 Elsevier Inc. All rights reserved.
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