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Biomedical subjects

D E Bice

Publications and source records attributed to D E Bice.

At least 37 records · Page 2Linked to original sources
PubMed1991

Comparative morphology and morphometry of alveolar macrophages from six species.

Pulmonary alveolar macrophages (PAM) were collected from normal, healthy mice, rats, dogs, cynomolgus monkeys, chimpanzees, and humans and evaluated for morphologic and morphometric characteristics. The PAM of mice, rats, and dogs were morphologically similar and had statistically similar frequency distributions for size. The cell size distribution for these three species was relatively homogeneous. The PAM of nonhuman primates and humans were morphologically heterogenous with sometimes prominent cytoplasmic vacuolation, irregular cell outlines, and increased numbers of multinucleated cells as compared to the PAM of rodents and dogs. The mean size of human PAM was statistically greater than that for all other species evaluated, including nonhuman primates. These data indicate that significant differences in PAM morphology and size exist among species.

Animals↗
PubMed1991

Long-term maintenance of localized antibody responses in the lung.

Immune memory cells for antibody production in the lung respond to antigen challenges, providing an important pulmonary defence. However, studies reported here suggested that long-term antibody production in the lung might also be important in pulmonary immune memory. After localized lung immunization and challenges, antibody production of specific IgG and IgA continued in the immunized lung lobes of dogs for months after the last antigen exposure. In addition, the evaluation of lung immunity in dogs immunized and challenged 3 years or 5 years previously (without additional antigen challenge) showed significantly higher levels of specific antibody in lavage fluid from the lung lobe exposed to antigen than in lavage fluids from control lung lobes. Cells from blood or from control lung lobes did not produce significant levels of specific antibody in vitro, whereas cells lavaged from the immunized lung lobes were producing specific antibody. Therefore, long-term antibody production by cells in lung lobes exposed to antigen probably contributed to antibody levels in serum and unexposed lung lobes. Traditionally, lymphoid tissues are believed to be responsible for long-term antibody production. However, antibody production in the lung for years without repeated antigen exposure suggested that other tissues might also be important in long-term antibody production. Maintenance of localized antibody production in the lung would be an important pulmonary defence against infectious agents, but might also play a key role in hypersensitivity lung diseases.

Animals↗
PubMed1990

The immunotoxicity of three nickel compounds following 13-week inhalation exposure in the mouse.

Groups of B6C3F1 mice were exposed to aerosols of nickel subsulfide (Ni3S2), nickel oxide (NiO), or nickel sulfate hexahydrate (NiSO4.6H2O) 6 hr/day, 5 days per week for 65 days to determine the immunotoxicity of these compounds. Exposure concentrations were 0.11, 0.45, and 1.8 mg Ni/m3 for Ni3S2, 0.47, 2.0, and 7.9 mg Ni/m3 for NiO; and 0.027, 0.11, and 0.45 mg Ni/m3 for NiSO4. Thymic weights were decreased only in mice exposed to 1.8 mg Ni/m3 Ni3S2. Increased numbers of lung-associated lymph nodes (LALN), but not spleen nucleated cells, were seen with all compounds. Nucleated cells in lavage samples were increased in mice exposed to the highest concentrations of NiSO4 and NiO and to 0.45 and 1.8 mg Ni/m3 Ni3S2. Increased antibody-forming cells (AFC) were seen in LALN of mice exposed to 2.0 and 7.9 mg Ni/m3 NiO and 1.8 mg Ni/m3 Ni3S2. Decreased AFC/10(6) spleen cells were observed in mice exposed to NiO, and decreased AFC/spleen were seen for mice exposed to 1.8 mg Ni/m3 Ni3S2. Only mice exposed to 1.8 mg Ni/m3 Ni3S2 had a decrease in mixed lymphocyte response. All concentrations of NiO resulted in decreases in alveolar macrophage phagocytic activity, as did 0.45 and 1.8 mg Ni/m3 Ni3S2. None of the nickel compounds affected the phagocytic activity of peritoneal macrophages. Only 1.8 mg Ni/m3 Ni3S2 caused a decrease in spleen natural killer cell activity. Results indicate that inhalation exposure of mice to nickel can result in varying effects on the immune system, depending on dose and physicochemical form of the nickel compound. These nickel-induced changes may contribute to significant immunodysfunction.

Aerosols↗
PubMed1990

Clearance, translocation, and excretion of beryllium following acute inhalation of beryllium oxide by beagle dogs.

Beagle dogs inhaled radiolabeled beryllium oxide (7BeO) particles that were calcined at either 500 or 1000 degrees C, resulting in either high (mean of 50 micrograms/kg body wt) or low (mean of 17 micrograms/kg body wt) initial lung burdens (ILBs) of both preparations of BeO. Levels of beryllium in whole body, tissue, and excreta were measured by external gamma-ray counting. Dogs were euthanized in pairs at 8, 32, 64, and 180 days after exposure to determine beryllium distribution in tissues. Beryllium oxide calcined at 1000 degrees C was retained more tenaciously in the lungs (62% of the ILB retained at 180 days after exposure) than BeO calcined at 500 degrees C (14% of the ILB retained at 180 days after exposure). Most of the beryllium that was cleared from the lungs and not excreted was translocated to the tracheobronchial lymph nodes, skeleton, liver, and blood. More beryllium was translocated to the skeleton and liver at 180 days after inhalation of BeO prepared at 500 degrees C than at 1000 degrees C. The predominant mode of excretion at early times after exposure was through the feces, with urinary excretion assuming predominance at later times. These data are important for interpreting the toxic effects of beryllium in the exposed dogs. Furthermore, because little is known concerning the retention and clearance of inhaled beryllium in man, these results provide information that may be used to understand the disposition of beryllium in accidentally exposed humans.

Administration, Inhalation↗
PubMed1990

Influence of preexisting pulmonary emphysema on susceptibility of rats to inhaled diesel exhaust.

The susceptibilities of normal rats and rats with preexisting pulmonary emphysema to chronically inhaled diesel exhaust were compared. Rats were exposed 7 h/day, 5 days/wk for 24 months to diesel exhaust at 3.5 mg soot/m3, or to clean air as controls. Emphysema was induced in one-half of the rats by intratracheal instillation of elastase 6 wk before exhaust exposure. Measurements included lung burdens of diesel soot, respiratory function, bronchoalveolar lavage, clearance of radiolabeled particles, pulmonary immune responses, lung collagen, excised lung weight and volume, histopathology, and mean linear intercept of terminal air spaces. Parameters indicated by analysis of variance to exhibit significant interactions between the influences of emphysema and exhaust were examined to determine if the effects were more than additive (indicating increased susceptibility). Although 14 of 63 parameters demonstrated emphysema-exhaust interactions, none indicated increased susceptibility. Less soot accumulated in lungs of emphysematous rats than in those of nonemphysematous rats, and the reduced accumulation had a sparing effect in the emphysematous rats. The results did not support the hypothesis that emphysematous lungs are more susceptible than are normal lungs to chronic exposure to high levels of diesel exhaust. The superimposition of effects of emphysema and exhaust, however, might still warrant special concern for heavy exposures of emphysematous subjects.

Animals↗
PubMed1990

Murine lung immunity to a soluble antigen.

Although it is known that soluble antigen is immunogenic when deposited in the respiratory tract, less is known about lung immunity to soluble antigen than is known about lung immunity to particulate antigen. To test the hypothesis that soluble antigen triggers antigen-specific immunity in the respiratory tract in a fashion similar to that reported for particulate antigen, we examined the development of local and systemic immunity in C57BL/6 mice after intratracheal (i.t.) instillation of a soluble, large molecular weight protein neoantigen, keyhole limpet hemocyanin (KLH). Specific anti-KLH IgG and IgM first appeared in the sera of mice on day 7 after primary immunization by i.t. instillation of KLH, with specific serum antibody concentrations remaining elevated at day 11. Cell populations prepared from lung-associated lymph nodes of immunized mice released specific anti-KLH IgG and IgM in vitro; peak levels were obtained from cells isolated 7 days after antigen instillation, with levels of specific antibody released by cells isolated on days 9 and 11 decreasing markedly. Cultured spleen cells obtained from mice after primary immunization released only low levels of specific IgM, and no specific IgG. No specific antibody was released by cell populations derived from the lungs of animals undergoing primary immunization. When presensitized mice were given an i.t. challenge with KLH, responses differed markedly from those following primary immunization. Lung-associated lymph node cell populations from challenged mice released greater amounts of specific antibody earlier than did cell populations from mice undergoing primary immunization.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Effect of four-week repeated inhalation exposure to unconjugated azodicarbonamide on specific and non-specific airway sensitivity of the guinea pig.

Reports of respiratory problems among industrial workers exposed repeatedly by inhalation to azodicarbonamide (ADA) raised concern that ADA might be a pulmonary sensitizer. We used a non-invasive method for measuring specific airway conductance to evaluate the potential for repeated inhalation of unconjugated ADA to cause specific or non-specific pulmonary sensitization in the guinea pig. Two groups of male Hartley guinea pigs were exposed 6 h/day, 5 days/week for 4 weeks to aerosolized ADA at 51 or 200 mg/m3, or to filtered air as controls. One group was tested for specific sensitization to ADA by measuring specific airway conductance during inhalation challenge with ADA before and on the third day after the 4-week ADA exposure. The ADA concentrations for the challenges were identical to the repeated exposure concentrations (51 or 200 mg/m3, 200 mg/m3 for controls). The other group was tested for non-specific airway sensitization by inhalation challenge with aerosolized histamine before and after the 4-week ADA exposure. Histamine was administered in stepwise increasing concentrations to elicit an airway response in each guinea pig. Skin tests for immunological responses to ADA, body weight and histopathology of the respiratory tract and skin test sites were also evaluated. The 4-week exposure to ADA did not result in either specific or non-specific airway sensitization. The ADA exposure did not induce positive skin reactions, influence body weight or cause histopathological responses. These results indicate that ADA, acting alone (i.e. not conjugated to a protein), is not a pulmonary sensitizer in the guinea pig exposed repeatedly for 4 weeks and challenged to simulate a 'Monday morning' exposure.

Administration, Inhalation↗
PubMed1989

Pulmonary immune response of dogs after exposure to 239PuO2.

This study evaluated the cell-mediated (CMI) and humoral immune responses in four Beagle dogs five to six years after single inhalation exposures to different monodisperse 239PuO2 aerosols (0.72-1.4 microns activity median aerodynamic diameter). These exposures resulted in initial lung burdens ranging from 19 to 35 kBq. Four nonexposed dogs were used as age-matched controls. Anesthetized dogs were immunized by instillation of sheep red blood cells (SRBC) into selected lung lobes. Cells and fluids were obtained serially from blood samples and by bronchoalveolar lavage of the saline- and SRBC-treated lung lobes at 5-20 days after immunization. The CMI response evaluated by the leukocyte procoagulant activity test was similar in the saline- and SRBC-treated lobes of both groups of dogs. The humoral immune response was measured by the enzyme-linked immunosorbent assay. No differences were shown between the amount of antibody measured in the sera or lung lavages from control or Pu-exposed dogs. Histopathology of the tracheobronchial lymph nodes from the Pu-exposed dogs showed them to be fibrotic with no lymphoid cells, suggesting that these tissues could not respond to the antigen deposited in the lungs. However, both mediastinal and sternal lymph nodes did contain lymphoid tissue, and were likely to be the lymphoid tissues that produced the immunity to the antigen deposited in the lungs of the exposed dogs. Although both exposed and control dogs produced immune responses to the antigen instilled into their lungs, differences were observed in the number of neutrophils in lung lavages from the control and exposed animals. There was a dramatic influx of neutrophils into both the saline- and SRBC-treated lung lobes of the Pu-exposed dogs that was not seen in the age-matched controls. This suggests that the inhaled 239PuO2 produced chronically-active inflammation in the lung which may contribute to recruitment of lymphocytes to the lung following intrapulmonary deposition of antigen. In conclusion, the immune responses induced by lung immunization of dogs that had inhaled 239PuO2 were not suppressed by large doses of chronic alpha irradiation of the lungs and tracheobronchial lymph nodes, indicating that local pulmonary immune responses are preserved despite severe radiation-induced alteration of these tissues.

Administration, Inhalation↗
PubMed1989

Bronchoalveolar lavage cytology in cynomolgus monkeys and identification of cytologic alterations following sequential saline lavage.

Total and differential cell counts were determined on cytolytic specimens obtained by fiberoptic bronchoscopy and bronchoalveolar lavage (BAL) of five normal cynomolgus monkeys. Total nucleated cell counts ranged from 100 to 430 cells/microliters. Macrophages were approximately 91% of total nucleated cells, while lymphocytes were 3%, neutrophils 4%, and eosinophils 2% of the initial BAL from each monkey. Less than 1% of the cells were mast cells and ciliated or nonciliated epithelial cells. The effects of repeated saline BAL on pulmonary cell populations were evaluated. Saline lavage of individual lung lobes resulted in a marked rise in circulating blood neutrophils at 4 hr after BAL; there was a similar rise in neutrophils in lavage fluids 24 hr after the initial lavage. Differential and total cell counts of both blood and lavage fluid returned to normal if subsequent lavages were spaced at 48-hr intervals. Lymphocytes were not present in saline-lavaged lung lobes, and protein levels of lavage fluids did not rise significantly. BAL produced a transient, reversible, intra-alveolar influx of neutrophils which was preceded by mobilization of bone marrow-stored neutrophils. Neutrophilia in the lavage fluid and blood was not detectable if lavage and blood sampling procedures were done at 48-hr intervals (which did not alter Ia antigen expression among BAL cells). These observations indicate that BAL is a valid method for sampling and assessing pulmonary cellular and fluid constituents if the procedures are done at intervals of at least 48 hr.

Animals↗
PubMed1989

Influence of experimental pulmonary emphysema on the toxicological effects from inhaled nitrogen dioxide and diesel exhaust.

This project examined the influence of preexisting, experimentally induced pulmonary emphysema on the adverse health effects in rats of chronic inhalation exposure to either nitrogen dioxide or automotive diesel-engine exhaust. Previous reports indicated that humans with chronic lung disease were among those most severely affected by episodic exposures to high concentrations of airborne toxicants. There were no previous reports comparing the effects of chronic inhalation exposure to components of automotive emissions in emphysematous and normal animals. The hypothesis tested in this project was that rats with preexisting pulmonary emphysema were more susceptible than rats with normal lungs to the adverse effects of the toxicant exposures. Young adult rats were housed continuously in inhalation exposure chambers and exposed seven hours per day, five days per week, for 24 months to nitrogen dioxide at 9.5 parts per million (ppm)2, or to diesel exhaust at 3.5 mg soot/m3, or to clean air as control animals. These concentrations were selected to produce mild, but distinct, effects in rats with normal lungs. Pulmonary emphysema was induced in one-half of the rats by intratracheal instillation of the proteolytic enzyme elastase six weeks before the toxicant exposures began. Health effects were evaluated after 12, 18, and 24 months of exposure. The measurements included respiratory function, clearance of inhaled radiolabeled particles, pulmonary immune responses to instilled antigen, biochemistry and cytology of airway fluid, total lung collagen, histopathology, lung morphometry, and lung burdens of diesel soot. The significance of influences of emphysema and toxicant exposure, and interactions between influences of the two treatments, were evaluated by analysis of variance. The elastase treatment resulted in pulmonary emphysema that was manifested by enlarged alveoli and alveolar ducts, and by ruptured alveolar septa. There was no accompanying inflammation and no alterations of bronchioles. The emphysema persisted throughout the study period, with little evidence of progression. Lung weight was increased, physiological lung volumes were enlarged, lung compliance was increased, and airflow was obstructed. Nitrogen dioxide exposure of normal rats caused mild epithelial hyperplasia and a thickening of the walls of terminal bronchioles, an extension of bronchiolar epithelium into proximal alveoli, and inflammation in proximal alveoli. Lung volume and weight and the lung collagen content were increased. Airway fluid indicators of cell damage and oxidant protective mechanisms were increased. Similar effects of nitrogen dioxide exposure were superimposed over the effects of emphysema in emphysematous nitrogen dioxide-exposed rats. Several parameters were affected similarly by nitrogen dioxide exposure and emphysema (for example, increased lung volume), and the combined effects tended to be additive.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1989

A canine model of beryllium-induced granulomatous lung disease.

Groups of beagle dogs were exposed by inhalation to attain either low or high initial lung burdens (ILB) of BeO calcined at 500 degrees or 1000 degrees C. Dogs were killed at 8, 32, 64, 180, and 365 days after exposure for evaluation of beryllium tissue burdens and histopathologic examination. Histologic lesions were characterized by perivascular and peribronchiolar infiltrates of lymphocytes and macrophages 8 days after exposure. These lesions progressed to distinct microgranulomas accompanied by patchy granulomatous pneumonia. Lesions were more severe in dogs exposed to 500 degrees C BeO. Additional dogs were sampled by bronchoalveolar lavage at 3, 6, 7, 11, 15, 18, and 22 months after exposure for characterization of lung cytology and lung immune responses. Lymphocyte percentages and numbers were increased in lavage samples 3 months after exposure in dogs with both the high and low ILB of 500 degrees C. Values for both parameters decreased rapidly thereafter. Dogs with either low or high ILB of 1000 degrees C-treated BeO displayed negligible to low and variable changes in both lymphocyte percentages and numbers. In vitro lymphocyte stimulation by beryllium was increased 180 and 210 days after exposure in dogs with the high ILB 500 degrees C BeO only. A marked degree of individual variation in both histologic lesions and lymphocyte responses among dogs was noted. Less soluble 1000 degrees C-treated BeO was retained in the lung longer than the more soluble 500 degrees C-treated material that was cleared almost entirely by 1 year after exposure. Because these changes are similar to those reported in humans with chronic beryllium disease, these data suggest that the beagle represents a good model to study histologic and immunologic aspects of this disease syndrome.

Aerosols↗
PubMed1988

Localized immune memory in the lung.

Antibody-forming cells (AFC) produced in the lung-associated lymph nodes after lung immunization enter the blood and accumulate mainly in the immunized lung. In lung interstitial tissues and alveoli, AFC mature into plasma cells and produce specific antibody. In addition to AFC, published data suggest that memory cells are also recruited to and/or are produced in immunized lung lobes, and that these memory cells can respond in the alveoli to secondary antigen challenges. The purpose of this study was to determine if memory cells induced in the lung by multiple antigen exposures could respond in vivo to challenges with low doses of antigen. The degree of inflammation produced by antigen doses that would allow the accumulation of AFC from the blood was evaluated. Beagle dogs were anesthetized, and a fiberoptic bronchoscope used to instill 10(6), 10(7), 10(8), 10(9), or 10(10) sheep red blood cells (SRBC) into individual lung lobes. Of these doses, only 10(9) and 10(10) SRBC significantly increased inflammation (increased number of neutrophils) or vascular permeability (increased total protein). The number of specific IgM AFC and concentration of anti-SRBC IgG antibody were significantly elevated only in lavage fluid from the lung lobes immunized with 10(9) and 10(10) SRBC. Four lung lobes were then given two additional challenges with 10(10) SRBC. In third and fourth challenges, these lung lobes received doses of SRBC of 10(4), 10(5), 10(6), 10(7), 10(8), and 10(9) SRBC. The results showed that significantly increased numbers of specific IgM AFC and concentrations of IgG antibody were found even at the lowest dose of antigen (10(4) SRBC) in the absence of increased inflammation or vascular permeability.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Immunopathologic effects of nickel subsulfide on the primate pulmonary immune system.

The effects of nickel subsulfide (Ni3S2) on the pulmonary immune system were evaluated in cynomolgus monkeys that had been previously immunized and repeatedly challenged with sheep red blood cells in specific lung lobes. After instillation of Ni3S2, at a final dose of 0.06 mumol/g lung, in one immunized and one control lobe of each monkey, bronchoalveolar lavage cells were evaluated for alterations in cell number and function. Neither numbers of antibody-forming cells nor natural killer (NK) cell conjugate formation were altered in immunized lobes of nickel-exposed animals regardless of individual lung lobe nickel exposure. Macrophage phagocytic activity was significantly decreased, and target cell killing by conjugate-forming NK cells was increased in all lobes independent of antigen or nickel exposure in all nickel-exposed animals. Histologic sections of nickel-exposed lobes were characterized by mild focal accumulations of macrophages and lymphocytes within the interstitium and alveoli and by perivenular lymphoid infiltration and follicle formation. We conclude that alveolar macrophages are sensitive to the toxic effects of nickel and that local instillation of Ni3S2 in the subhuman primate lung results in suppression of pulmonary alveolar macrophage function accompanied by a secondary increase in NK cell-mediated killing of target cells.

Animals↗
PubMed1987

Identification of plasma cells in lung alveoli and interstitial tissues after localized lung immunization.

Large numbers of antibody-forming cells (AFC) can be identified with the Jerne plaque assay in immunized lung lobes of the beagle dog after localized instillation of particulate antigen. Published data suggest that these AFC are secreting antibody and are responsible for increased levels of specific antibody in immunized lung lobes. If AFC in the lung are actively secreting antibody, there should be an increase in the number of mature plasma cells in lung lobes exposed to antigen. The purposes of this study were to evaluate the number of lymphoid cells present in immunized and control lung lobes and to determine if lung immunization produces a localized increase in the number of plasma cells. Sheep red blood cells (SRBC), autologous dog red blood cells, and saline were instilled into specific lung lobes of beagle dogs with the aid of a fiberoptic bronchoscope. Light and transmission electron microscopy studies of tissues from lung lobes instilled with SRBC showed perivascular infiltrates and intra-alveolar accumulations of lymphoid cells which were not present in control lung lobes. The morphology of these lymphoid cells ranged from small lymphocytes through mature plasma cells. From 5% to 15% of the cells present in the interstitial tissues and alveoli of immunized lung lobes were plasma cells. These observations suggest that lymphoid cells which entered the SRBC immunized lung can mature to plasma cells which are probably responsible for the local production of antigen-specific antibody.

Animals↗
PubMed1987

Migration of neutrophils from lung to tracheobronchial lymph node.

Translocation of particulate antigen deposited in the lung to tracheobronchial lymph nodes (TBLN) is important in the induction of pulmonary immune responses. We have previously shown that alveolar macrophages can contribute to particle translocation to TBLN, but whether neutrophils can also contribute to this process is not known. To determine if neutrophils can carry particles to the TBLN, dog neutrophils were elicited by instillation of red or green fluorescent microspheres into individual lung lobes. Autologous neutrophils that had phagocytized fluorescent microspheres were then instilled into an unexposed lobe of the same dog's lung. After 24 hr, the TBLN of instilled dogs had numerous neutrophils, 99% of which contained either red or green fluorescent microspheres but not both. Use of the two different colored microspheres as labels precluded the possibility that neutrophils had phagocytized the microspheres in the TBLN. In a second experiment, dogs were depleted of peripheral blood neutrophils by injections of hydroxyurea. Hydroxyurea-treated and normal dogs were instilled with fluorescent microspheres and killed after 40 h. Hydroxyurea treatment reduced neutrophil accumulation in the lung by 79% and reduced particle translocation to the TBLN by 80%. Results of these experiments indicate that neutrophils are similar to pulmonary alveolar macrophages (PAM) in their ability to phagocytize particles in the lung and then migrate to the TBLN.

Animals↗
PubMed1987

Comparative lung immunotoxicity of inhaled quartz and coal combustion fly ash.

Some inhaled particles that are deposited in the terminal airways and alveoli clear to the lung-associated lymph nodes, and insoluble particles have a long half-life in these tissues. Because the lung-associated lymph nodes are essential in the induction of immunity after lung immunization, the accumulation of inhaled particles in these tissues could alter immune responses that develop after lung immunization. This study evaluated the effects of inhaled insoluble fly ash particles or alpha quartz on the immune functions of lung-associated lymph nodes. F344 rats were exposed for 20 days by inhalation of fly ash from a fluidized bed combustor (FBC) or a pulverized coal combustor (PCC). Rats were similarly exposed to quartz particles (Min-U-Sil). Control rats were exposed to filtered air. Groups of ten exposed and ten control rats from each group were immunized by intratracheal instillation of 10(8) sheep red blood cells at 4, 6, 40, and 52 weeks after the start of exposures. The cellularity of the lung-associated lymph nodes and antibody-mediated immunity were evaluated at 7 days after immunization. Tissues from lung and lung-associated lymph nodes were taken for histopathology. The inhalation of FBC fly ash, PCC fly ash, and quartz particles all significantly increased the number of lymphoid cells in the lung-associated lymph nodes at each of the sacrifice times. However, FBC fly ash had no significant effect on antibody immunity, while both PCC fly ash and quartz caused suppression of antibody responses at 52 weeks after the start of exposure. Histopathology data showed that exposure to quartz and PCC fly ash caused significant cellular changes in lungs and lung-associated lymph nodes, while FBC fly ash had less effect. These data indicate that an acute exposure (20 days) to relatively insoluble particles significantly increased the cellularity of the lung-associated lymph nodes for up to 52 weeks after the start of the exposure, but the pulmonary toxicity of the particles inhaled appeared to influence the effects of the exposure on antibody immune responses.

Animals↗
PubMed1987

The pulmonary antibody-forming cell response in the guinea pig after intratracheal immunization.

Guinea pigs were immunized by an intratracheal instillation of 5 X 10(9) sheep red blood cells (sRBCs) with or without the immunoadjuvant maleic vinyl ether-2 (MVE). At 6 days post immunization, a peak IgM antibody-forming cell (AFC) response was detected in lung-associated lymph nodes (LALNs), lung tissue, lavage fluid, blood, and spleen. The time course of the response in the LALNs was similar to that of the response of the popliteal lymph node after footpad immunization. The use of MVE significantly enhanced this response. In addition, immunization with the sRBCs enhanced the phagocytic activity of the lung macrophages. The magnitude and kinetics of the AFC response seen in the guinea pig lung is compared to the response seen in other animals.

Animals↗