High bronchoalveolar levels of tumor necrosis factor and its inhibitors, interleukin-1, interferon, and elastase, in patients with adult respiratory distress syndrome after trauma, shock, or sepsis.

Intrapulmonary activation of leukocytes and release of cellular mediators and enzymes are involved in the pathophysiology of the adult respiratory distress syndrome (ARDS). To investigate a possible role of local cytokines, we measured bronchoalveolar fluid (BALF) and plasma levels of tumor necrosis factor alpha (TNF-alpha) and its soluble inhibitors (sTNF-RI + RII), interleukin-1 beta (IL-1 beta), interferon-alpha (IFN-alpha), and granulocyte elastase in 14 patients at risk for ARDS and in 35 patients developing ARDS after trauma, sepsis, or shock. During clinical development of severe ARDS, BALF cytokines increased markedly: TNF-alpha from 116 +/- 36 to 10,731 +/- 5,048 pg/ml (mean +/- SEM), p = 0.001; sTNF-RI + RII from 3.7 +/- 1.4 to 24.6 +/- 2.6 ng/ml, p less than 0.05; and IL-1 beta from 7,746 +/- 5,551 to 42,255 +/- 19,176 pg/ml, p = 0.01. Plasma cytokines were not increased in most patients, nor were they correlated with the development or severity of ARDS. BALF elastase was higher in patients developing ARDS than in those at risk but not going into pulmonary failure (0.97 +/- 0.26 versus 0.28 +/- 0.13 U/ml, p = 0.026), and the highest values were observed in the early stages of severe ARDS (1.85 +/- 0.39 U/ml). BALF elastase levels correlated with IFN-alpha (r = 0.72, p less than 0.001). In conclusion, local release of TNF-alpha and IL-1 beta, possibly by pulmonary macrophages or other cells, and/or accumulation in the lung is associated with the development of ARDS.(ABSTRACT TRUNCATED AT 250 WORDS)

[1]  J. Kelley.  Cytokines of the lung. , 1992, The American review of respiratory disease.

[2]  A. Fowler,et al.  Tumor necrosis factor levels in serum and bronchoalveolar lavage fluid of patients with the adult respiratory distress syndrome. , 1991, The American review of respiratory disease.

[3]  C. Dinarello.  The proinflammatory cytokines interleukin-1 and tumor necrosis factor and treatment of the septic shock syndrome. , 1991, The Journal of infectious diseases.

[4]  M. Schaller,et al.  Plasma levels of tumor necrosis factor in the adult respiratory distress syndrome. , 1991, The American review of respiratory disease.

[5]  J. Schellekens,et al.  Prognostic Values of Tumor Necrosis Factor/Cachectin, Interleukin-l, Interferon-α, and Interferon-γ in the Serum of Patients with Septic Shock , 1990 .

[6]  E. A. Havell,et al.  Roles of tumor necrosis factor and macrophages in lipopolysaccharide-induced accumulation of neutrophils in cutaneous air pouches , 1990, Infection and immunity.

[7]  S. Suter,et al.  Relation between tumor necrosis factor-alpha and granulocyte elastase-alpha 1-proteinase inhibitor complexes in the plasma of patients with cystic fibrosis. , 1989, The American review of respiratory disease.

[8]  G. Campbell,et al.  Elevated interleukin-1 release by human alveolar macrophages during the adult respiratory distress syndrome. , 1989, The American review of respiratory disease.

[9]  J. Grassi,et al.  Production of monoclonal antibodies against interleukin-1α and -1β: Development of two enzyme immunometric assays (EIA) using acetylcholinesterase and their application to biological media , 1989 .

[10]  M. Singer,et al.  TUMOUR NECROSIS FACTOR IN BRONCHOPULMONARY SECRETIONS OF PATIENTS WITH ADULT RESPIRATORY DISTRESS SYNDROME , 1989, The Lancet.

[11]  R. Strieter,et al.  Differential regulation of tumor necrosis factor-alpha in human alveolar macrophages and peripheral blood monocytes: a cellular and molecular analysis. , 1989, American journal of respiratory cell and molecular biology.

[12]  M. Molyneux,et al.  Tumor necrosis factor and disease severity in children with falciparum malaria. , 1989, The New England journal of medicine.

[13]  D. Dehring,et al.  Intravascular macrophages in pulmonary capillaries of humans. , 1989, The American review of respiratory disease.

[14]  A. Malik,et al.  Macrophages activated by fibrin increase albumin permeability across pulmonary artery endothelial monolayers. , 1989, The American review of respiratory disease.

[15]  J. Ellner,et al.  Dyscoordinate expression of tumor necrosis factor-alpha by human blood monocytes and alveolar macrophages. , 1989, The American review of respiratory disease.

[16]  S. Weiss.  Tissue destruction by neutrophils. , 1989, The New England journal of medicine.

[17]  B. Schleiffenbaum,et al.  Interleukin 1 and tumor necrosis factor stimulate human vascular endothelial cells to promote transendothelial neutrophil passage. , 1989, The Journal of clinical investigation.

[18]  M. Wiseman,et al.  DIAGNOSTIC CRITERIA FOR ADULT RESPIRATORY DISTRESS SYNDROME: TIME FOR REAPPRAISAL , 1989, The Lancet.

[19]  E. Girardin,et al.  Tumor necrosis factor and interleukin-1 in the serum of children with severe infectious purpura. , 1988, The New England journal of medicine.

[20]  T. Raffin,et al.  Tumor necrosis factor causes increased pulmonary permeability and edema. Comparison to septic acute lung injury. , 1988, The American review of respiratory disease.

[21]  K. Tracey,et al.  Cachectin: a hormone that triggers acute shock and chronic cachexia. , 1988, The Journal of infectious diseases.

[22]  Kevin J. Tracey,et al.  Anti-cachectin/TNF monoclonal antibodies prevent septic shock during lethal bacteraemia , 1987, Nature.

[23]  N. Voelkel,et al.  Platelet-activating factor mediates hemodynamic changes and lung injury in endotoxin-treated rats. , 1987, The Journal of clinical investigation.

[24]  A. Waage,et al.  ASSOCIATION BETWEEN TUMOUR NECROSIS FACTOR IN SERUM AND FATAL OUTCOME IN PATIENTS WITH MENINGOCOCCAL DISEASE , 1987, The Lancet.

[25]  J. D. Albert,et al.  Shock and tissue injury induced by recombinant human cachectin. , 1986, Science.

[26]  J. Gamble,et al.  Stimulation of neutrophils by tumor necrosis factor. , 1986, Journal of immunology.

[27]  J. Rinaldo,et al.  Mediation of ARDS by leukocytes. Clinical evidence and implications for therapy. , 1986, Chest.

[28]  R. Colman,et al.  Neutrophil elastase-releasing factors in bronchoalveolar lavage from patients with adult respiratory distress syndrome. , 1985, The American review of respiratory disease.

[29]  P. Suter,et al.  Pulmonary extraction of serotonin and propranolol in patients with adult respiratory distress syndrome. , 1985, The American review of respiratory disease.

[30]  T. Petty,et al.  Adult respiratory distress syndrome: risk with common predispositions. , 1983, Annals of internal medicine.

[31]  R. Spragg,et al.  Pathogenesis of the adult respiratory distress syndrome. Evidence of oxidant activity in bronchoalveolar lavage fluid. , 1983, The Journal of clinical investigation.

[32]  R. Rogers,et al.  Current concepts: positive end-expiratory pressure in adult respiratory failure. , 1982, The New England journal of medicine.

[33]  R. Rogers,et al.  Adult respiratory-distress syndrome: changing concepts of lung injury and repair. , 1982, The New England journal of medicine.

[34]  R. Spragg,et al.  Studies on the pathogenesis of the adult respiratory distress syndrome. , 1982, The Journal of clinical investigation.

[35]  A. Fein,et al.  Elastolytic activity in pulmonary lavage fluid from patients with adult respiratory-distress syndrome. , 1981, The New England journal of medicine.

[36]  M. J. Moore,et al.  Complement-induced granulocyte aggregation: an unsuspected mechanism of disease. , 1980, The New England journal of medicine.

[37]  J. Travis,et al.  Human leukocyte granule elastase: rapid isolation and characterization. , 1976, Biochemistry.

[38]  O. P. Dinnick,et al.  UNSAFE ANÆSTHETIC SUPPLY SYSTEMS , 1975, The Lancet.

[39]  A. Forrest,et al.  Letter: Procaine and malignant hyperthermia. , 1974, Lancet.

[40]  J. Murray,et al.  Plasma tumor necrosis factor in patients with septic shock. Mortality rate, incidence of adult respiratory distress syndrome, and effects of methylprednisolone administration. , 1990, The American review of respiratory disease.

[41]  M. Gee,et al.  Arachidonic acid metabolites as mediators of lung injury during intravascular complement activation. , 1985, Progress in biochemical pharmacology.