Interactions between neutrophils and cytokines in blood and alveolar spaces during ARDS

Am J Respir Crit Care Med. 1996 Sep;154(3 Pt 1):594-601. doi: 10.1164/ajrccm.154.3.8810592.


Although the pathogenesis of the acute respiratory distress syndrome (ARDS) is complex and poorly understood, several observations point to an important role of interactions between polymorphonuclear neutrophils (PMN) and cytokines in this process. We therefore studied certain parameters involved in PMN transendothelial migration (adhesion molecule expression and cytoskeletal organization) in patients with ARDS (n = 14) in comparison with other ventilated patients (n = 15). We found that in the basal state, both whole-blood PMN and alveolar PMN obtained by bronchoalveolar lavage (BAL) were activated, as shown by decreased L-selectin CD62L and increased beta 2 integrin CD11b expression, as well as decreased F-actin content. The degree of PMN activation increased with the degree of lung injury and with the levels of tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), and interleukin-8 (IL-8). Moreover, the capacity of ex vivo stimulation of alveolar PMN by a bacterial peptide was low in ARDS and could partly account for the high susceptibility of these patients to lung infection. Therefore, ARDS-associated lung injury could be caused, at least in part, by inappropriate adhesion and transendothelial migration of proinflammatory cytokine-primed PMN.

Publication types

  • Clinical Trial
  • Comparative Study
  • Controlled Clinical Trial

MeSH terms

  • Actins / blood
  • Aged
  • Bronchoalveolar Lavage Fluid / chemistry
  • CD18 Antigens / blood
  • Cytokines / blood*
  • Humans
  • L-Selectin / blood*
  • Middle Aged
  • Neutrophils / metabolism*
  • Pneumonia / blood
  • Pneumonia / complications
  • Pneumonia / immunology*
  • Pulmonary Alveoli / immunology*
  • Respiration, Artificial
  • Respiratory Distress Syndrome / blood
  • Respiratory Distress Syndrome / complications
  • Respiratory Distress Syndrome / immunology*


  • Actins
  • CD18 Antigens
  • Cytokines
  • L-Selectin