In vivo uptake of inhaled particles by airway phagocytes is enhanced in patients with mild asthma compared with normal volunteers.

BACKGROUND: The uptake of inhaled particulate matter by airway phagocytes is an important defence mechanism contributing to the clearance of potentially toxic substances, including aeroallergens, from the lung. Since airway monocytes and macrophages can also function as antigen presenting cells, their ability to engulf materials deposited on the airway surface is of particular interest in patients with allergic asthma. To determine whether airway mononuclear phagocytes of patients with allergic asthma might have enhanced phagocytic activity, the in vivo uptake of inhaled radiolabelled particles was compared in 10 patients with mild allergic asthma and 8 healthy (non-allergic) individuals. METHODS: Phagocyte function was assessed by quantifying the proportion of radioactivity associated with cellular and supernatant fractions of induced sputum 2 h after inhalation of radiolabelled sulfur colloid particles. All subjects were pretreated with albuterol before sputum induction. A standardised breathing pattern was used to target aerosol deposition in the bronchial airways. RESULTS: In vivo particle uptake by airway cells was significantly greater in patients with asthma than in healthy volunteers (57.2% (95% CI 46.5% to 67.9%) vs 22.3% (95% CI 4.9% to 39.6%), p<0.01), as was in vitro phagocytosis of opsonised zymosan-A bioparticles. There was also a significant correlation (r = 0.85, p<0.01) between the percentage of sputum mononuclear phagocytes and the percentage uptake of particles in the patients with asthma but not in the control subjects. CONCLUSIONS: In vivo particle uptake by airway macrophages is enhanced in persons with mild asthma. Enhanced uptake and processing of particulate antigens could contribute to the pathogenesis and progression of allergic airways disease and may contribute to the increased risk of disease exacerbation associated with particulate exposure.

Salmonella enterica serotype Javiana infections associated with amphibian contact, Mississippi, 2001.

Salmonella Javiana is a Salmonella serotype that is restricted geographically in the United States to the Southeast. During the summer of 2001, the number of reported S. Javiana infections in Mississippi increased sevenfold. To identify sources of infection, we conducted a case-control study, defining a case as an infection with S. Javiana between August and September in a Mississippi resident. We enrolled 55 cases and 109 controls. Thirty (55%) case patients reported exposure to amphibians, defined as owning, touching, or seeing an amphibian on one's property, compared with 30 (29%) controls (matched odds ratio 2.8, P=0.006). Contact with amphibians and their environments may be a risk factor for human infection with S. Javiana. The geographic pattern of S. Javiana infections in the United States mimics the distribution of certain amphibian species in the Southeast. Public health officials should consider amphibians as potential sources of salmonellosis, and promote hand washing after contact with amphibians.

Effects of inhaled iron oxide particles on alveolar epithelial permeability in normal subjects.

Pulmonary inflammation secondary to oxidant generation catalyzed by transition metals associated with inhaled particles is one factor postulated to underlie the acute health effects of particulate air pollution. We postulated that inhaled iron oxide particles with associated amounts of soluble iron should induce mild pulmonary inflammation and lead to altered alveolar epithelial integrity and altered gas exchange. To test this hypothesis we examined the effects of inhaled iron oxide particles on alveolar epithelial permeability. Sixteen healthy subjects inhaled aerosols of iron oxide particles (1.5 microm mass median aerodynamic diameter) having either high or low water-soluble iron content [3.26 +/- 0.25 (SE) and 0.14 +/- 0.04 microg soluble iron/mg of particles, respectively] for 30 min at an average mass concentration of 12.7 mg/m(3). Alveolar epithelial permeability was assessed by measuring the pulmonary clearance of an inhaled radiolabeled tracer molecule ((99m)Tc-DTPA, diethylene triamine pentaacetic acid) using a gamma camera at 1/2 h and 24 h post particle exposure. Carbon monoxide lung diffusing capacity (DL(CO)) and spirometry were also performed before and after breathing the iron oxide. As a control, on a separate day, the procedures were duplicated except that the subject breathed particle-free air. For those subjects breathing aerosols with high soluble iron, we found no significant difference in DTPA clearance half-times after breathing particles versus particle-free air either at 1/2 h (97.4 +/- 15.4 vs. 116.1 +/- 15.5 min, respectively) or 24 h postinhalation (105.1 +/- 13.8 vs. 106.9 +/- 12.9 min, respectively). Likewise, for those subjects breathing aerosols with low soluble iron content we found no significant difference in DTPA clearance half-times after breathing particles versus particle-free air either at 1/2 h (108.6 +/- 31.9 vs. 95.6 +/- 10.8 min, respectively) or 24 h postinhalation (130.0 +/- 18.0 vs. 105.8 +/- 13.7 min, respectively). We found no significant differences in DL(CO) between particle exposures and air exposures. Minor differences in spirometric measurements were noted but were not statistically significant. We conclude that inhalation of iron oxide particles did not cause an appreciable alteration of alveolar epithelial permeability, lung diffusing capacity, or pulmonary function in healthy subjects under the studied conditions.

Cellular and biochemical response of the human lung after intrapulmonary instillation of ferric oxide particles.

Bronchoalveolar lavage (BAL) was used to sample lung cells and biochemical components in the lung air spaces at various times from 1 to 91 d after intrapulmonary instillation of 2.6 microm-diameter iron oxide particles in human subjects. The instillation of particles induced transient acute inflammation during the first day post instillation (PI), characterized by increased numbers of neutrophils and alveolar macrophages as well as increased amounts of protein, lactate dehydrogenase, and interleukin-8 in BAL fluids. This response was subclinical and was resolved within 4 d PI. A similar dose-dependent response was seen in rats 1 d after intratracheal instillation of the same particles. The particles contained small amounts of soluble iron (240 ng/mg) and possessed the capacity to catalyze oxidant generation in vitro. Our findings indicate that the acute inflammation after particle exposure may, at least partially, be the result of oxidant generation catalyzed by the presence of residual amounts of ferric ion, ferric hydroxides, or oxyhydroxides associated with the particles. These findings may have relevance to the acute health effects associated with increased levels of ambient particulate air pollutants.

Retention and intracellular distribution of instilled iron oxide particles in human alveolar macrophages.

Bronchoalveolar lavage (BAL) was used to sample retention of particles within the alveolar macrophage (AM) compartment at various times from 1 to 91 d following intrapulmonary instillation of 2. 6-microm-diameter iron oxide (Fe2O3) particles in human subjects. Particles were cleared from the lavagable AM compartment in a biphasic pattern, with a rapid-phase clearance half-time of 0.5 d and long-term clearance half-time of 110 d, comparable to retention kinetics determined by more traditional methods. The intracellular distribution of particles within lavaged AMs was similar in bronchial and alveolar BAL fractions. AMs with high intracellular particle burdens disappeared from the lavagable phagocytic AM population disproportionately more rapidly (shorter clearance half-time) than did AMs with lower particle burdens, consistent with the occurrence of a particle redistribution phenomenon as previously described in similar studies in rats. The rates of AM disappearance from the various particle burden categories was generally slightly slower in bronchial fractions than in alveolar fractions. The instillation of particles induced a transient acute inflammatory response at 24 h postinstillation (PI), characterized by increased numbers of neutrophils and alveolar macrophages in BAL fluids. This response was subclinical and was resolved within 4 d PI.

Disruption of normal iron homeostasis after bronchial instillation of an iron-containing particle.

The atmosphere constitutes a prime vehicle for the movement and redistribution of metals. Metal exposure can be associated with an oxidative stress. We tested the hypothesis that, in response to an iron-containing particle, the human respiratory tract will demonstrate an increased expression of both lactoferrin and ferritin as the host attempts to transport and store the metal in a chemically less-reactive form and therefore diminish the oxidative stress the particle presents. Subjects (n = 22) were instilled with 20 ml of saline and 20 ml of an iron-containing particle suspended in saline in a right middle lobe bronchus and a lingular bronchus, respectively. At either 1, 2, or 4 days after this exposure, the volunteer was lavaged for a sample of the lower respiratory tract, and concentrations of L-ferritin, transferrin, and lactoferrin were measured by enzyme immunoassay, immunoprecipitin analysis, and enzyme-linked immunosorbent assay (ELISA), respectively. Transferrin receptor was also quantified by ELISA. The concentrations of L-ferritin in the lavage fluid of lung exposed to particles were significantly increased relative to the levels of the protein in the segment exposed to saline. Relative to saline instillation, transferrin was significantly diminished after exposure to the iron-containing particle, whereas both lactoferrin and transferrin receptor concentrations in the segment of the lung exposed to the particle were significantly elevated. We conclude that instillation of an iron-containing particle was associated with a disequilibrium in iron metabolism in the lower respiratory tract. The response included increased ferritin and lactoferrin concentrations, whereas transferrin concentrations diminished. This coordinated series of reactions by the host effects a decrease in the availability of catalytically reactive iron to likely diminish the consequent oxidative stress to the human host.

Retention of insoluble particles after local intrabronchial deposition in dogs.

Recent studies have challenged the generally accepted hypothesis that bronchial particle clearance is complete within 24-48 h postdeposition. We studied bronchial retention of inert particles using a bronchoscope and microspray nozzle to localize deposition in a bronchus while avoiding alveolar deposition. Six-microliter aliquots (444 kBq) of submicrometer (number mean diameter = 0.22 microns, geometric standard deviation = 1.75) technetium-99m-labeled (99mTc) sulfur colloid (SC) particles (n = 6) or the unbound radiolabel 99mTc-pertechnetate (99mTcO4-; n = 3) were sprayed onto a 5-mm-diam bronchus in halothane-anesthetized dogs. Radioactivity at the deposition site and clearance pathway was monitored externally with a gamma camera beginning immediately postspray. Bronchial retention of SC was 8.5 +/- 2.4 and 1.5 +/- 0.7% at 3 and 24 h postspray, respectively. Tracheal mucus velocity was measured at 10.4 +/- 2.2 mm/min. For comparison, clearance of inhaled submicrometer SC particles was also measured in the same dogs. Retention of inhaled aerosolized SC (peripheral lung deposition) was 98.1 +/- 1.1 and 76.3 +/- 1.8% at 3 and 24 h, respectively. 99mTcO4- cleared from the bronchi slightly more rapidly than did SC. Radioactivity was readily detected in the blood after deposition of 99mTcO4- but not of SC. Thus SC cleared by mucociliary transport, whereas 99mTcO4- cleared predominantly by transepithelial absorption. We conclude that clearance of submicrometer particles from a 5-mm conducting airway is very nearly complete by 24 h, with approximately 92% of the clearance occurring within the first 3 h postdeposition.

Eosinophilic gastroenteritis with encapsulated nematodes in a horse.

A 3-year-old Quarter Horse gelding admitted for evaluation of weight loss, signs of depression, and dermatitis of the coronary bands was found to have eosinophilic gastroenteritis. Intralesional nematodes identified as Strongylus edentatus were seen in multiple microscopic sections of the small colon, suggesting a parasitic cause of the disease.

Sclerosing encapsulating peritonitis in three dogs.

A condition resembling human sclerosing encapsulating peritonitis was identified in 3 young large-breed dogs. All 3 dogs had similar clinical signs: ascites, vomiting, and excessive borborygmus. The condition was discovered at laparotomy and confirmed histologically. Laparotomy revealed a sac-like formation totally or partially occupying the peritoneal cavity. The predominant histologic abnormality was marked peritoneal and serosal fibrosis. None of the dogs had a favorable response to treatment, and euthanasia was performed because of development of abdominal distention.

Histology and morphometry of Strongylus vulgaris-mediated equine mesenteric arteritis.

Histological and morphometric evaluation of equine cranial mesenteric arteries was performed on 239 and 89 arteries, respectively. Histological examination revealed that thrombosis and the severity of inflammation varied on a seasonal basis and were directly associated with larval presence. Intimal and adventitial fibrosis were generally of greater severity than medial fibrosis. Fibrosis of the vasa vasorum was less frequent than fibrosis of the artery itself. Morphometry revealed a significant increase in intimal, adventitial and, to a lesser extent, medial area in affected as compared with normal arteries. This change was due to the accumulation of collagen and was considered to result in decreased arterial elasticity. The luminal area varied widely among affected arteries.

Morphometric and ultrastructural study of postnatal lung growth and development in calves.

The objectives of this study were to characterize basic patterns of postnatal lung growth in 1- to 150-day-old Holstein calves and to identify periods of accelerated lung growth and times of epithelial cell development that might correlate with periods of heightened susceptibility to pulmonary injury by infective agents and dietary toxins. Calves had fully developed alveoli at birth. There was an age-associated increase in total alveolar surface area and alveolar number, which was most marked in calves older than 30 days. Lung volume and body weight increases were also most marked when calves were older than 30 days. Mean bronchiolar cross-sectional area increased significantly (P less than 0.05) with age, and there was a significant (P less than 0.05) decrease in the percentage of terminal bronchioles with diameters less than 3 x 10(4) microns between 1 and 150 days. In newborn calves, nonciliated bronchiolar epithelial cells retained fetal characteristics of differentiation, including abundant cytoplasmic glycogen and sparse agranular endoplasmic reticulum. Glycogen deposits were depleted, and agranular endoplasmic reticulum was developed in nonciliated cells by the time calves were 30 days old. We concluded that bronchiolar epithelium in calves is well differentiated by the time they are 30 days old and that lung growth in calves raised in semi-isolation begins most rapidly when calves are approximately 30 days old.

Influence of acute pulmonary interstitial inflammation on kinetics of phagocytosis by alveolar macrophages.

The pulmonary alveolar macrophage (PAM) is central to lung cellular defenses and is a potential participant in lung injury, but little is known about the influence of the nature and anatomic pattern of acute lung injury on PAM function. To assess the relationship between ongoing pulmonary inflammation and PAM function, we evaluated PAM phagocytic kinetics in a model system of experimental interstitial adjuvant pneumonitis (EIAP) in calves. PAMs were obtained from lung one and seven days postinduction (dpi) of EIAP. Lesions were typical of EIAP, characterized by acute multifocal to coalescing exudative interstitial pneumonitis at 1 dpi, which progressed to granulomatous interstitial pneumonitis by 7 dpi. The total recoverable lung cells and percentage of neutrophils (PMNs) were elevated (P less than 0.01) from animals with EIAP at both 1 and 7 dpi, and there was a four-fold increase (P less than 0.01) in the PAM yield by 7 dpi. Linear regression equations revealed that a larger proportion of control PAMs were phagocytic than were PAMs from animals with EIAP. The mean initial phagocytic rates of PAM following acute lung injury were significantly elevated (P less than 0.05) over controls; this difference was concentration dependent and required a phagocytic bead stimulus concentration in excess of 12.5 x 10(6) beads/ml. PAMs from animals with EIAP had a greater maximum rate of phagocytosis (Vmax) and Km than control PAMs. PAMs from animals with EIAP had a slightly higher proportion of cells which phagocytosed multiple beads. Levels of beta-glucuronidase were elevated (P less than 0.02) in PAM from animals with EIAP at 7 dpi. The results document enhanced PAM phagocytic function in EIAP and differ from our previous experiments in which depressed PAM phagocytic indices were obtained in a model of virus-induced acute bronchiolitis and alveolitis. The functional activities of the PAMs thus appear to be modified by injury-specific events in the lung microenvironment which may, in part, reflect the nature and anatomic pattern of developing pulmonary inflammatory reactions.

Acute inflammatory lung injury retards pulmonary particle clearance.

The deposition, retention, and clearance of inhaled cobalt oxide particles from the lungs of calves with acute inflammatory lung injury induced by parainfluenza-3 virus (PI-3) were examined. Acute pulmonary inflammation was induced by nebulization with 10(9) TCID50 of PI-3 virus on two successive days, and animals were subsequently exposed to an aerosol of particulate cobalt oxide (geometric mean diameter 0.54-0.65 microns) seven days post-virus infection (dpi). Pulmonary lesions at 7 dpi were typical of PI-3 pneumonitis and were characterized by patchy aveolitis and bronchiolitis with accumulations of neutrophils, macrophages, fibrin, and inflammatory debris. Calves were killed at 0, 7, and 21 days post-aerosol exposure (dpe) to evaluate particle clearance and retention by assay for cobalt in lung tissues, bronchoalveolar washings, and tracheobronchial lymph nodes. Control animals had a typically biphasic clearance pattern with rapid initial clearance of 50% of the initial lung burden (ILB) by 7 dpe followed by slower prolonged clearance. Clearance was significantly retarded (P less than 0.05) in calves with viral-induced acute inflammatory lung injury; 90% of the ILB was retained at 7 dpe. Essentially all particles recoverable by bronchoalveolar lavage were intracellular within pulmonary alveolar macrophages (PAM) in both experimental and control groups, but interstitial sequestration of particles within PAM was commonly observed only in the lungs of calves with viral pneumonitis. Pneumonic calves also exhibited retarded translocation of particles to regional lymph nodes. The results document impaired particulate clearance from acutely inflamed lungs, and implicate decreased mucociliary clearance and interstitial sequestration within PAM as the major contributing factors. These functional alterations would be expected to enhance the progression of virus-induced acute pulmonary inflammatory injury.

Preliminary investigations on the effects of a Strongylus vulgaris larval extract, mononuclear factors and platelet factors on equine smooth muscle cells in vitro.

Factors involved in the proliferation of equine vascular smooth muscle cells were studied in vitro. The most prominent proliferative responses in cultured vascular smooth muscle cells were induced by Strongylus vulgaris larval antigen extract (LAE) and platelet-derived factors. Less significant proliferative responses were obtained with conditioned media from S. vulgaris LAE stimulated and from unstimulated equine mononuclear leukocytes. Additionally, vascular smooth muscle cells exposed to S. vulgaris LAE developed numerous perinuclear vacuoles and were more spindle-shaped than control or smooth muscle cells exposed to other factors. Equine mononuclear leukocytes exposed to LAE developed prominent morphological changes, including enlargement, clumping and increased numbers of mitotic figures.

Generation and characterization of respirable metallic oxide aerosols for pulmonary clearance studies in calves.

An aerosol generating system capable of producing inert, insoluble, non-toxic, respirable, submicronic particles suitable for deposition, retention and clearance studies in the lungs of calves was designed and tested. The machine generated high volume outputs of respirable aerosols by nebulization of an aqueous solution of metallic ions, drying the droplet aerosol, thermal degradation in the presence of oxygen to form insoluble oxides, and subsequent cooling of the aerosol. Aqueous solutions of ferric nitrate, ferric chloride, ferric citrate, ferric oxalate, zinc acetate, lead acetate, cobalt nitrate, cobalt chloride and cobalt acetate were examined, and the resultant aerosols characterized by particle size distribution, shape, aerosol mass concentration, and production of toxic by-products. Iron oxide and cobalt oxide aerosols were judged suitable for inhalation studies in calves, and cobalt oxide was selected for pulmonary clearance studies due to the low background content of cobalt in lung tissue. The cobalt oxide aerosol selected had a geometric mean diameter (GMD) of 0.54 to 0.65 micron with a dimensionless geometric standard deviation (GSD) of 1.41 to 1.71, a mass aerosol concentration of 124 to 335 mg/m3, and a NO2 contamination of 5 to 33 ppm. The cobalt oxide particles were measurably polydisperse, but virtually all particles were smaller than 2.0 microns making the aerosol totally respirable.

Effects of Newcastle disease virus infection on the binding, phagocytic, and bactericidal activities of respiratory macrophages of the turkey.

Effects of Newcastle disease virus (NDV) infection on the binding, phagocytic, and bactericidal activities of turkey respiratory macrophages were studied. Respiratory macrophages of the turkey demonstrated the presence of immunoglobulin (Ig) G and complement receptors but lacked IgM receptors. Respiratory macrophages from NDV-infected turkeys showed little or no depression of binding of sheep erythrocyte-IgG complexes and sheep erythrocyte-IgM-complement complexes to their appropriate membrane receptors. In contrast, respiratory macrophages from NDV-infected turkeys showed significant (P less than or equal to 0.05) depression of phagocytosis of similar complexes. Bacterial killing by respiratory macrophages from NDV-infected turkeys was significantly (P less than or equal to 0.05) inhibited.

Solid-state 15N NMR of oriented lipid bilayer bound gramicidin A'.

Highly oriented samples of lipid and gramicidin A' (8:1 molar ratio) have been prepared with the samples extensively hydrated (approximately 70% water v/w). These preparations have been shown to be completely in a bilayer phase with a transition temperature of 28 degrees C, and evidence is presented indicating that the gramicidin is in the channel conformation. An estimate of the disorder in the alignment of the bilayers parallel with the glass plates used to align the bilayers can be made from the asymmetry of the nuclear magnetic resonances (NMR). Such an analysis indicates a maximal range of disorder of +/- 3 degrees. Uniformly 15N-labeled gramicidin has been biosynthesized by Bacillus brevis grown in a media containing 15N-labeled Escherichia coli cells as the only nitrogen source. When prepared with labeled gramicidin, the oriented samples result in high-resolution 15N NMR spectra showing 12 resonances for the 20 nitrogen sites of the polypeptide. The frequency of the three major multiple resonance peaks has been interpreted to yield the approximate orientation of the N-H bonds in the peptide linkages with respect to the magnetic field. These bond orientations are only partially consistent with the extant structural models of gramicidin.

Alveolar macrophage phagocytic kinetics following pulmonary parainfluenza-3 virus infection.

Qualitative and quantitative evaluations of the cellular components of bronchoalveolar washings of calves with experimental parainfluenza-3 virus pneumonitis and control calves were made. Calves were exposed to 10(9) TCID50 of PI-3 by intranasal aerosol exposure and bronchoalveolar cells obtained 7 days after infection by volume-controlled bronchopulmonary lavage. Transient tachypnea and pyrexia occurred in all infected calves, and virus was recoverable at 7 days from nasal swabs and lung tissue. Pulmonary lesions were typical of viral pneumonitis, characterized by patchy alveolitis and bronchiolitis with accumulations of cells and inflammatory debris. The mean total lavage cell yield was elevated in the virus-infected calves, and the percentage of neutrophils was elevated (P less than 0.05). Increased numbers of pulmonary alveolar macrophages (PAM) were also recovered but the difference was not significant. Linear regression equations showed that a decreased proportion of PAM from virus-infected animals were phagocytic. The mean initial phagocytic rates of macrophages from calves with viral pneumonitis were significantly decreased (P less than 0.05) over controls. This difference was concentration dependent and required a phagocytic stimulus in excess of 12.5 X 10(6) beads/ml. Studies of phagocytic kinetics showed that PAM from calves with viral pneumonitis had a lower Vmax than PAM from control calves, but that Km values were comparable. No differences in PAM beta-glucuronidase and acid phosphatase activity were observed. These results indicate depressed phagocytic function in PI-3 virus-inflamed lungs relative to controls. In concert with virus-induced airway lesions, such in vivo depression of PAM phagocytic functions would be expected to depress pulmonary particulate clearance and lung defense mechanisms.

Tracheal mucus transport rate and bacterial clearance in turkeys exposed by aerosol to La Sota strain of Newcastle disease virus.

Tracheal mucus transport rate (TMTR) and quantitative clearance of aerosolized Escherichia coli from the trachea, lung, and air sac were measured in healthy unanesthetized turkeys and in turkeys exposed by aerosol to a La Sota vaccine strain of Newcastle disease virus (NDV). The TMTR of uninfected turkeys was 42.4 +/- 14.7 cm/min. The TMTR of NDV-infected turkeys was depressed on days 3 through 7 postexposure (PE); depression was significant (P less than or equal to 0.05) on day 7 PE. Tracheal E. coli clearance in NDV-infected turkeys was reduced on days 4 through 9 PE, significantly so on day 5 PE (P less than or equal to 0.01). Depression of TMTR and tracheal E. coli clearance were associated histologically with replacement of normal pseudostratified columnar epithelium by 3 to 8 layers of immature nonciliated cells. E. coli clearance by the lung and air sac of NDV-infected turkeys was depressed on days 5 through 9 PE.

Volume-controlled bronchopulmonary lavage of normal and pneumonic calves.

Saline bronchopulmonary lavage of the right lung of 16 anesthetized calves was performed using a single-lumen cuffed endotracheal tube. The initial volume of saline introduced was based on the functional residual capacity (FRC) of the right lung lobes as determined from the proportional weights of the right (58% of total FRC) and left (42% of total FRC) lung lobes. Calves were divided into "pneumonic" and "normal" groups based on clinical signs. Five sequential washes were done on each calf. There was no difference in the percentage of total lavage fluid volume recoverable between normal (83.8 +/- 4.2%) and pneumonic (81.1 +/- 8.2%) calves. Cell yield in the initial wash was consistently greater than in subsequent washes for both normal (12.7 +/- 6.6 X 10(6) cells/kg body weight) and pneumonic (58.1 +/- 37.6 X 10(6) cells/kg body weight) calves, and constituted 62.0% (normal) and 75.4% (pneumonic) of the total recoverable cell yield. Total cell yields were higher (P less than 0.05) in pneumonic calves, primarily due to neutrophil leukocytes (PMN). Neutrophils constituted 53.7 +/- 25% of the total cell yield in the pneumonic calves, but only 12.3 +/- 9.5% in the normal calves. The pulmonary alveolar macrophage (PAM) was the major recoverable cell in normal calves (85.7 +/- 8.7% of total lavage cells). Macrophages constituted a smaller (42.9 +/- 23.5) percentage of the total lavage cells in the pneumonic group due to increased PMN numbers. Viability of recovered cells from the pneumonic calves (91.5 +/- 4.8%) was lower than for the normal calves (94.1 +/- 2.5%), but the difference was not significant.(ABSTRACT TRUNCATED AT 250 WORDS)