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Biomedical subjects

B W Robinson

Publications and source records attributed to B W Robinson.

At least 91 records · Page 5Linked to original sources
PubMed1989

Indomethacin augments lymphokine-activated killer cell generation by patients with malignant mesothelioma.

Human malignant mesothelioma (MM) cells are resistant to natural killer (NK) cell lysis but susceptible to lysis by lymphokine-activated killer (LAK) cells from control individuals. The present study was performed to determine the capacity of patients with MM (n = 22) and individuals occupationally exposed to asbestos (the major population at risk of developing this disease, n = 52) to generate LAK cells capable of effectively lysing human mesothelioma cells. Compared to controls (n = 20), both patient groups demonstrated significantly depressed LAK cell activity against mesothelioma tumor cell targets (55 +/- 3% lysis by controls vs 34 +/- 3% lysis by patients with MM, P less than 0.005; and 45 +/- 3% lysis by asbestos-exposed individuals, P less than 0.025). Addition of 10 micrograms/ml indomethacin during LAK cell generation restored normal LAK cell activity for patients with MM (52 +/- 6% lysis of cultured human MM cells, P = NS compared to controls), suggesting that the defective cytolytic cell function observed in some patients with MM is a result of prostaglandin-induced immunosuppression. The ability of indomethacin to restore suppressed LAK cell activity in patients with MM suggests that the concomitant use of this agent in ex vivo LAK cell generation and in patients undergoing interleukin/LAK cell therapy may be beneficial.

Asbestos↗
PubMed1989

Study of human epithelial cell detachment and damage: development of a model.

Detachment of epithelial structures from underlying basement membrane (BM) represents an important component of a number of human disease processes e.g. airway and alveolar diseases, gastrointestinal ulceration, and retinal diseases. This study describes a method of evaluating human epithelial cell detachment from BM that is simple, rapid, inexpensive, quantifiable and which, because it utilizes BM rather than tissue culture plastic, more closely mimics the in vivo situation than other methods. In this model human amnionic epithelial cells attached to their underlying BM are isolated from fresh placentae and mounted in a multi-well chemotaxis assembly. These membranes can be studied with the epithelial cell monolayer intact. Protease-induced detachment of the epithelial cells from the underlying BM was readily quantifiable using light microscopy and spectroscopy. Following removal of the native amnionic epithelial cells, immunoperoxidase staining for the BM attachment proteins laminin, fibronectin, and type IV collagen demonstrated that these molecules remain intact. The BM could also be used as an attachment surface to reconstitute other epithelial cell monolayers. Cultured human amnionic cells and human respiratory epithelial cells were both able to attach to the denuded BM in the absence of serum (% attachment = 85 +/- 15% and 92 +/- 8% respectively, P = 0.8). Natural BM was a better substrate for epithelial cell attachment than tissue culture plastic in that, in the absence of serum, cultured epithelial cell attachment to tissue culture plastic was 20 +/- 4% of the value for BM (P less than 0.05). Furthermore, cells attached to plastic adhered less effectively than to BM in that trypsin concentrations required to induce 50% cell detachment were 0.72 +/- 0.4 for plastic and 62 +/- 13 BAEE U/ml for BM (P less than 0.001). In view of the complex protein interactions known to be involved in the anchorage of human epithelial cells to BM, it is likely this model will be a useful tool for evaluating the mechanisms underlying human epithelial cell attachment and detachment in a variety of normal and disease situations.

Amnion↗
PubMed1989

The role of bronchoalveolar lavage in the assessment of diffuse lung diseases.

Bronchoalveolar lavage is a safe and simple technique for sampling the inflammatory cells of the lung. However, while its use in the evaluation of pulmonary pathogenic mechanisms is both well accepted and described, its clinical utility is more controversial. Marked variation in results may occur through variation in the lavage procedure. Standardisation of the lavage technique and laboratory processing of the specimen are essential for reliable results. This review examines the current clinical role of bronchoalveolar lavage in the assessment of patients with diffuse lung diseases, and immunocompromised patients with pulmonary infiltrates. In this latter category, for patients with Acquired Immunodeficiency Syndrome, lavage is of equal efficacy to lung biopsy and can establish the cause of pulmonary infiltrates in over 90% of cases. Bronchoalveolar lavage can detect abnormalities in patients with diffuse lung diseases prior to the development of irreversible fibrosis. Lavage features have been described for sarcoidosis, cryptogenic fibrosing alveolitis, extrinsic allergic alveolitis, connective tissue diseases, and asbestosis. In cryptogenic fibrosing alveolitis lavage data may be used to indicate a subsequent deterioration in the patient's condition, or predict a favourable response to therapy.

Alveolitis, Extrinsic Allergic↗
PubMed1989

Asbestos and cancer: human natural killer cell activity is suppressed by asbestos fibers but can be restored by recombinant interleukin-2.

Inhalation of asbestos fibers is associated with a marked increase in the risk of developing pulmonary malignancy, particularly bronchogenic carcinoma. As natural killer (NK) cells are specialized lymphocytes that are considered to have an important in vivo role in the recognition and destruction of malignant cells, we examined the capacity of asbestos fibers (chrysotile, amosite, and crocidolite) to interfere with the NK activity of nylon wool-nonadherent, human blood lymphocytes (51Cr-release assay, K562 target cells, 14 h effector-to-target ratio = 50:1). Final asbestos concentrations used were 1 to 1,000 micrograms/ml. None of the fibers altered spontaneous target cell lysis or lymphocyte viability. All types of asbestos suppressed NK activity in a dose-dependent fashion. This effect was most marked with chrysotile, which exerted a profound inhibitory effect on blood NK cell activity; at 100 micrograms/ml, NK activity was inhibited 84 +/- 2% (p less than 0.001). The suppressive effects of asbestos were exerted directly on the NK cells (large granular lymphocytes, 91 +/- 2% inhibition at 100 micrograms/ml; p less than 0.001). Exposure of lymphocytes to recombinant interleukin-2 (IL-2, 150 units/ml) for 24 h prior to exposure to asbestos restored the level of activity to 99 +/- 6% of the original value (p less than 0.001), and lung lymphocytes that were exposed to IL-2 in vivo (active sarcoidosis) were resistant to suppression by asbestos. Similar results were observed in a group of patients with asbestosis. This suppression of NK activity may contribute to the increased susceptibility of asbestos-exposed persons to the development of pulmonary malignancy.

Asbestos↗
PubMed1989

Lysis of human malignant mesothelioma cells by natural killer (NK) and lymphokine-activated killer (LAK) cells.

Malignant mesothelioma is an aggressive tumor of the pleura for which, at present, there is no effective therapy. As interleukin-2 (IL-2) and lymphokine-activated killer (LAK) cells lyse many solid tissue malignancies that are unresponsive to conventional forms of therapy, the aim of this study was to evaluate the susceptibility of human malignant mesothelioma cells to lysis by natural killer (NK) and LAK cells. Using a 4-h 51Cr release assay, malignant mesothelioma cell lines grown from six different patients were found to be resistant to NK cell lysis (less than 10% lysis as compared to 50 +/- 3% lysis of the standard NK-sensitive target, K562, p less than 0.001). These malignant mesothelioma cells were, however, susceptible to lysis by LAK cells (58 +/- 4% lysis, p less than 0.001 compared to NK lysis). Similar results were seen using fresh mesothelioma cell targets (4 +/- 2% and 34 +/- 12% lysis for NK and LAK cells, respectively). Optimal LAK cell activation against these targets was achieved by incubating peripheral blood mononuclear cells (2 to 4 x 10(6)/ml) in culture medium containing 1,000 units/ml IL-2 for 3 to 14 days. The degree of LAK cell activation was dependent on the serum source used in culture, with autologous serum being more effective than pooled human AB serum or fetal calf serum at generating LAK cell activity in vitro (p less than 0.05). The results of this study demonstrate that although human malignant mesothelioma cells are resistant to NK cell lysis, IL-2-activated LAK cells effectively kill these targets.(ABSTRACT TRUNCATED AT 250 WORDS)

Cell Line↗
PubMed1989

Gallium lung scanning and bronchoalveolar lavage in crocidolite-exposed workers.

Gallium lung scanning is widely used to evaluate pulmonary inflammation in patients with interstitial lung disease but has not previously been reported in crocidolite-exposed workers. In order to characterize the pulmonary inflammation caused by crocidolite inhalation, GLS and BAL findings were related to chest x-ray film changes graded according to the ILO classification of roentgenograms of pneumoconioses. In individuals with roentgenographic evidence of asbestosis (CXR greater than or equal to 1/0, n = 15), 13 had a positive GLS and 13 had an abnormal BAL. In asbestos-exposed individuals with equivocal chest x-ray film changes (CXR 0/1, n = 12), six had a positive GLS and six had BAL changes (both GLS and BAL abnormal in three). In individuals with a normal chest x-ray film (CXR 0/0 n = 8), two had a positive GLS and two BAL changes (both abnormal in 1). These data demonstrate that most subjects with crocidolite-induced asbestosis have an abnormal GLS and BAL. In addition, many individuals with asbestos exposure and equivocal or no chest x-ray film changes have an abnormal GLS and/or BAL, suggesting the presence of active subclinical pulmonary inflammation in these individuals.

Asbestos↗
PubMed1989

Effect of nedocromil sodium on neutrophil and eosinophil-induced epithelial cell desquamation in a human in vitro epithelial model.

A human amniotic epithelial membrane preparation was used as a model to study epithelial responses to neutrophils and eosinophils, obtained from normal subjects using Percoll density gradient methods, and activated by phorbyl myristate acetate (PMA). Incubation of activated neutrophils with the epithelial membrane resulted in epithelial cell desquamation, probably due to release of proteases. Activated eosinophils resulted in epithelial cell damage but no desquamation, an action that appeared to be mimicked by major basic protein (MBP). The addition of nedocromil sodium did not significantly inhibit neutrophil-induced epithelial cell desquamation. In one preliminary experiment, nedocromil sodium (10(-4) to 10(-5) mol/L) inhibited epithelial cell desquamation induced by a mixed population of eosinophils and neutrophils.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1988

Bronchoalveolar lavage sampling of airway and alveolar cells.

Bronchoalveolar lavage (BAL) cell counts are used to assess 'alveolitis' in patients with interstitial lung diseases (ILD) but inflammatory cells from airways can contribute to the differential cell count. To determine what BAL volume samples airway cells in patients with ILD we measured the proportion of bronchial epithelial cells (BECs) in four successive 25 ml aliquots in a single lung subsegment in 23 patients with ILD (cryptogenic fibrosing alveolitis (CFA) four, rheumatoid lung (RL) three, asbestosis (ASB) 11, sarcoidosis (SARC) five). Cells recovered from the first two 25 ml lavages exhibited higher proportions of BECs (15 +/- 4% and 9 +/- 2% respectively) than those from the remaining two aliquots (3 +/- 1%, 3 +/- 1%, each P less than 0.01), suggesting that the first 50 ml BAL preferentially samples airway cells compared to the second 50 ml BAL. To evaluate airway and alveolar inflammatory cell proportions in ILD we performed two separate 50 ml BALs (samples I and II) in a single subsegment in 38 patients with ILD (CFA seven, RL five, ASB 19, SARC seven) and measured the proportions of recovered cells in each sample separately and combined. Seven control individuals were also studied. Sample I contained 1-67% (mean 26 +/- 3%) of the total recovered cells. Neutrophil (PMN) proportions were higher in sample I compared to sample II in CFA (20 +/- 6 vs 8 +/- 2%), RL (30 +/- 9 vs 8 +/- 2%) and ASB (12 +/- 2 vs 7 +/- 1%), P less than 0.05 for each, but were similar in samples I and II in patients with SARC (3 +/- 1 vs 2 +/- 1%) and controls (2 +/- 1 vs 2 +/- 1%). In combined samples (I + II), absolute PMN proportions were up to 8% higher than in sample II alone whereas absolute lymphocyte proportions were up to 8% less than in sample II alone. These data suggest that separate processing of the fluid recovered from the first 50 ml BAL in ILD patients provides information on the location of inflammatory cells and improves the accuracy of BAL cell counts.

Adult↗
PubMed1988

Production of plasminogen activator by alveolar macrophages in normal subjects and patients with interstitial lung disease.

Increased production of the serum protease plasminogen activator is associated with tissue damage. The in vitro production of plasminogen activator by alveolar macrophages obtained by bronchoalveolar lavage was studied in 22 normal subjects and 28 patients with interstitial lung disease to determine whether plasminogen activator is produced by normal alveolar macrophages and whether this is increased in patients with interstitial lung disease. Plasminogen activator activity, measured with an iodine-125 labelled fibrin release assay, was found to be dependent on time, effector cell numbers, and plasminogen concentration. Plasminogen activator production by alveolar macrophages from 14 normal non-smokers and eight normal smokers was similar and the mean value was 0.78 (SEM 0.16) urokinase (UK) units x 10(-8)/cell/hour. Alveolar macrophages from the seven patients with cryptogenic fibrosing alveolitis and six patients with histiocytosis-X produced more plasminogen activator (1.89 (0.25) and 4.54 (1.3) x 10(-8) UK units/cell/hour respectively) than macrophages from normal subjects (p less than 0.05), whereas those from 15 patients with sarcoidosis did not (1.09 (0.2) x 10(-8) UK units/cell/hour). Exposure of normal alveolar macrophages to immune complexes enhanced plasminogen activator production to 2.07 (0.27) x 10(-8) UK units/cell/hour, whereas exposure to products of activated T cells and to purified gamma interferon reduced plasminogen activator production (to 0.38 (0.11) and 0.62 (0.11) x 10(-8) UK units/cell/hour respectively). These studies show that plasminogen activator is produced by normal human alveolar macrophages and that its production is increased in patients with cryptogenic fibrosing alveolitis and histiocytosis-X.

Antigen-Antibody Complex↗
PubMed1988

Increased pulmonary gamma interferon production in asbestosis.

In order to determine if disordered cellular immune processes are present in the lungs of persons with asbestosis, we performed bronchoalveolar lavage (BAL) on 26 patients with either crocidolite- or chrysotile-induced pulmonary asbestosis and measured the spontaneous release of gamma interferon (IFN gamma), a marker of increased cellular immune activity. For comparison, 18 control subjects and 7 patients with active pulmonary sarcoidosis were also studied. Recovered BAL cells were cultured for 24 h (5 x 10(6)/ml), and the supernatant was assayed for interferon by determining inhibition of cytopathic effect on encephalomyocarditis virus-induced lysis of WISH cells and characterized by monoclonal anti-IFN gamma antibody inhibition. Nine (35%) patients with asbestosis released increased amounts of IFN gamma, up to 320 units/ml, the levels seen in the sarcoidosis patients. All control subjects released less than or equal to 10 units/ml. All interferon released was IFN gamma. In asbestosis patients, IFN gamma production was not related to a history of cigarette smoking, there was no significant difference in the ratio of helper/inducer (Leu-3) to suppressor/cytotoxic (Leu-2) cells in IFN gamma producers compared to non-IFN gamma producers (p greater than 0.05), and IFN gamma production correlated significantly with serum IgG levels (p less than 0.001) but not with the levels of IgM, IgA, antinuclear factor, or rheumatoid factor. These data suggest that active cellular immune processes are present in the lungs of a proportion of patients with asbestosis.

Asbestosis↗
PubMed1988

Neutrophil chemotactic factor release and neutrophil alveolitis in asbestos-exposed individuals.

Alveolar neutrophil accumulation occurs in asbestosis. To evaluate a possible role for release of neutrophil chemotactic factor (NCF) in the pathogenesis of asbestosis, spontaneous NCF release from alveolar macrophages obtained by bronchoalveolar lavage (BAL) in eight individuals with asbestosis, 13 asbestos-exposed individuals without asbestosis, and five control subjects has been studied. Alveolar macrophages were incubated in medium (four hours; 37 degrees C), and neutrophil responses to the supernatants were assayed in a microchemotaxis chamber. Alveolar macrophages from subjects with asbestosis released more NCF (97 +/- 19 neutrophils per high-power field [N/HPF]) than controls (3 +/- 1 N/HPF; p less than 0.01). Alveolar macrophages from individuals with asbestos exposure and increased BAL neutrophil proportions (n = 7) released more NCF (93 +/- 24 N/HPF) than individuals with asbestos exposure and normal BAL neutrophil proportions (n = 6; 11 +/- 6 N/HPF; p less than 0.02). The results show that spontaneous NCF release occurs in asbestosis and that NCF release is associated with neutrophil alveolitis in asbestos-exposed individuals without asbestosis, suggesting a pathogenic role for NCF in mediating this neutrophil alveolitis. The results of the study also suggest that the presence of crackles is a better predictor of the presence of neutrophil alveolitis than is an abnormal chest x-ray film.

Asbestos↗
PubMed1988

Limiting-dilution analysis of T cells extracted from solid human lung tissue: comparison of precursor frequencies for proliferative responses and lymphokine production between lung and blood T cells from individual donors.

This study evaluates the frequency and functions of immunocompetent T cells at the clonal level in solid human lung tissue versus peripheral blood. Enzymatic digestion of slices of histologically normal human lung yielded 18-42 x 10(6) viable mononuclear cells per gram wet weight tissue, of which 60-72% were lymphocytes; based upon these recoveries and the known weight of adult lung, the (median) lung parenchymal lymphocyte population can be estimated as 6 x 10(9), being of the same order as the blood pool and 15-30-fold that recoverable by broncho-alveolar lavage. Flow cytometric analysis indicated that the bulk of these lymphocytes was OKT3+/T11+ (CD3/CD2) T cells. Purified blood and lung T cells from each subject were cultured at limiting dilution in the presence of PHA, irradiated feeder cells and recombinant human IL-2. The mean frequency estimates for PHA-responsive T cells in these populations were 1 in 1.23 (81%) and 1 in 3.22 (31%) for blood and lung, respectively. This difference was seen for T cells from each donor and was highly significant by paired t-test (P less than 0.002). Analysis of surface phenotypes and functions of individual blood and T-cell clones indicated comparable frequencies for OKT4 (CD4) and OKT8 (CD8) expression, TNF production and mitogen-induced cytotoxicity. However, a striking inverse relationship was observed between the overall frequency of IL-2-producing clones (79% for blood versus 47% for lung) and interferon-gamma (IFN-gamma)-producing clones (46% versus 87%). These differences were found for each subject, and both were highly significant (P less than 0.001) by paired t-test. The available literature suggests that the majority of these lung T cells represent transient immigrants derived from the blood. Accordingly, the functional differences we have observed suggest either selective trapping within the lung vascular bed of peripheral blood T cells of certain functional phenotypes or alternatively selection/modulation of T cells by lung-derived factors during their transit through the tissue.

Adult↗
PubMed1987

Natural killer (NK)-resistant human lung cancer cells are lysed by recombinant interleukin-2-activated NK cells.

Natural killer (NK) cells are active in host defence against tumors. In order to determine if NK cells have the capacity to lyse human lung cancer cells, we evaluated blood NK cell activity against human lung carcinoma lines representing each of the commonest histological types of lung cancer, NCI-H157 (large cell), LICM107 and NCI-H146 (small cell), NCI-H226 (squamous cell), and LICM26 (adeno), and compared the results to their activity against a standard NK-sensitive target, K562, using a 16-hr 51Cr-release assay. At effector to target (E:T) ratios up to 50:1, NK activity was very low against each of the lung cancer cell lines compared to the K562 cells (NCI-H157 10 +/- 2%, LICM107 12 +/- 2%, NCI-H146 14 +/- 5%, NCI-H226 8 +/- 5%, and LICM26 7 +/- 3%, compared to K562 60 +/- 3%, P less than 0.001, for each compared to K562 cells). Recombinant interleukin 2 (IL-2) produced a dose-dependent augmentation of NK activity against each of the lung cancer cell lines, with doses as low as 0.25 U/ml being effective. The highest level of boosting was seen against NCI-H157 cells where NK activity (E:T, 50:1, IL-2, 250 U/ml) increased from 9 +/- 2 to 56 +/- 7%, P less than 0.001). Only brief exposure to IL-2 was necessary for augmentation to occur, with as little as 5 min being required for activation, although increased exposure times produced increased levels of augmentation. NK cells appeared to be the IL-2-responsive lytic cell population in these experiments as Leu 11b-depleted lymphocytes expressed little IL-2-mediated augmentation of activity against these target cells, and most of this IL-2-mediated augmentation of activity was located in the large granular lymphocyte-enriched fraction of the lymphocyte population. We conclude that normal blood NK cell activity against human lung cancer cell lines is low but that this activity can be markedly augmented by brief exposure of NK cells to low doses of recombinant IL-2, suggesting a potential role for IL-2 in the immunotherapy of human lung cancer.

Antibodies, Monoclonal↗
PubMed1987

Comparison of bronchoalveolar lavage helper/suppressor T-cell ratios in sarcoidosis versus other interstitial lung diseases.

In order to compare the frequency of elevated lymphocyte proportions and elevated Leu3/Leu2 (helper/inducer to suppressor/cytotoxic) ratios in sarcoidosis with those in clinically similar interstitial lung diseases (ILDs), bronchoalveolar lavage (BAL) lymphocyte proportions and Leu3/Leu2 ratios were determined for 20 patients with sarcoidosis and 30 patients with other (non-sarcoidosis) ILDs [cryptogenic fibrosing alveolitis (seven), lung connective tissue disease (seven), extrinsic allergic alveolitis (four), lymphoproliferative disease (two), and asbestosis (ten)], as well as in eight control subjects. BAL lymphocyte proportions were elevated above control values in 19 (95%) patients with pulmonary sarcoidosis (mean value 36 +/- 3%) but also in 12 (39%) patients with non-sarcoidosis ILDs (mean value 17 +/- 4%). Leu3/Leu2 ratios were over 2.5 in 15 (75%) of the sarcoidosis patients (mean ratio 4.4 +/- 1). In all control subjects, however, and in all but one of the non-sarcoidosis groups, Leu3/Leu2 ratios were below 2.5 (p less than 0.001 for each compared to sarcoidosis patients). Helper/suppressor ratios over 2.5 are found in the majority of our sarcoidosis patients and, unlike raised lymphocyte proportions alone, are not commonly seen in other ILDs, suggesting that evaluation of BAL helper/suppressor cell ratios may be of value in the investigation of patients with ILD.

Adult↗
PubMed1986

Alveolitis of pulmonary asbestosis. Bronchoalveolar lavage studies in crocidolite- and chrysotile-exposed individuals.

Bronchoalveolar lavage (BAL) findings in 27 individuals with crocidolite- or chrysotile-induced asbestosis were compared to BAL findings in 29 unexposed control subjects. Alveolitis, defined as an increase in the proportions and/or absolute numbers of inflammatory cells present in BAL fluid compared to values in control subjects, was present in 26 (96 percent) subjects with asbestosis. Most exhibited a neutrophil-eosinophil alveolitis, with neutrophil proportions increased to 7.4 +/- 0.7 percent and eosinophil proportions increased to 2.2 +/- 0.4 percent, compared to 2 +/- 0.5 percent and 0.4 +/- 0.01 percent, respectively, in control subjects (p less than 0.01 for both neutrophils and eosinophils). An increase in the total number of neutrophils and eosinophils per ml of lavage fluid was also seen (neutrophils 23 +/- 5 and eosinophils 13 +/- 4 per ml; p less than 0.05 compared to control subjects). Severity of the alveolitis, defined by the neutrophil or eosinophil proportions, was independent of a history of exposure to cigarette smoke. The pattern and severity of alveolitis in crocidolite- and chrysotile-induced asbestosis were similar. There was a significant correlation between duration of exposure to asbestos and neutrophil proportions (p less than 0.01). No significant difference in the severity of the alveolitis was observed between individuals with radiologic and physiologic evidence of asbestosis compared to those with asbestos exposure and crackles alone, suggesting that, in asbestosis as in other chronic interstitial lung diseases, radiologic and physiologic parameters do not reflect the severity of the alveolitis. This study demonstrates that a neutrophil-eosinophil alveolitis is present in individuals with crocidolite- and chrysotile-induced asbestosis, that this alveolitis is independent of cigarette smoking, and that the severity of the BAL changes is not reflected in radiologic and physiologic changes.

Asbestos↗
PubMed1986

Extraction of immune and inflammatory cells from human lung parenchyma: evaluation of an enzymatic digestion procedure.

The inflammatory and immune cell populations of the human lung parenchyma have not been characterized in detail. This report describes a novel and efficient procedure for their extraction. Histologically normal human lung tissue samples from pneumonectomy specimens were sliced to 0.5 mm, and digested in collagenase/DNAse. Viable mononuclear cell yields ranged from 15-48 X 10(6)/g, and were markedly in excess of reported methods employing mechanical tissue disruption, which normally yield populations containing almost exclusively macrophages. The lung digest population was examined by flow cytometry using monoclonal antibodies against cell surface receptors, and found to comprise up to 40% T lymphocytes, 10% B lymphocytes and 30% macrophages, contaminated by less than 1% peripheral blood cells. Based upon these figures, the recoverable lung parenchymal lymphoid cell pool appears considerably larger than previously recognized, being of the same order as the peripheral blood pool. Initial functional studies suggest that such cellular activities as antigen-specific T cell proliferation, antigen-presentation, interleukin 1 production and natural killer cell activity survive the extraction process, and controlled enzymatic digestion experiments with peripheral blood cells indicate that the degree of enzyme-mediated damage to these functions and to cell-surface structures, was minimal. The extraction method thus appears suitable for studying the types and functions of human parenchymal lung cells in health and disease.

Aged↗