Bronchial neutrophilia in patients with noninfectious status asthmaticus.

Cellular events that occur in status asthmaticus (SA) remain poorly investigated. Autopsy studies frequently emphasized about the presence of eosinophils in bronchial airway wall, whereas recent studies reported increased number of neutrophils in patients dying of sudden-onset fatal asthma. Mucus plugs occluding the bronchial lumen are almost constant features during SA. Bronchial lavage (BL) may be useful to remove mucus plugs in cases of atelectasis and/or refractory SA. We investigated the contribution of different cell types and cellular mediators (neutrophil elastase, eosinophil cationic protein [ECP], histamine, interleukin-8 [IL-8]) to the pathogenesis of SA. We studied 16 BL from eight patients undergoing mechanical ventilation (MV) for SA (time interval from onset of MV = Day 0 to Day 11), four BL from patients undergoing MV without preexisting respiratory disease (V), 11 BL from patients with stable asthma (A) and eight BL from healthy controls (C). SA exhibited higher number and percentage of neutrophils (81.5 +/- 4.5%) than V (44.3 +/- 12.2) (p < 0.05), A (6.9 +/- 2.7) and C (9.5 +/- 3.8) (p < 0.0001), and higher number of eosinophils than V, A, and C (p < 0.01). Neutrophil elastase, ECP, and IL-8 levels were dramatically increased in SA. Histamine was higher in SA than in C and V (p < 0.05). Bronchial neutrophilia was not related to concomitant bacterial infection as bacteriological cultures were positive in only three BL. Eosinophils, mast cells and histamine were higher in BL performed within the first 48 h of MV (p < 0.05) than in BL performed later on. Our results indicate that bronchial inflammation in SA differs from bronchial inflammation in mild asthma. Persistent bronchial neutrophilia is associated with increased eosinophils and mast cells in the early phase of SA. Neutrophils may result in tissue damage and participate to the shedding of the epithelium in SA.

[1]  P. Howarth,et al.  The effect of treatment with oral corticosteroids on asthma symptoms and airway inflammation. , 1997, American journal of respiratory and critical care medicine.

[2]  C. Delacourt,et al.  Gelatinases in epithelial lining fluid of patients with adult respiratory distress syndrome. , 1997, The American journal of physiology.

[3]  S. Holgate,et al.  Cellular infiltration of the airways in asthma of varying severity. , 1996, American journal of respiratory and critical care medicine.

[4]  A. James,et al.  Airway structure and inflammatory cells in fatal attacks of asthma. , 1996, The European respiratory journal.

[5]  D. Thornton,et al.  Analysis of respiratory mucus glycoproteins in asthma: a detailed study from a patient who died in status asthmaticus. , 1995, American journal of respiratory cell and molecular biology.

[6]  M. Sears,et al.  Exacerbations of asthma without sputum eosinophilia. , 1995, Thorax.

[7]  Jesse B. Hall,et al.  The assessment and management of adults with status asthmaticus. , 1995, American journal of respiratory and critical care medicine.

[8]  Kwang Woo Kim,et al.  Prominent neutrophilic inflammation in sputum from subjects with asthma exacerbation. , 1995, The Journal of allergy and clinical immunology.

[9]  B. Make,et al.  Standards for the diagnosis and care of patients with chronic obstructive pulmonary disease. American Thoracic Society. , 1995, American journal of respiratory and critical care medicine.

[10]  H. Boushey,et al.  Analysis of induced sputum to examine the effects of prednisone on airway inflammation in asthmatic subjects. , 1994, The Journal of allergy and clinical immunology.

[11]  J. Oates,et al.  Effect of oral prednisone on airway inflammatory mediators in atopic asthma. , 1994, American journal of respiratory and critical care medicine.

[12]  D. Smith,et al.  Bronchoalveolar lavage in asthma. An update and perspective. , 1993, The American review of respiratory disease.

[13]  T. Standiford,et al.  Cytokines. 2. Cytokines and lung inflammation: mechanisms of neutrophil recruitment to the lung. , 1993, Thorax.

[14]  A. James,et al.  The structure of large and small airways in nonfatal and fatal asthma. , 1993, The American review of respiratory disease.

[15]  C E Reed,et al.  Sudden-onset fatal asthma. A distinct entity with few eosinophils and relatively more neutrophils in the airway submucosa? , 1993, The American review of respiratory disease.

[16]  F. Mitsunobu,et al.  Changes in the proportions of bronchoalveolar lymphocytes, neutrophils and basophilic cells and the release of histamine and leukotrienes from bronchoalveolar cells in patients with steroid-dependent intractable asthma. , 1993, International archives of allergy and immunology.

[17]  P. W. Johnston,et al.  T lymphocytes and activated eosinophils in airway mucosa in fatal asthma and cystic fibrosis. , 1992, The American review of respiratory disease.

[18]  C. Smith,et al.  Endothelial leukocyte adhesion molecule-1 mediates antigen-induced acute airway inflammation and late-phase airway obstruction in monkeys. , 1991, The Journal of clinical investigation.

[19]  Simon Ra,et al.  Safety and possible efficacy of fiberoptic bronchoscopy with lavage in the management of refractory asthma with mucous impaction. , 1991 .

[20]  C. Corrigan,et al.  Cultured peripheral blood mononuclear cells derived from patients with acute severe asthma ("status asthmaticus") spontaneously elaborate a neutrophil chemotactic activity distinct from interleukin-8. , 1991, The American review of respiratory disease.

[21]  K. Offord,et al.  Exposure to an aeroallergen as a possible precipitating factor in respiratory arrest in young patients with asthma. , 1991, The New England journal of medicine.

[22]  R. Simon,et al.  Safety and possible efficacy of fiberoptic bronchoscopy with lavage in the management of refractory asthma with mucous impaction. , 1991, Annals of allergy.

[23]  J. Bousquet,et al.  Eosinophilic inflammation in asthma. , 1990, The New England journal of medicine.

[24]  L. Fabbri,et al.  Neutrophils and asthma. , 1989, The European respiratory journal. Supplement.

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

[26]  S. Holgate,et al.  Early and late-phase bronchoconstriction after allergen challenge of nonanesthetized guinea pigs. I. The association of disordered airway physiology to leukocyte infiltration. , 1988, The American review of respiratory disease.

[27]  G. Gleich,et al.  The eosinophilic leukocyte and the pathology of fatal bronchial asthma: evidence for pathologic heterogeneity. , 1987, The Journal of allergy and clinical immunology.

[28]  Phillips Yy,et al.  Standards for the diagnosis and care of patients with chronic obstructive pulmonary disease (COPD) and asthma. This official statement of the American Thoracic Society was adopted by the ATS Board of Directors, November 1986. , 1987, The American review of respiratory disease.

[29]  M. Schwarz,et al.  Bronchoalveolar lavage fluid neutrophils increase after corticosteroid therapy in smokers with idiopathic pulmonary fibrosis. , 2015, The American review of respiratory disease.

[30]  S. Lam,et al.  Effect of bronchial lavage volume on cellular and protein recovery. , 1985, Chest.

[31]  H. Sampson,et al.  Dermal deposition of eosinophil-granule major basic protein in atopic dermatitis. Comparison with onchocerciasis. , 1985, The New England journal of medicine.

[32]  K Aas,et al.  Heterogeneity of Bronchial Asthma , 1981, Allergy.

[33]  B. Cardell,et al.  Death in Asthmatics , 1959 .

[34]  J. Trounce,et al.  A Clinical and Pathological Study of Fatal Cases of Status Asthmaticus , 1953, Thorax.