[Influenza following heart transplantation in a patient, an unusual cause of viral pneumonia].
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Anti-Bacterial Agents↗
Biomedical subjects
F B Michel
Publications and source records attributed to F B Michel.
Serum fragment of cytokeratin subunit 19 measured by CYFRA 21-1 immunoradiometric assay as a marker of lung cancer.
Cytokeratin 19 is a subunit of cytokeratin intermediate filament expressed in simple epithelia and their malignant counterparts. Therefore, it is expressed by respiratory epithelium cells and has been detected in lung cancer specimens. An immunoradiometric assay was used to detect a fragment of the cytokeratin 19, referred to as CYFRA 21-1, in the serum of 165 patients with histologically proved lung cancer (128 non-small cell and 37 small cell lung cancers). This prospective study was conducted to evaluate the reliability of this immunoradiometric assay and to identify the relationship between serum CYFRA 21-1 and different features of lung cancer including prognosis. The minimal detectable concentration detected by this assay was 0.06 ng/ml. The reliability of the immunoradiometric assay was demonstrated by the linear relationship between CYFRA 21-1 measurement and dilution of the serum, the reproducibility of the dosage in intraassay and interassay, and the high sensitivity of the method in discriminating low CYFRA 21-1 concentrations. Using a threshold of 3.6 ng/ml, sensitivity and specificity were 0.52 and 0.87, respectively. The sensitivity of the marker was highest in squamous cell carcinoma and lowest in small cell carcinoma. In non-small cell lung cancer patients, the marker varied significantly according to both stage of the disease (Kruskal-Wallis, 13.7; P < 0.005) and performance status (Kruskal-Wallis, 9.16; P < 0.05) inasmuch as a high serum CYFRA 21-1 level was associated with advanced stages, mediastinal lymph nodes, and poor performance status. Consequently, the marker was significantly lower in patients who were operated upon when compared with unresectable ones. Lung cancer patients with serum CYFRA 21-1 over 3.6 ng/ml proved to have a significantly shorter overall survival than those with a normal serum level (log rank, P = 0.007; Wilcoxon, P = 0.001). The negative prognostic effect of CYFRA 21-1 was highly significant in squamous cell carcinomas whereas it was nonsignificant for the other histologies. In Cox's model analysis, performance status, stage grouping, and CYFRA 21-1 were the only significant determinants of survival. This study supports the use of the serum fragment of cytokeratin subunit 19 CYFRA 21-1 as an independent prognostic marker of squamous cell carcinoma of the lung.
Adult↗
Effect of nedocromil sodium on sulfidopeptide leukotrienes-stimulated human alveolar macrophages in asthma.
Alveolar macrophages (AM) may take part in the amplification of the inflammatory mechanism involved in asthma. During an asthma attack, mast cells and eosinophils release arachidonic acid derivative mediators of inflammation such as sulfidopeptide leukotrienes. Among them, LTC4 has been shown to be present in bronchoalveolar fluid. In asthmatic patients, we showed that the ability of AM to transform LTC4 into its derivatives LTD4 and LTE4 was related to the intensity of the local inflammation observed during endoscopy. AM from asthmatics incubated in the presence of LTC4 or LTE4, generated LTB4 and 5-HETE, which are potent chemoattractants. Nedocromil sodium (10(-4) M) decreased LTB4 releasability and intracellular 5-HETE concentrations in zymosan-stimulated AM from asthmatic patients, and was shown to decrease the LTC4 or LTE4-promoted formation of LTB4 and 5-HETE.
Adolescent↗
Precision of conjunctival provocation tests in right and left eyes.
BACKGROUND: Conjunctival provocation tests (CPTs) are used for assessing the efficacy of antiallergic treatments, but their reproducibility is not well characterized. A study was carried out to assess the reproducibility of CPTs and the release of mediators during CPTs. METHODS: Both eyes of 30 grass-pollen-allergic patients were challenged with threefold increasing concentrations of a standardized orchard grass pollen extract. The positivity of the CPT was assessed by a cumulative symptom score. The release of mediators was examined by means of histamine (radioimmunoassay), prostaglandin D2 and leukotrienes C4 and D4 (enzyme immunoassay). RESULTS: There was a significant correlation between the concentrations of allergen inducing a positive CPT in both eyes (p < 0.0001, Spearman). All but one patient had a significant release of at least one mediator. After allergen CPT there was a significant release in both eyes in 13 of 20 patients for prostaglandin D2, 11 of 19 for leukotrienes C4 and D4 and 15 of 18 for histamine. The correlations between the levels of mediators released during diluent and allergen challenges in both eyes were significant for prostaglandin D2 (diluent and allergen challenges) and leukotrienes C4 and D4 (allergen challenge). CONCLUSION: Considering the whole group of patients, CPT is reproducible in both eyes, but the results are less satisfactory when patients are examined individually.
Adult↗
Airway macrophages from patients with asthma do not proliferate.
BACKGROUND: Macrophages are involved in asthma, but their pulmonary turnover is unknown. We compared the ability of bronchoalveolar lavage (BAL) and bronchial macrophages to proliferate in normal subjects and patients with asthma. METHODS: BAL cells from eight patients with asthma and eight normal volunteers were separated with a discontinuous Percoll gradient (Pharmacia Fine Chemicals, Uppsala, Sweden). In a first experiment, nuclei of each alveolar macrophage (AM) fraction, stained with propidium iodide, were analyzed for DNA content with a flow cytometer, and the proportions of cells in the G0/G1, S, and G2 + M phases were determined. In a second experiment, expression of Ki-67-related antigen was sought on AMs by immunocytochemistry. Macrophages from 10 patients with asthma and 10 normal volunteers were studied in biopsy specimens by means of immunohistochemistry with a panmacrophage monoclonal antibody (HAM-56) and a monoclonal antibody against proliferating cell nuclear antigen. RESULTS: The proportions of BAL AMs in the different phases of the cell cycle were similar in normal subjects and patients with asthma for all fractions, and the percentage of cells in S and G2 +/- M phases ranged from 7.3% to 11.3%. Under 1% of BAL AMs expressed Ki-67-related antigen. None of the macrophages present in the biopsy specimens expressed proliferating cell nuclear antigen. CONCLUSIONS: This study does not indicate that an important source of airway macrophages is local proliferation.
Adolescent↗
Eosinophilic and neutrophilic inflammation in asthma, chronic bronchitis, and chronic obstructive pulmonary disease.
BACKGROUND: Eosinophils but not neutrophils may play a role in the airway inflammation of asthma. In chronic bronchitis (CB) and chronic obstructive pulmonary disease (COPD), neutrophils are present in the airways. To differentiate among the pathology of asthma, CB, and COPD eosinophils and neutrophils were studied in peripheral blood, bronchial biopsy specimens, and bronchoalveolar lavage fluid (BALF). METHODS: We studied nine nonsmoking healthy subjects, 20 nonsmoking patients with asthma, 10 nonatopic smoking patients with CB (forced expiratory volume in 1 second: 98.4% +/- 11.3%) and 17 patients with COPD (forced expiratory volume in 1 second: 51.2% +/- 14.3%). Eosinophils were characterized by their enumeration in biopsy specimens (EG2 monoclonal antibody), peripheral blood, and BALF and by measurement of eosinophil cationic protein in BALF. Neutrophils were characterized by their enumeration in biopsy specimens (anti-elastase monoclonal antibody) and BALF and by measurement of neutrophil-specific myeloperoxidase in BALF. RESULTS: In patients with asthma we found degranulated eosinophils in biopsy specimens and significantly increased eosinophil cationic protein levels in BALF. In patients with CB or COPD, eosinophil numbers in biopsy specimens were not significantly different from those of patients with asthma, but cells were not degranulated and eosinophil cationic protein levels in BALF were similar to those of normal subjects. In patients with CB or COPD neutrophils were not increased in the mucosa, but neutrophil numbers and myeloperoxidase levels in BALF were significantly increased. CONCLUSION: The percentages of neutrophils in BALF were greater in patients with COPD than in those with CB, suggesting a role in the chronic airflow limitation.
Adult↗
Immunohistochemical study of P-glycoprotein distribution in lung cancer.
Indirect immunoperoxidase was used to determine the reactivity of C219 (P-glycoCHEK C219, Centocor Diagnostics, Malvern, PA), a monoclonal antibody (Mab) with high affinity for an internal epitope of the P-glycoprotein encoded by the multidrug resistance (MDR1) gene, in 40 surgically resected primary lung tumours. C219 reactivity was qualitatively classified in seven small cell lung cancers (SCLC), 29 non small cell lung cancers (NSCLC), and four carcinoid tumours. Ploidy was analysed by means of static cytometry using a computer-assisted image processor following Feulgen staining of cytologic prints of 32/40 lung tumours. Indirect immunoperoxidase reactivities of Mabs S-L 11.14 and MOC-1 were also studied to characterize the expression of cluster 1 lung cancer antigens and hence to determine among the NSCLC those which expressed the neural cell adhesion molecule (NCAM). Eighteen (45%) lung tumours strongly expressed P-glycoprotein as an immunostaining of many islets of malignant cells or almost all malignant cells. In addition, 8/40 tumours (20%) showed a weak reactivity (few immunostained cells) and 14/40 (35%) no reactivity. There was no difference of reactivity when NSCLC were compared with SCLC. The expression of P-glycoprotein in NSCLC did not vary significantly when the stage of disease was considered. Among the 29 NSCLC, 10 (36%) expressed S-L 11.14 and MOC-1. The NCAM positive NSCLC did not show any difference of P-glycoprotein expression in comparison with NCAM negative ones. Finally, C219 immunoperoxidase reactivity did not significantly differ according to the ploidy status. In conclusion, the internal epitope of the P-glycoprotein encoded by the MDR1 gene is frequently expressed by lung tumours of any histological type. This expression is not higher in Stage III and IV lung cancers in comparison with Stage I and II ones, or in NSCLC in comparison with SCLC either. Thus, the C219 related epitope seems to have a weak implication in the lower chemosensitivity of both advanced stages and NSCLC.
ATP Binding Cassette Transporter, Subfamily B, Mem↗
Clinical evaluation of serum tumour marker CA 242 in non-small cell lung cancer.
CA 242, a novel tumour carbohydrate antigen present in serum (upper limit of normal values: 20.0 U ml-1), has been measured in a group of 102 pathologically confirmed non-small cell lung cancer patients. The aim of the present prospective study was to identify any relationship between pre-treatment serum CA 242 level and different features of lung cancer including prognosis. Serum CA 242 was measured using the delayed europium lanthanide fluoroimmunometric assay. Sensitivity and specificity were 28.5% and 95.6% respectively. Its level was significantly lower in squamous cell carcinoma in comparison with non-squamous histologies (adenocarcinoma and large cell carcinoma). The CA 242 level was higher in metastatic disease (median: 15.3 U ml-1) in comparison with non-metastatic (median: 7.9 U ml-1; Mann Whitney U test; P < 0.003), and increased significantly from stage I to stage IV. In 50 patients who underwent chemotherapy, the serum CA 242 level was higher in non-responder patients when compared with responders (median: 16.8 U ml-1 and 9.5 U ml-1 respectively; Mann Whitney; P < 0.02). Univariate analysis of the entire population showed serum CA 242 levels were not related to survival. However, patients with unresectable non-small cell lung cancer and elevated CA 242 level proved to have a significantly shorter survival than those with a CA 242 < 20 U ml-1. In Cox's model analysis, stage of the disease and performance status were the only significant determinants of survival. We conclude that a high level of serum CA 242 (1) is significantly related to the stage of disease, (2) predictive of no response to chemotherapy but seems to add weak prognostic information to stage of disease and performance status, the main prognostic determinants of non-small cell lung cancer.
Adult↗
Modulation of eicosanoid and histamine release from human dispersed lung cells by terfenadine.
Terfenadine is an H1-blocker that may have antiallergic properties. A study was carried out to examine the ability of terfenadine to inhibit the release of histamine and arachidonic-acid-derived mediators from human lung cells. Cells were dispersed from fresh human lung tissue obtained from four accident victims whose hearts were donated for transplantation and four lung cancer resections. Cells were dispersed by enzymatic digestion with type XIV protease and chymopapain, and this resulted in a cell population containing approximately 5% mast cells. The remaining cells were mainly macrophages. The cells were challenged with anti-IgE at a 1/1000 dilution. Cells were challenged without terfenadine and after a preincubation of 0.1, 1, and 10 mumol terfenadine. The release of PGD2 and LTC4/D4 was assessed with an EIA. Histamine was assayed by RIA with a monoclonal antibody against acylated histamine. A release of both eicosanoids and histamine was observed in all experiments. An inhibition of eicosanoids was observed at both 1 and 10 mumol terfenadine (median percentage of inhibition of PGD2: 38.00 +/- 15.65 and 56.00 +/- 13.12; median percentage of inhibition of LTC4/D4: 37.5 +/- 19.80 and 52.5 +/- 26.8). On the other hand, histamine release was not blocked by terfenadine. Terfenadine inhibits, in a dose-dependent manner, the release of eicosanoids after challenge of dispersed lung cells by anti-IgE, and this effect may have some clinical relevance.
Aged↗
Heterogeneity of atopy. I. Clinical and immunologic characteristics of patients allergic to cypress pollen.
The heterogeneity of pollen-allergic persons is well known but poorly characterized. Cypress is one of the major pollen-producing plants of the Mediterranean area. A study was undertaken to characterize the symptoms presented by patients allergic to cypress pollen and the heterogeneity of the IgE immune response between patients allergic only to cypress pollen and those who are polysensitized. Eighty-nine patients allergic to cypress pollen were studied, 26 being allergic only to cypress pollen. The IgE response was assessed by skin prick tests and the titration of serum total IgE and cypress-specific IgE by RAST. Clinical reactivity was assessed by symptom scores during the cypress pollen season and skin tests. Pollen counts were obtained. The clinical reactivity was similar in both patient groups. Rhinitis was present in all patients, conjunctivitis in 73.7-88.5%, and asthma in only 7.4-19.2%. The age of onset of symptoms caused by cypress pollen allergy was significantly greater in patients allergic to cypress pollen only. Total serum IgE was within the normal range in the cypress pollen group and significantly lower than in the polysensitized groups. Cypress pollen RAST was higher in the polysensitized group. We concluded that conjunctivitis is particularly common in cypress pollen allergy. Patients allergic only to cypress pollen may be unique in their way of expressing serum total IgE levels.
Adolescent↗
Increased expression of adhesion molecules (ICAM-1 and LFA-1) on alveolar macrophages from asthmatic patients.
In the airways inflammation observed in asthma, activated macrophages are present in increased numbers. Adhesion molecules are required for the cell:cell contacts between leukocytes and endothelial cells or other leukocytes, and they are induced by inflammatory stimuli. We studied the expression of two adhesion molecules (ICAM-1 and LFA-1) on alveolar macrophages recovered by bronchoalveolar lavage from 11 normal subjects and 13 asthmatic patients by using immunocytochemistry. Two specific monoclonal antibodies were used, and the reaction was revealed by the alkaline phosphatase-antialkaline phosphatase (APAAP) method. The percentage of cells expressing ICAM-1 or LFA-1 was significantly increased in asthmatic patients, as compared with normal subjects (P < 0.001 and P < 0.002, respectively; Mann-Whitney U test), and there was a significant correlation with the percentage of cells expressing both markers in asthma (P < 0.03, Spearman rank test). This study highlights the importance of macrophages in the inflammation of asthma and suggests that macrophage interactions with other cells play a role in this inflammation.
Adult↗
Functional and phenotypic characteristics of bronchial epithelial cells obtained by brushing from asthmatic and normal subjects.
Bronchial epithelial cells may be involved in the pathogenesis of asthma releasing several inflammatory mediators such as interleukins and lipoxygenase products. In this study we evaluated the spontaneous and A23128-induced release of 15-HETE, PGE2 and fibronectin as well as the spontaneous expression of HLA-DR and ICAM-1 molecules by bronchial epithelial cells obtained by bronchial brushing from 35 asthmatic and 27 normal subjects. The release of fibronectin and 15-HETE was studied using the EIA and RIA techniques. The expression of HLA-DR and ICAM-1 molecules was studied using the APAAP and the immunofluorescence methods. Bronchial epithelial cells from asthmatics released higher amounts of 15-HETE and fibronectin both spontaneously (p < 0.002, p < 0.05, respectively) or after stimulation with calcium ionophore compared with normals. On the other hand, PGE2 release was significantly higher only after stimulation with calcium ionophore (p < 0.002). The spontaneous expression of HLA-DR and ICAM-1 (p < 0.001) was significantly higher on epithelial cells from asthmatics than in normal subjects. Finally, the severity of asthma significantly correlated with the release of 15-HETE (p < 0.02) and the expression of HLA-DR and ICAM-1 respectively (p < 0.001 and p < 0.002, respectively). This study indicates that bronchial epithelial cells are in an activated state in asthma and that the degree of activation is correlated to the severity of the disease.
Adult↗
Cells and mediators in bronchoalveolar lavage of asthmatic patients: the example of eosinophilic inflammation.
Bronchoalveolar lavage (BAL) greatly improved our understanding of asthma allowing to demonstrate the key role of inflammation in the pathogenesis of the disease. BAL is a safe procedure, even in severe patients when properly performed. BAL samples large and small airways and alveoli. Cells and mediators may be measured in BALF but they only represent an indirect estimation of the bronchial inflammation. Before performing BAL, the clinical status of the patients should be ascertained and drugs taken may have to be withdrawn. BALF markers should follow some requirements: (1) markers should be released by cells that are pertinent to airways inflammation (and reparation) in asthma, and, if possible they should be specific of a single cell type, (2) the enumeration of cells or titration of the marker or of its metabolites should be specific and sensitive, (3) if possible the titration should not be modified by the sampling procedure, (4) pilot studies should have demonstrated that the cell is increased or the secretory product is released during challenge in asthmatic subjects, (5) studies in a large number of patients should have demonstrated that the levels of the marker are increased in chronic asthmatics, that these levels are correlated with the severity of the disease and are decreased during effective anti-inflammatory treatment, and (6) if possible the cell or marker should be specific to asthma (but at present there is no such cell or marker). Eosinophils and granule secretory products follow most of these requirements. BAL represents an important research tool to assess the effects of therapeutic interventions.
Asthma↗
Functional characteristics of bronchial epithelium obtained by brushing from asthmatic and normal subjects.
Airways epithelial cells may be involved in the pathogenesis of asthma, but their role remains to be determined. Epithelial cells can release large amounts of 15-hydroxy-eicosatetranoic acid (15-HETE) and smaller amounts of prostaglandin E2 (PGE2) as well as fibronectin, a mediator involved in epithelial repair after injury. Epithelial cells obtained after bronchial brushing of 16 asthmatic (age 38 +/- 5 yr) and 11 normal subjects (age 36 +/- 5 yr) were studied. The percentage of epithelial cells was assessed by immunocytochemistry using an anti-cytokeratin antibody. The viability of the cells was assessed by trypan blue exclusion. The release of 15-HETE PGE2 and fibronectin was studied in resting cells and after A23187 calcium ionophore stimulation. Epithelial cells always comprised more than 86% of cells recovered, and the viability of epithelial cells was significantly (p < 0.001, Mann-Whitney U test) greater in normal subjects (54 +/- 5%) compared with asthmatic subjects (13 +/- 1%). The release of 15-HETE and fibronectin by resting epithelial cells was significantly greater in asthmatics (p < 0.05, Mann-Whitney U test) than in normal subjects. A23187 significantly (p < 0.05, Wilcoxon W test) increased the release of 15-HETE and fibronectin. There was no significant difference in the release of PGE2 by resting cells from either asthmatics or normal subjects, but challenge with A23187 induced a significant (p < 0.03, Wilcoxon W test) increase in PGE2 from cells of asthmatics but not from cells of normal subjects. This study shows that epithelial cells are activated and less viable in asthma and suggests a role for these cells in asthma.
Adult↗
Mast cells' contribution to the fibrosing alveolitis of the scleroderma lung.
Fibrosing alveolitis is frequently seen in scleroderma. Although usually causing progressive symptomatology, it may be found in patients reporting no respiratory symptoms. Mast cells may play a role in the pathogenesis of skin fibrosis in scleroderma. We determined the mast cells and other cellular content, as well as measuring the inflammatory mediators in the bronchoalveolar lavage fluid (BALF) in 17 scleroderma patients and nine control subjects to correlate BALF features with fibrosing alveolitis as determined by lung function testing and high-resolution computed tomographic scans. Bronchoalveolar lavage cells were enumerated after May-Giemsa-Grünwald (MGG), alcian blue, and safranine blue staining. Histamine, tryptase, eosinophil cationic protein, hyaluronic acid, and neutrophil-specific myeloperoxidase were measured by radioimmunoassay. In comparison with normal subjects the BALF of scleroderma patients showed an increased percentage of mast cells (p < 0.002, Mann-Whitney U test), and increased levels of histamine (p < 0.005), tryptase (p < 0.02), and hyaluronic acid (p < 0.004). The BALF of the eight scleroderma patients with an abnormal chest X-ray had a significantly greater number of mast cells (p < 0.04, Mann-Whitney U test), and significantly higher levels of histamine (p < 0.03, Mann-Whitney U test) and tryptase (p = 0.02, Mann-Whitney U test) than the nine scleroderma patients with a normal chest X-ray. This study demonstrates the importance of mast cells and mast-cell activation in the pathogenesis of the fibrosing alveolitis of scleroderma.
Adult↗
HLA-DR and ICAM-1 expression on bronchial epithelial cells in asthma and chronic bronchitis.
HLA-DR and ICAM-I molecules play an important role in cellular interactions, and their expression can be induced by inflammatory stimuli. We evaluated the spontaneous expression of HLA-DR and ICAM-1 on epithelial cells obtained by bronchial brushing from 27 asthmatic patients, 10 chronic bronchitis (CB) patients, and 19 normal subjects. In all cases > 90% pure epithelial cells were obtained. HLA-DR and ICAM-1 were characterized using monoclonal antibodies and revealed by immunocytochemistry (APAAP technique). In asthma, the percentage of cells expressing HLA-DR and ICAM-1 was significantly increased by comparison with normal values (p < 0.001) and GB (p < 0.001; HLA-DR; p < 0.003; ICAM-1) and was correlated with the clinical score of Aas (p < 0.001, HLA-DR; p < 0.001, ICAM-1) and the FEV1 (p < 0.001, HLA-DR; p < 0.002; ICAM-1). In CB, expression of both markers was slightly but significantly increased by comparison with normal subjects and was correlated with FEV1 (p < 0.02, HLA-DR; p < 0.03, ICAM-1). In addition, the expression of HLA-DR and ICAM-1 was significantly correlated. This study suggests that epithelial cells are in an activated state in asthma and that the extent of expression of these markers may be specific to asthma, not a general feature of chronic inflammation.
Adult↗
Neural cell adhesion molecule and prognosis of surgically resected lung cancer.
The prognostic significance of the expression of neural cell adhesion molecule (NCAM), a neuroendocrine antigen in lung cancer, was analyzed by an indirect immunoperoxidase method in 97 surgically treated patients. Reactivity of MOC-1 and S-L 11.14, both cluster-1 monoclonal antibodies directed against NCAM, was positive in all nine small-cell lung cancers and in 16 of 88 (18%) non-small-cell lung cancers. For the latter group, this expression demonstrated a phenotypic heterogeneity that was mainly observed in poorly differentiated squamous cell carcinomas and in stage N2 non-small-cell lung cancers. Patients with NCAM-positive non-small-cell lung cancer proved to have a shorter survival than those with NCAM-negative disease. In Cox's model for multivariate analysis, nodal status and histology were the main independent determinants of prognosis. We therefore concluded that NCAM expression in non-small-cell lung cancer is correlated to nodal status and that it indicates a poor prognosis. These findings confirm that the diversification of lung cancer phenotype leads to tumor progression and brings a negative prognosis to surgically resected non-small-cell lung cancer. However, nodal status remains the most important prognostic variable, suggesting that NCAM expression is only one of numerous biological events that promote tumor progression.
Adenocarcinoma↗
Activation by histamine of bronchial epithelial cells from nonasthmatic subjects.
Histamine is a major mediator of the mast cells that are present between epithelial cells in asthma. In asthma, there is an increased expression of ICAM-1 and HLA-DR and an increased spontaneous release of fibronectin. The effect of histamine was tested on bronchial epithelial cells obtained by bronchial brushing from 22 nonasthmatic subjects. The activation of epithelial cells was assessed by immunocytochemical analysis of the expression of membrane markers (ICAM-1 and HLA-DR) using the alkaline phosphatase-anti-alkaline phosphatase method and the release of fibronectin (enzyme immunoassay). Time-response (three experiments) and dose-response (six experiments) curves showed that the maximal effect was obtained after an incubation time of 24 h and a dose of 1 microM of histamine. For this time course and concentration, there was a highly significant increase in the number of cells expressing ICAM-1 (before histamine: 10 +/- 11%; after histamine: 32 +/- 20%; P < 0.001) and HLA-DR (before histamine: 8 +/- 7%; after histamine: 23 +/- 20%; P < 0.001) and in the release of fibronectin (before histamine: 30 +/- 20 ng/10(5) viable cells; after histamine: 61 +/- 35 ng/10(5) viable cells; P < 0.003). Cycloheximide blocked these effects, suggesting that histamine requires protein synthesis for its action. Pyrilamine (H1-blocker) and ranitidine (H2-blocker) at a concentration of 10 microM decreased the effect of histamine. However, there was no additive effect when both antagonists were added. This study suggests that mast cells present in the airways have a role in the activation of epithelial cells.
Adult↗