Inflammatory cytokines in patients with persistence of the acute respiratory distress syndrome.

Abstract

To determine the relationship between airspace cytokines and cellular inflammatory responses in patients with the acute respiratory distress syndrome (ARDS), we performed bronchoalveolar lavage (BAL) in 82 prospectively identified, mechanically ventilated patients on Days 3, 7, 14, and/or 21 after the onset of ARDS. We studied the relationships between bronchoalveolar lavage fluid (BALF) cell populations and the concentrations of two potent neutrophil (PMN) chemoattractants, interleukin-8 (IL-8) and epithelial cell-derived neutrophil activator-78 (ENA-78); two potent monocyte chemoattractants, monocyte chemotactic peptide-1 (MCP-1) and macrophage inflammatory peptide-1 alpha (MIP-1 alpha); and the early response cytokine interleukin-1 beta (IL-1 beta) and its naturally occurring antagonist, IL-1 receptor antagonist protein (IRAP). We found that all of these cytokines were significantly increased regardless of the duration of ARDS. IL-8 and ENA-78 were the cytokines most strongly and consistently correlated with PMN concentrations in the lung fluids of patients with ARDS, and the correlations were independent of the other cytokines or coexisting lung infection. None of the cytokines tested correlated with macrophage concentrations. MCP-1 was directly correlated with lung injury score on Days 7, 14, and 21. Although neither IL-8 nor ENA-78 was associated with outcome, levels of IL-1 beta measured on Day 7 were associated with an increased risk of death (odds ratio [OR] = 2.8; 95% confidence interval [CI] = 1.1 to 7.4). These data demonstrate potential molecular mechanisms of the persistent inflammatory process in the lungs of patients with ARDS.

Thoracotomy procedures effect cytokine levels after thoracoabdominal esophagectomy

“…Leukocyte activation and free radical release, proteases, arachidonic acid metabolites, inflammatory and anti-inflammatory cytokines result in the increased alveolar-capillary membrane permeability (21)(22)(23)(24).…”

Hyperoxia-induced signal transduction pathways in pulmonary epithelial cells☆

“…Upon exposure to hyperoxia, ROS evoke pulmonary cells to increase the secretion of chemoattractants and other proinflammatory cytokines that leads to leukocyte recruitment to the lung. Recruited leukocytes, including neutrophils and monocytes, accumulate within the pulmonary circulation, interstitium and air spaces and are significant sources of additional ROS, as well as proteinases, and antimicrobial peptides [18][19][20][21]. Therefore, the interactions between ROS and leukocytes establish a vicious cycle that initiates and/or exacerbates lung injury.…”

Prostaglandin E2 Mediates IL-1β-Related Fibroblast Mitogenic Effects in Acute Lung Injury through Differential Utilization of Prostanoid Receptors

“…Several cytokines and chemokines that may modulate fibroblast proliferation have been identified in pulmonary edema fluid (or bronchoalveolar lavage) from patients at risk for, or with established, ALI, including TNF-␣, ILs 1 and 8 (IL-1, IL-8), growthrelated oncogenes (gro-␤, MIP-2-␣), epithelial neutrophil-activating protein 78, and platelet-derived growth factor (1,(17)(18)(19)(20). The finding that transient overexpression of IL-1␤ using an adenoviral vector induces pulmonary fibrosis in rat lungs indicates that IL-1␤ acts as a potent profibrotic cytokine in vivo (21); however, its mechanism of action has not been elucidated.…”