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Biomedical subjects

M Laviolette

Publications and source records attributed to M Laviolette.

At least 91 records · Page 5Linked to original sources

In vitro leukotriene (LT) C4 synthesis by blood eosinophils from atopic asthmatics: predominance of eosinophil subpopulations with high potency for LTC4 generation.

We compared the leukotriene (LT) C4 generation by the eosinophil density subpopulations isolated from the blood of asthmatics and normal subjects. Using discontinuous Percoll gradients, eosinophil subpopulations with densities of 1.075, 1.078, 1.081, 1.084, 1.087 and 1.100 g/ml were isolated from the blood of six atopic asthmatics and seven normals. In normals, most eosinophils (94%) were recovered in the density fractions (1.084, 1.087, and 1.100 g/ml). In asthmatics, the eosinophil density profile was shifted towards lower cell density: the eosinophil subsets 1.078, 1.081 and 1.084 g/ml were increased 4.5, 30.3 and 8.9-fold respectively compared to normals (p less than 0.0001); the intermediate subsets, the hypodense 1.081 and normodense 1.084 g/ml fractions being the predominant subpopulations. The ability of asthmatic eosinophil subsets 1.078 to 1.087 g/ml to release LTC4 was measured by reversed-phase HPLC, LTC4 production was highest with the normodense 1.084 g/ml eosinophil subset (149 +/- 28 pmol/10(6) eosinophils, p less than 0.01 compared to the 1.081 fraction). The eosinophils from the hypodense 1.081 g/ml fraction also released more LTC4 (112 +/- 19 pmol/10(6) eosinophils) than the 1.078 and 1.087 g/ml fractions (70 +/- 16 and 67 +/- 12 respectively, p less than 0.01). These results show that, compared to normals, blood of mild atopic asthmatics contains an elevated number of eosinophils of intermediate density which have a high capacity for LTC4 production.

Adult↗

Influence of natural antigenic exposure on bronchoalveolar lavage in subjects with pollen-induced rhinitis.

To determine if atopic subjects without asthma naturally exposed to antigens to which they are sensitized demonstrate evidence of lower airway inflammation, we studied 10 subjects with recurrent seasonal allergic rhinitis to pollens. Each subject had a monthly methacholine challenge and two bronchoalveolar lavages (BAL), one during symptoms of allergic rhinitis and one out of season. The percentage of macrophages, lymphocytes, neutrophils, eosinophils, and mast cells in the lavage fluid were determined on Diff-Quik, nonspecific esterase, or toluidine blue-stained cytocentrifuge preparations. The total number of cells recovered on BAL was 23.2 +/- 3.5 X 10(6) (mean +/- SEM) (13.3 +/- 2.3 X 10(4) cells per milliliter) in season, during symptoms of allergic rhinitis, and 33.8 +/- 7.4 X 10(6) (15.2 +/- 3.1 X 10(4) cells per milliliter) out of season (p greater than 0.05). BAL cell-differential counts (percent) in/out season were similar for macrophages (89.0/84.6), lymphocytes (9.1/12.8), neutrophils (1.3/2.1), eosinophils (0.5/0.5), epithelial cells (0.37/0.46), and mast cells (0.0008/0.0013). Blood eosinophil counts, taken, respectively, in and out of season, were 135.5 +/- 26.8 X 10(6)/L and 102.8 +/- 20.6 X 10(6)/L (p greater than 0.05). Although overall airway responsiveness increased slightly during the pollen season, it did not reach statistical significance (geometric mean of provocative concentration causing a 20% fall in FEV1 [milligrams per milliliter], 98.8 during antigenic exposure compared to 121.4 out of season) (p greater than 0.05. These observations suggest that in subjects without asthma, no changes in cell differential are detected on BAL at the time of maximal symptoms of allergic rhinitis.

Adult↗

Inhibitory effects of MK-886 on arachidonic acid metabolism in human phagocytes.

1. We have investigated the inhibitory activity of compound MK-886 (formerly L-663,536), an indole derivative, on 5-lipoxygenase product synthesis in various human phagocytes stimulated with either the ionophore A23187, in the presence and absence of exogenous arachidonic acid, or platelet-activating factor (PAF). The lipoxygenase products were analysed by reversed-phase h.p.l.c. 2. MK-886 inhibited the formation of 5-hydroxy-eicosatetraenoic acid (5-HETE), leukotriene B4 (LTB4), its omega-oxidation products and 6-trans-isomers with an IC50 value of 10-14 nM in A23187-stimulated neutrophils. In the same system, nordihydroguaiaretic acid (NDGA), AA-861 and L-655,240 showed IC50 values of 250-510, 110-420 nM and 1.7-3.9 microM, respectively. 3. MK-886 inhibited 5-lipoxygenase product synthesis in A23187-stimulated blood eosinophils and monocytes, and in neutrophils primed with granulocyte-macrophage colony-stimulating factor and stimulated with PAF with IC50 values of 1-13 nM. 4. The inhibitory activity of MK-886 was not reversed by addition of 10 microM arachidonic acid to A23187-stimulated neutrophils. 5. Compound MK-886 had no effect on 15-lipoxygenase product synthesis in blood eosinophils and neutrophils up to a concentration of 1 microM. 6. At 100 nM compound MK-886 had no significant effects on calcium ion mobilization, superoxide anion production and actin polymerization in neutrophils. 7. In conclusion, MK-886 is a very potent and specific inhibitor of both LTB4 and LTC4 synthesis in various types of human phagocytes.

Actins↗

Inhibition of human alveolar macrophage production of leukotriene B4 by acute in vitro and in vivo exposure to tobacco smoke.

The number of neutrophils in the lungs of cigarette smokers is increased. This could be a consequence of the chemotactic mediator synthesis by alveolar macrophages (AM). In order to evaluate the possible role of leukotriene B4 (LTB4) in this condition, we studied the formation of LTB4 by nonsmokers' AM exposed in vitro and in vivo to cigarette smoke and by smokers' AM. In the absence of stimulus or upon stimulation, nonsmokers' AM exposed in vitro to tobacco smoke formed less LTB4 than did nonexposed AM, e.g., the cells incubated with arachidonic acid and ionophore produced, respectively, 241 +/- 132 and 425 +/- 106 pmol LTB4/10(6) cells (mean +/- SEM) (P less than 0.01). In other experiments, smokers' AM were incubated in absence of stimulus and produced less LTB4 than did nonsmokers' AM; during a 3-h incubation, smokers' and nonsmokers' adherent AM released, respectively, 3 +/- 2 and 40 +/- 28 pmol LTB4/10(6) cells (P less than 0.05). Similarly stimulated smokers' AM produced less LTB4 than did nonsmokers' AM, e.g., the cells incubated with arachidonic acid and ionophore formed, respectively, 225 +/- 41 and 573 +/- 150 pmol LTB4/10(6) cells (P less than 0.05). In a group including mild smokers and nonsmokers, in vivo exposure to the smoke of 4 cigarettes produced a decrease in the release of LTB4 by AM, e.g., in the presence of arachidonic acid and ionophore, nonexposed and exposed AM produced, respectively, 198 +/- 38 and 143 +/- 38 pmol LTB4/10(6) cells (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Predictive value of bronchoalveolar lavage cells and serum precipitins in asymptomatic dairy farmers.

In 1981 to 1982, we reported that many (19/43) asymptomatic dairy farmers, especially those with positive serum precipitins, had a lymphocytic alveolitis. We reevaluated, six and seven years later, 33 of the initial 43 farmers to verify their outcome. The restudied group included 31 men and 2 women between 24 and 67 years of age. In both studies, 24 were nonsmokers and 9 were exsmokers. Each farmer answered a questionnaire, had a physical examination, blood withdrawal for precipitin analysis, a chest roentgenogram, and pulmonary function tests (forced expiratory flows and diffusion capacity). At restudy, one subject had developed symptoms suggestive of sub-acute farmer's lung and now had inspiratory crackles; six had chronic morning cough and sputum production. Serum precipitins were positive in 10 subjects, whereas 16 had been positive at the initial study. Precipitins reverted from positive to negative in eight subjects and from negative to positive in six. Chest roentgenograms were normal in 23 subjects, while discrete interstitial abnormalities were noted in nine. One subject had significant pulmonary infiltrates. Results of current pulmonary function tests were (% predicted, mean +/- SEM) DL(CO) 114.8 +/- 3.0, FEV1 108.1 +/- 2.4, FVC 105.4 +/- 1.1. No correlations were found between these data and the lymphocytes or mast cells found in the bronchoalveolar lavage (BAL) at the initial study of 1981 and 1982. We conclude that bronchoalveolar lavage cell counts of asymptomatic farmers have no long-term clinical significance.

Adult↗

Metabolism of arachidonic acid through the 5-lipoxygenase pathway in normal human peritoneal macrophages.

Peritoneal macrophages (PM), obtained from 39 healthy women with normal laparoscopy findings, were stimulated with the ionophore A23187 or/and arachidonic acid (AA) both in adherence and in suspension. AA lipoxygenase metabolites were determined by reversed-phase HPLC. The major metabolites identified were 5-hydroxyeicosatetraenoic acid (5-HETE), leukotriene (LT)B4 and LTC4. The 20-hydroxy-LTB4, 20-carboxy-LTB4, and 15-HETE were not detected. Incubations of adherent PM with 2 microM A23187 induced the formation of LTB4, 110 +/- 19 pmol/10(6) cells, 5-HETE, 264 +/- 53 pmol/10(6) cells and LTC4, 192 +/- 37 pmol/10(6) cells. When incubated with 30 microM exogenous AA, adherent PM released similar amounts of 5-HETE (217 +/- 67 pmol/10(6) cells), but sevenfold less LTC4 (27 +/- 12 pmol/10(6) cells) (p less than 0.01). In these conditions LTB4 was not detectable. These results indicate that efficient LT synthesis in PM requires activation of the 5-lipoxygenase/LTA4 synthase, as demonstrated previously for blood phagocytes. When stimulated with ionophore, suspensions of Ficoll-Paque-purified PM produced the same lipoxygenase metabolites. The kinetics of accumulation of the 5-lipoxygenase/LTA4 synthase products in A23187-stimulated adherent cells varied for the various metabolites. LTB4 reached a plateau by 5 min, whereas LTC4 levels increased up to 60 min, the longest incubation time studied. Levels of 5-HETE were maximal at 5 min, and then slowly decreased with time. Thus, normal PM, in suspension or adherence, have the capacity to produce significant amounts of 5-HETE, LTB4, and LTC4. The profile of lipoxygenase products formed by the PM and the reactivity of this cell to AA and ionophore A23187 are similar to those of the human blood monocyte, but different from those of the human alveolar macrophage.

Adult↗

Bronchoalveolar lavage cell differential on microscope glass cover. A simple and accurate technique.

We describe a quick and easy technique to perform cell differentials on bronchoalveolar lavage: the microscope glass cover. Lavage fluids of 72 subjects were analyzed by 3 techniques: glass cover, filter, and cytocentrifuge preparations. Seventy-seven other lavages were analyzed by glass cover and cytocentrifuge preparations alone. Data for the 72 subjects studied by all 3 techniques showed that the cell counts on glass cover and filter preparations were similar, e.g., lymphocytes, 19.2% (range, 0.5 to 94%) and 20.9% (range, 3 to 95%), respectively (Spearman's correlation coefficient, 0.98). However, on cytocentrifuge preparations, lymphocyte counts were lower (8.3%; range, zero to 87%) and macrophage counts were higher (p less than 0.005). Comparison of glass cover and cytocentrifuge preparation mixtures with varying amounts (20 to 80%) of purified blood leukocytes labeled with 51Cr (greater than or equal to 72% lymphocytes) showed that a significant amount of radioactive cells was lost during the cytocentrifuge technique in contrast to the glass cover technique. Because neutrophils represented a low proportion of lavage cells, we also evaluated cell suspensions with known neutrophil contents (10 to 70%); we found no difference in neutrophil counts obtained with the 3 techniques. Lavage data analysis of 40 young nonsmoking volunteers showed that glass cover lymphocyte count was also higher than counts on cytocentrifuge preparations: 16.5% (range, 3 to 45%) and 8.2% (range, 2.5 to 35%), respectively. In this group, the distribution of glass cover lymphocyte percentages was normal (p = 0.21, chi 2 test), and the one-tailed 95% confidence interval was 18.6 to 34.7% (mean plus 1.65 standard deviation).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

Effect of mefenamic acid on bronchial tone in vivo.

Prostaglandins (PG) are very potent mediators which can dilate or constrict the bronchi. In order to evaluate the role of PG in the homeostasis of bronchial tone, we studied the effects of mefenamic acid, a potent cyclooxygenase inhibitor, on the pulmonary function tests of 20 volunteers. The subjects were studied randomly in two sessions, one with a placebo and one with mefenamic acid. Tablets (drug or placebo) were taken for 2 days with the pulmonary function tests performed in the afternoon of the second day. Sessions were performed at least 2 days apart. Parameters measured, including forced vital capacity, forced expiratory volume in 1 s, expiratory flows, functional residual capacity and specific airway conductance (SGaw), were similar in both sessions. The SGaw, which was previously reported to increase with cyclooxygenase inhibitors, was 0.23 +/- 0.06 s-1 X cm H2O-1 in the placebo session and 0.24 +/- 0.06 in the mefenamic acid session (mean +/- SD). This study shows that cyclooxygenase inhibitors have no effect on airway tone and strongly suggests that endogenous PG do not participate in the homeostasis of normal bronchial tone.

Adolescent↗

Prognostic significance of bronchoalveolar lymphocytosis in farmer's lung.

In 1983, we studied and reported the clinical and bronchoalveolar lavage (BAL) data of 26 patients with a history of previous farmer's lung. Most of these subjects (24 of 26) had a BAL lymphocytosis. In 1985, we restudied 14 of these subjects. Each subject had a clinical evaluation, chest roentgenogram, pulmonary function tests, and bronchoalveolar lavage. Results show that only 1 subject had evidence of an episode of acute recurrent disease, and only 1 had clinically progressive disease; however, 6 complained of chronic cough and sputum production. There were some fluctuations in individual pulmonary functions, with a significant decrease in FVC during the 2-yr period. The total number of cells on repeated lavage was 55.20 X 10(6) +/- 41.10 X 10(6) (mean +/- SD). This was not statistically different from the results obtained 2 yr earlier (69.5 X 10(6) +/- 43.01 X 10(6)). The percentage of BAL lymphocytes was also similar between the 2 studies, with abnormal values (greater than 20%) in 13 of 14 subjects (47.2 +/- 19.2). The BAL lymphocyte subsets, measured by monoclonal antibody in 8 subjects, showed a wide range of values, with individual OKT4/OKT8 ratios remaining similar at both studies. There were no correlations between changes seen in individual pulmonary function and BAL lymphocytosis. We conclude that a high intensity lymphocytic alveolitis, which persists after an acute episode of farmer's lung, does not predict the outcome of the disease.

Adult↗

Comparison of 5- and 15-lipoxygenase activities in blood and alveolar leukocyte preparations from normal subjects and patients with eosinophilia.

The arachidonic acid lipoxygenase metabolites of polymorphonuclear leukocyte (PMNL) preparations obtained from 31 subjects with eosinophilia (eosinophil content of PMNL preparations: 27.0%, 4-73, median with range) and 29 normal donors (4.5%, 0-15) were analyzed by reversed phase high performance liquid chromatography. More leukotriene (LT) C4 and 15-hydroxyeicosatetraenoic acid (HETE) (p less than 0.001) and less LTB4 (p less than 0.005) were found in eosinophil-rich preparations in comparison to controls on incubations with ionophore and arachidonic acid. In incubations with arachidonic acid alone, only small amounts of 5-lipoxygenase metabolites were produced by both groups, but the PMNL preparations from patients with eosinophilia showed higher capacity to release LTC4 and 15-HETE (p less than 0.005). In the eosinophil-rich preparations, the percentage of eosinophils correlated positively with the production of LTC4 and negatively with LTB4 (p less than 0.05, incubations with ionophore +/- arachidonic acid), and positively with 15-HETE (p less than 0.01, incubations with arachidonic acid +/- ionophore). Moreover the eosinophil-rich preparations produced more LTC4 per eosinophil in incubations with arachidonic acid alone (p less than 0.001) than normal PMNL preparations. The predominant release of LTC4 and 15-HETE by eosinophils was further confirmed by the analysis of bronchoalveolar lavage cells. Lavage cells containing eosinophils released LTC4 and 15-HETE while normal bronchoalveolar lavages, which were poor in eosinophils, did not produce detectable amount of LTC4 and 15-HETE. These results show that eosinophils release preferentially LTC4 and 15-HETE in contrast to LTB4 for the neutrophils.

Adolescent↗

Bronchoalveolar lavage in farmers' lung disease: diagnostic and physiological significance.

A group of 92 farmers had clinical evaluation, pulmonary function tests, and bronchoalveolar lavage (BAL). There were 12 patients with acute farmers' lung disease (FLD) (group 1) and 37 farmers who had had acute FLD, of whom 22 were still on their farm (group 2) and 15 had ceased contact (group 3); others were normal dairy farmers, 23 serology positive to Micropolyspora faeni (group 4), 20 serology negative (group 5), and 42 normal controls (group 6). Of the 134 subjects, 59 had an increase in alveolar lymphocytes (greater than 22% lymphocytes in BAL) (12 in group 1, 19 in group 2, six in group 3, 14 in group 4, five in group 5, and three in group 6). Within each group there was no correlation between BAL lymphocytes (% and absolute number) and most pulmonary function tests. It is concluded that although an increase in BAL lymphocytes is always seen in acute FLD it may also be seen in the absence of clinically evident disease and that BAL lymphocytosis does not correlate with physiological changes in FLD.

Acute Disease↗

Relationships between radiographic change, pulmonary function, and bronchoalveolar lavage fluid lymphocytes in farmer's lung disease.

Ninety four dairy farmers were investigated by chest radiography, pulmonary function tests, and bronchoalveolar lavage. They were divided into five groups--1: 11 subjects with acute farmer's lung; 2: 25 subjects with previously diagnosed farmer's lung who had stayed on their farm; 3: 15 farmers with previously diagnosed farmer's lung who had left the farm; 4: 23 precipitin positive symptomless farmers; 5: 20 precipitin negative symptomless farmers. The study evaluated the relationships between radiographic changes measured with a scoring system derived from the International Labour Office (ILO) classification, the results of pulmonary function tests, and bronchoalveolar lavage fluid. Thirty eight subjects had radiographic evidence of interstitial pulmonary infiltrates. Group 1 had the highest percentage of lymphocytes recovered by bronchoalveolar lavage (mean 66.3 (SD 19.2]. For all subjects carbon monoxide transfer factor (TLCO) and total lung capacity were negatively correlated with radiographic changes (r = -0.45 and -0.30; p less than 0.001 and less than 0.01 respectively). TLCO was also negatively correlated with radiographic change in group 2 (r = -0.59, p less than 0.005). The percentage of lavage lymphocytes was correlated with radiographic changes for all subjects (r = 0.36, p less than 0.001), but this correlation was not seen within groups. This study shows good correlation between radiographic abnormalities, pulmonary function changes and the cellular composition of bronchoalveolar lavage fluid.

Adolescent↗

Bronchoalveolar lavage in pulmonary mycotoxicosis (organic dust toxic syndrome).

Two cases of pulmonary mycotoxicosis (organic dust toxic syndrome) are described in which bronchoalveolar lavage was undertaken during the acute phase and after recovery. Both cases occurred after exposure to mould dust in a silo in the course of removing the top mouldy layer of silage or oats at the start of unloading. The workers suffered an acute febrile illness accompanied by cough and dyspnoea. One patient had impaired ventilatory function and both had arterial desaturation in the acute phase. There was mild impairment of diffusing capacity (transfer factor). Bronchoscopy showed inflammation of the bronchial mucosa in one patient. Fungal spores were cultured from the lavage fluid in both patients. In both patients there was an increase in the percentage of neutrophils in the lavage fluid without increase in lymphocytes. The immunoglobulin concentration in the lavage fluid was normal. At the follow up lavage the neutrophils had returned to normal while a mild lymphocytosis of the lavage fluid was seen in both patients.

Acute Disease↗

Role of prostaglandins in marihuana-induced bronchodilation.

In vitro evidence suggests that physiological effects of marihuana may be mediated by prostaglandins via the stimulation of phospholipase A2. To verify if marihuana could act by this route in vivo, we tested the effects of acetylsalicylic and mefenamic acids, inhibitors of cyclooxygenase, on marihuana-induced bronchodilation and tachycardia. In 11 healthy volunteers, marihuana smoking (7 mg/kg, 1.7% delta 9-tetrahydrocannabinol) produced a significant increase in specific airway conductance (from 0.262 +/- 0.033 to 0.360 +/- 0.050 s-1 X cm H2O-1, mean +/- SE, p less than 0.01), forced expiratory volume in 1 s (4.02 +/- 0.22-4.27 +/- 0.25 liter, p less than 0.05) and heart rate (73.2 +/- 2.0-108.5 +/- 5.2 beats/min, p less than 0.001). In a second session, acetylsalicylic or mefenamic acid was taken for 30 h before marihuana smoking. No inhibition of marihuana-induced increase of specific airway conductance, forced expiratory volume in 1 s and heart rate was found. These findings suggest that the bronchodilation and the tachycardia induced by marihuana smoking in humans are not mediated by prostaglandins.

Adult↗

Decreased leukotriene B4 synthesis in smokers' alveolar macrophages in vitro.

Recent studies have shown that alveolar macrophages (AM) are able to release leukotrienes (LTs). Since cigarette smoking inhibits the cyclooxygenase pathway of arachidonic acid metabolism in the AM, we evaluated the LT production by AM from smokers and nonsmokers. AM were obtained from 35 volunteers, 16 nonsmokers, and 19 smokers. The cells were incubated under various conditions including stimulation with 30 microM arachidonic acid, 2 microM ionophore A23187, or both. Each experiment was performed in parallel using cells from a smoker and a nonsmoker. Lipoxygenase products were analyzed by reverse-phase high performance liquid chromatography. After stimulation, nonsmokers' AM produced LTB4 and 5-hydroxy-eicosatetraenoic acid (5-HETE). In incubations of AM with arachidonic acid and ionophore, the amounts of products formed were: LTB4, 317 +/- 56 pmol/10(6) cells and 5-HETE, 1,079 +/- 254, mean +/- SEM. No metabolites were generated under control conditions (no stimulation). In all incubations performed, the peptido-LTs (LTC4, LTD4, and LTE4) were undetectable. In comparison with AM from nonsmokers, those from smokers showed a 80-90% reduction of 5-HETE and LTB4 synthesis (P less than 0.05 to P less than 0.001 according to stimulatory conditions). This defective lipoxygenase metabolite production in AM from smokers was observed over a wide range of stimuli concentrations and incubation times; AM from smokers also had lower levels of intracellular (esterified) 5-HETE than nonsmokers' AM. We also studied blood polymorphonuclear leukocytes (PMNL) and no difference in the synthesis of 5-lipoxygenase products in these cells was noticed between smokers and nonsmokers. These data show that cigarette smoking causes a profound inhibition of the 5-lipoxygenase pathway in AM but not in blood PMNL.

Adult↗

Persistent bronchoalveolar lymphocytosis in asymptomatic farmers.

We previously demonstrated that 14 of 23 asymptomatic dairy farmers with positive precipitins and 5 of 20 without precipitins had an alveolar lymphocytosis (greater than 22%). To verify the outcome of this lymphocytosis, we restudied, 2 or 3 yr later, 27 of these subjects. No subject had had symptoms suggestive of farmer's lung disease either prior to the initial study or between the 2 studies. All were still on their farm. Physical examination and chest roentgenograms were normal for all subjects at both studies. Pulmonary function tests showed a small but significant change in RV (101.8 +/- 20.4% to 118.7 +/- 27.6% of predicted, p less than 0.05) and FVC (98.0 +/- 12.6% to 94.3 +/-9.5%, p less than 0.05), whereas TLC, FEV1, and DLCO showed no changes. Lymphocytes from BAL were still increased in 9 of 12 subjects, whereas 3 had returned to normal; of the 15 subjects with previous normal values, 3 now had an abnormal lavage lymphocytosis. There was no correlation between lung function variations and the percentage of lymphocytes in the previous or the present BAL. We conclude that a bronchoalveolar lymphocytosis is a persistent phenomenon in a large number of asymptomatic dairy farmers, and that this finding is not related to significant disease, at least in the time span studied.

Adult↗

Relationship among antigen contact, alveolitis, and clinical status in farmer's lung disease.

We studied 41 subjects with a history of farmer's lung disease who had been free of acute episodes for at least one year. Twenty-six were still in daily contact with hay (group 1), and 15 had ceased all antigenic exposure (group 2). While the incidence of dyspnea was similar in both groups, coughing and sputum were more frequent in group 1. Inspiratory crackles were frequent in group 1 subjects (15 of 26) and absent in all group 2 subjects. In both groups, a high percentage of lymphocytes was demonstrated by bronchoalveolar lavage: 52.5% +/- 21.1% (mean +/- SD) and 26.3% +/- 18.7%, respectively. Lymphocytic alveolitis (greater than 22% lymphocytes) was more common in group 1 (23 of 26) than in group 2 (6 of 15). There was no relationship between functional abnormalities and the intensity of the alveolitis. We conclude that lymphocytic alveolitis may persist after an acute episode of farmer's lung disease, but the intensity of the alveolitis is not associated with functional alterations.

Acute Disease↗