Expression of acute-phase cytokines, surfactant proteins, and epithelial apoptosis in small airways of human acute respiratory distress syndrome

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• 作者：Ruy Camargo Pires-Neto ; PhD^a ; ^ruy@usp.br ; Maina Maria Barbosa Morales ; PhD^a ; Tatiana Lancas ; PhD^a ; Nicole Inforsato ; MD^a ; Maria Irma Seixas Duarte ; PhD^a ; Marcelo Britto Passos Amato ; PhD^b ; Carlos Roberto Ribeiro de Carvalho ; PhD^b ; Luiz Fernando Ferraz da Silva ; PhD^a ; Thais Mauad ; PhD^a ; Marisa Dolhnikoff ; PhD^a
• 关键词：ARDS ; Respiratory epithelium ; Apoptosis ; Cytokines ; Surfactant protein
• 刊名：Journal of Critical Care
• 出版年：2013
• 出版时间：February, 2013
• 年：2013
• 卷：28
• 期：1
• 页码：111.e9-111.e15
• 全文大小：599 K

文摘

Purpose

Recent 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 Methods

We studied the lungs of 31 patients with ARDS (Pao₂/fraction of inspired oxygen ¡Ü 200, 45 ¡À 14 years, 16 men) and 11 controls (52 ¡À 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.

Results

Acute 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.

Conclusion

Distal 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.