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Biomedical subjects

M Laviolette

Publications and source records attributed to M Laviolette.

At least 55 records · Page 3Linked to original sources
PubMed1997

Effects of repeated swine building exposures on normal naive subjects.

Exposure to swine confinement buildings has a negative impact on respiratory health. A short exposure to this environment results in an acute airway inflammatory response. The present study was performed to confirm and further define the acute effects of working in a swine building, and to determine whether these effects are reproducible. Seven previously nonexposed normal subjects underwent evaluations that included hourly measurement of forced expiratory volume in one second (FEV1), methacholine challenge (the provocative concentration producing a 20% fall in FEV1 (PC20)), bronchoalveolar lavage (BAL), nasal lavage (NL), and blood analyses, before (control) and after each of two 5 h exposures to a swine building environment. The exposures were conducted 8 days apart. The levels of total dust, endotoxins, and ammonia (NH3) in the confinement building were measured on each day of exposure. Both exposures resulted in a significant reduction in FEV1 (mean+/-SEM change in FEV1: control = 7+/-2%; exposure 1 = 15+/-3%; exposure 2 = 23+/-3%), decrease in PC20 (median value (25th-75th percentile): 223 (23-256), 20 (15-198) and 20 (11-71), respectively; p=0.05) and increase in BAL cells (129+/-20, 451+/-43 and 511+/-103x10(3) cells x mL(-1), respectively) and NL cells (6+/-4, 126+/-58 and 103+/-26x10(3) cells x mL(-1), respectively), mostly neutrophils. Levels of interleukin-8 (IL-8), but not interleukin-1 (IL-1) or tumour necrosis factors (TNF-alpha), increased both in BAL and nasal fluids with exposure. In normal naive subjects, repeated exposure to the environment of a swine building induced a marked and reproducible reduction in forced expiratory volume in one second, increase in airway responsiveness, and increased neutrophilic inflammatory response. These results could not be accounted for by any of the environmental factors measured.

Adult↗
PubMed1997

Bronchial subepithelial fibrosis correlates with airway responsiveness to methacholine.

OBJECTIVES: To evaluate the relationships between airway subepithelial collagen deposition and epithelial desquamation with airflow obstruction and hyperresponsiveness in different types of asthma and other respiratory conditions such as chronic cough and allergic rhinitis. DESIGN AND PARTICIPANTS: We compared the histopathologic features observed on bronchial biopsy specimens obtained from 80 subjects: 38 with different types of asthma, 19 with chronic cough, 13 with allergic rhinitis, and 10 normal control subjects. Each subject had a questionnaire on respiratory symptoms and medication needs, measurements of expiratory flows and methacholine responsiveness, allergy skin prick tests, and a bronchoscopy with bronchial biopsies. None of the subjects studied used bronchial anti-inflammatory agents. RESULTS: Different degrees of bronchial subepithelial fibrosis were present in asthmatic subjects, the most intense being observed in occupational asthma; a subepithelial deposition of collagen was also found in subjects with allergic rhinitis, although it was less intense than in asthma and irregularly distributed under the basement membrane. On global analysis, we found a significant correlation between individual provocative concentration of methacholine inducing a 20% fall in FEV1 (PC20) and subepithelial fibrosis intensity (rs=-0.70, p<0.001). The degree of epithelial desquamation was correlated with that of subepithelial fibrosis (rs=0.36, p=0.02) in subjects with normal airway responsiveness, but it was not correlated with the PC20 (rs=0.10, p>0.05). Neither the degree of subepithelial fibrosis nor epithelial desquamation was correlated with the FEV1. CONCLUSION: These results suggest that structural airway changes such as subepithelial collagen deposition may be significant determinants or markers of a process that results in airway hyperresponsiveness.

Adult↗
PubMed1996

Dexamethasone and cyclosporin A modulation of cytokine expression and specific antibody synthesis in an allergic bronchopulmonary aspergillosis murine model.

We previously demonstrated that, in C57B1/6 mice, cyclosporin A enhanced and dexamethasone inhibited the Aspergillus fumigatus-induced pulmonary eosinophilia and total IgE levels. To evaluate whether these effects were related to the modulation of T-lymphocyte recruitment and activation and cytokine expression, we performed immunohistochemical staining for T-cell surface marker CD3 and CD4, cell activation marker CD25, and cytokines granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin-4 (IL-4) and interleukin-5 (IL-5) on lung tissue sections from mice exposed to Aspergillus fumigatus and treated or not with dexamethasone or cyclosporin A. Dexamethasone significantly inhibited Aspergillus fumigatus-induced increased number of activated T cells and cytokine-expressing cells in parallel with a decrease in pulmonary eosinophils. In contrast, cyclosporin A did not decrease these immunological events but enhanced the lung eosinophil recruitment. Moreover, dexamethasone prevented the production of immunoglobulins against 76 and 36 kD antigen proteins and cyclosporin A against 76 and 18 kD antigen proteins. These results indicate that dexamethasone down-regulates and cyclosporin A up-regulates lung eosinophil recruitment and total IgE production, probably via the modulation of T-lymphocyte activation and GM-CSF, IL-4 and IL-5 expression. Both drugs inhibit Aspergillus fumigatus-specific antibody synthesis, but their suppressive actions are selective to different antigenic components.

Animals↗
PubMed1996

Immunohistochemical detection of GM-CSF, IL-4 and IL-5 in a murine model of allergic bronchopulmonary aspergillosis.

BACKGROUND: Granulocyte macrophage-colony stimulating factor (GM-CSF), interleukin-4 (IL-4) and IL-5 are important in tissue eosinophil accumulation and high IgE production in allergic inflammatory reaction. OBJECTIVE: We examine lung GM-CSF, IL-4 and IL-5 expression in a murine model of allergic bronchopulmonary aspergillosis (ABPA) characterized by eosinophil and lymphocyte lung infiltration and elevated serum IgE level. METHODS: C57BL/6 mice were intranasally treated three times a week for 1, 2 or 3 week(s) with Aspergillus fumigatus (Af) antigen or saline and were sacrificed on days 7, 14 and 21. Immunohistochemical analyses for GM-CSF, IL-4 and IL-5 were performed on lung sections. RESULTS: Af treatment induced a remarkable pulmonary eosinophil influx. Increased numbers of lung T lymphocytes and GM-CSF positive cells were observed on days 14 and 21. IL-4 and IL-5 positive cells were increased significantly only on day 14. Immunostained serial sections showed that most (> or = 98%) cytokine positive cells were CD3 positive. Few eosinophils (< 2% of cytokine positive cells) were immunoreactive for GM-CSF and IL-5. Significant correlations were found between the number of GM-CSF and IL-5 positive cells, and the number of eosinophils in Af-treated lung (r = 0.62, P < 0.05 and r = 0.52, P < 0.05 respectively), and between the number of IL-4 positive cells and the serum total IgE level (r = 0.64, P < 0.01). CONCLUSIONS: Our data suggest a role for T lymphocyte GM-CSF, IL-4 and IL-5 in Af-induced mouse pulmonary eosinophilia and increased serum IgE production and further support the importance of T helper (TH2) cells in the pathogenesis of ABPA.

Animals↗
PubMed1996

Morphologic and functional properties of bronchial cells isolated from normal and asthmatic subjects.

Recent advances in biomedical sciences have led to the development of various methods for the evaluation of the physiopathology of respiratory diseases. This study reports morphologic and functional features of cells isolated by a new method from bronchial biopsies of normal and asthmatic subjects. Both epithelial and fibroblastic cells were isolated from the same biopsies using collagenase. The cells were cultured for several passages and stored frozen. Two selective culture media were used in order to obtain pure epithelial and fibroblastic cell populations. Immunofluorescence analysis of intermediate filaments, keratins, and vimentin confirmed the type of the isolated cells. The proportions of alpha-actin-expressing cells varied among the fibroblastic cell populations isolated from normal and asthmatic subjects. Interestingly, the population containing high numbers of alpha-actin-expressing cells and presenting the fastest collagen contraction kinetic was isolated from bronchial biopsies of an asthmatic subject. Moreover, the fibroblastic cells that showed the best contractile properties 24 h after their seeding in floating collagen gels were isolated from bronchial biopsies of asthmatic patients having PC20 values below 1 mg/ml. On the basis of these data, we propose a new approach to isolate, culture and characterize human bronchial cells in vitro.

Adult↗
PubMed1996

Reactive airways dysfunction syndrome (RADS) following exposure to toxic gases of a swine confinement building.

We describe the case of a 58 year old male, who developed a reactive airways dysfunction syndrome (RADS) after exposure to a high level of toxic gases in a swine confinement building. This previously healthy, nonatopic man developed moderate, partially reversible, airway obstruction and increased responsiveness within a month after the toxic exposure. The circumstances of the incident and the concomitant death of two sows make it likely that hydrogen sulphide was the causative agent. To our knowledge, this is the first case of reactive airways dysfunction syndrome reported from swine confinement buildings and, therefore, should raise awareness of this potential risk in that work environment.

Administration, Inhalation↗
PubMed1996

A randomized, double-blind, placebo-controlled study of lorazepam as premedication for bronchoscopy.

To our knowledge, no study has clearly demonstrated the advantage of sedative premedication for bronchoscopy. In a double-blind study, we evaluated the efficacy of oral lorazepam as premedication for bronchoscopy. One hundred patients were randomly assigned to receive placebo (group A) or lorazepam (2 mg) (group B) approximately 1.5 h before bronchoscopy. Immediately after the procedure and the following day, a questionnaire addressing the patient's perception of the procedure was administered. Specifically, subjects were asked to grade the bronchoscopy as very easy, easy, difficult, or very difficult to tolerate and if they would agree to a second bronchoscopy if believed necessary. In addition, their recollection of the procedure was graded as clear, indistinct, or not at all. No difference was found between the two groups for age, duration of the bronchoscopy, and the answers to the questionnaire administered immediately after the procedure. Most patients from both groups found their level of sedation adequate. On the following day, however, group B reported with lower frequency that the technique was difficult or very difficult (38.0% vs 65.3% for group A; p < 0.005) and that they would be less reluctant to a repeated bronchoscopy (30.0% vs 57.1% for group A; p < 0.015). Moreover, their recollection of the procedure was now less precise than for those who had received the placebo (p < 0.005). This suggests that the difference observed between the two groups at 24 h was related to the amnesic effect of lorazepam. We conclude that lorazepam, by improving patient's perception of the bronchoscopy, is a useful premedication and may facilitate patient's investigation when a second bronchoscopy becomes necessary.

Bronchoscopy↗
PubMed1996

Gene expression of interleukin-2 in purified human peripheral blood eosinophils.

To verify the hypothesis that eosinophils produce interleukin-2 (IL-2), a cytokine essential for lymphocyte activation, the expression of IL-2 was examined in peripheral blood eosinophils obtained from normal, atopic, asthmatic and hypereosinophilic subjects. Purified blood cell preparations were > 95% eosinophils, the remaining cells being neutrophils. Based on morphological observations and on CD3 expression, no lymphocytes were detected in these eosinophil preparations. The expression of IL-2 mRNA was detected by reverse transcriptase polymerase chain reaction (RT-PCR) in total RNA extracted from purified eosinophils stimulated with granulocyte-macrophage colony-stimulating factor (GM-CSF), with or without calcium ionophore (A23187). In-cell RT-PCR combined with in situ hybridization further confirmed that it was the eosinophils that expressed IL-2 mRNA. Moreover, in this experiment IL-2 mRNA expression increased upon costimulation with A23187 and GM-CSF suggesting that a steady-state level of IL-2 mRNA was inducible. Finally, IL-2 was detected in purified eosinophils by immunochemistry. These data, obtained by different techniques, demonstrate that eosinophils can express IL-2. An IL-2-mediated eosinophil-lymphocyte interaction could contribute to the chronic state of cell activation in inflamed tissues where these cells are implicated.

Asthma↗
PubMed1996

Tumor necrosis factor-alpha and interleukin-1 alpha expression in a murine model of allergic bronchopulmonary aspergillosis.

Tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 alpha (IL-1 alpha) are two important proinflammatory cytokines that may be involved in allergic inflammatory processes. We recently developed a murine model of allergic bronchopulmonary aspergillosis characterized by eosinophilic and lymphocyte lung infiltration and increased serum and bronchoalveolar lavage immunoglobulin E concentration. In this study we examined the expression of TNF-alpha and IL-1 alpha in the lung tissue sections of C57BL/6 mice that were intranasally challenged with Aspergillus fumigatus antigen or saline on the first 3 days of each week and sacrificed on days 4, 7, 14, and 21. Compared with the control mice, A. fumigatus treated mice had a remarkable increase of TNF-alpha and IL-1 alpha expression in the lung on days 4, 14, and 21, with a slight increase on day 7. The major types of cells expressing TNF-alpha and IL-1 alpha included alveolar macrophages, endothelial cells, and bronchiolar and alveolar epithelial cells. Consistent with increased expression of TNF-alpha and IL-1 alpha, intercellular adhesion molecule-1 expression also was upregulated in the lung of A. fumigatus treated mice; its time course and cell types were similar to those of TNF-alpha and IL-1 alpha expression. These results suggest that TNF-alpha and IL-1 alpha may be involved in the A. fumigatus induced inflammatory process and that upregulated intercellular adhesion molecule-1 expression may represent one of the roles played by TNF-alpha and IL-1 alpha in this murine model.

Animals↗
PubMed1996

Lower airways remodeling in nonasthmatic subjects with allergic rhinitis.

We analyzed by immunohistochemistry the distribution of types I, II, III, IV, V, and VII collagens, laminin, and fibronectin in the bronchial biopsy specimens of nonasthmatic subjects with seasonal allergic rhinitis (n = 8) and compared these results with those found in mild stable allergic asthmatics (n = 6) and normal controls (n = 5). The content of type I and III collagens was increased in rhinitic subjects compared with controls. These collagens were focally deposited in the reticular basement membrane area. Three subjects with allergic rhinitis had no fibronectin deposition in their basement membrane, as in controls, whereas the other five had a focal fibronectin deposition. In asthmatic patients, type I and III collagens and fibronectin were more abundant and more uniformly distributed underneath the basement membrane than they were in rhinitic subjects. Expression of type II, IV, V, and VII collagens and laminin were similar in the three groups. Electron microscopic and immunohistochemical analyses of bronchial mucosa showed a network of myofibroblasts beneath the epithelium in rhinitis as in asthma subjects. These data show that the irregularly distributed subepithelial fibrosis observed in subjects with allergic rhinitis results from the deposition of type I and III collagens and fibronectin, probably produced by bronchial myofibroblasts. These results suggest the presence of an active structural remodeling in the lower airways of allergic rhinitic subjects that is similar in nature to that seen in asthma, although less marked.

Adult↗
PubMed1995

Increased expression of intercellular adhesion molecule-1 (ICAM-1) in a murine model of pulmonary eosinophilia and high IgE level.

T lymphocytes and eosinophils are probably involved in the pathogenesis of allergic bronchopulmonary aspergillosis (ABPA), a disease characterized by pulmonary eosinophilia and high serum and lavage IgE levels. We recently developed a murine model of ABPA. To investigate the mechanisms of T lymphocyte and eosinophil recruitment to the lung in this disease, we examined the expression of ICAM-1 in the lung tissue of mouse challenged with Aspergillus fumigatus (Af) antigen. C57B1/6 mice were intranasally exposed to Af (Af group) or saline (control group) three times a week for 1, 2 or 3 weeks. On days 4, 7, 14 and 21, mice were killed and lung tissue was fixed in acetone and embedded in glycol methacrylate. Serial 2-microns sections were stained with chromotrope 2R and MoAbs against ICAM-1, CD11a/CD18 (LFA-1) and CD3. Af-challenged mice presented significant increases in eosinophil, T lymphocyte and LFA-1-positive cell count and up-regulated expression of ICAM-1 in the lung tissue at all the time points examined. ICAM-1 expression intensity correlated with the number of T lymphocytes (r = 0.59, P < 0.01), LFA-1-positive cells (r = 0.68, P < 0.001), but not of eosinophils (r = -0.24, P > 0.05). These findings suggest that up-regulation of ICAM-1 expression is involved in the inflammatory process of this murine model of ABPA, and that this up-regulation may be more relevant to the the T lymphocyte accumulation in the lung.

Animals↗
PubMed1995

Evaluation of an asthma self-management education program.

The goal of this study was to evaluate a self-management education program for asthmatics. This was a case-controlled retrospective study with a "1 year before and 1 year after" assessment of the proposed education program. It was carried out in the Quebec City metropolitan area, tertiary-center setting. The intervention group included 42 patients, 14 men and 28 women, aged 15-71 years. A control group of 42 patients was matched for age, sex, and medication needs. Neither of the 2 groups had previously received structured asthma education. The intervention group received 3 training sessions on asthma and its treatment, the use of action plans and self-measurement of peak expiratory flow, and was offered individual teaching by a specialized educator or telephone consultation. Evaluation of asthma knowledge was made before and after the teaching sessions and 1 year later. The control group received their usual care. The primary clinical outcome measures included frequency of asthma-related emergency-room (ER) visits, hospitalizations, absenteeism from work, and quality of life, measured 1 year prior to initiation of the educational program and for 1 year after, using questionnaires, chart reviews, and interviews. The control group was evaluated only during the last year of the study. Knowledge of asthma and its management was significantly improved immediately after the program and 1 year later (both p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Absenteeism↗
PubMed1995

Increased maximal airway response to methacholine during seasonal allergic rhinitis in nonasthmatic subjects: relationships with airway wall thickness and inflammation.

This study was carried out to determine whether the increase in airway responsiveness induced by natural antigenic exposure in nonasthmatic subjects is associated with an increase in maximal bronchoconstrictor response (MBR), and if these changes could be due to an increase in airway wall thickness from allergen-induced increase in airway inflammation. In 11 nonasthmatic subjects with seasonal allergic rhinitis, a methacholine challenge was obtained monthly, during and out of pollen exposure. Each subject had a high-resolution chest tomography in and out of the pollen season, to determine the relative thickness of the right intermediary bronchus over its total diameter (T/D), as well as inflammatory cell counts, apparent basement membrane thickness as an indication of subepithelial fibrosis and epithelial desquamation in bronchial biopsy specimens. In season, the mean provocative concentration of methacholine producing a 20% decrease in forced expiratory volume in one second (PC20) decreased from 51.5 to 25.8 mg.mL-1, and the maximal post-methacholine fall in forced expiratory volume in one second (delta FEV1,max) or forced vital capacity (delta FVC) and the slope of the dose response curve (DRS) increased compared with out of season: delta FEV1,max 44 +/- 5 vs 25 +/- 5%; delta FVC 34 +/- 5 vs 16 +/- 4%; and slope of DRS 14.1 +/- 2.8 vs 6.9 +/- 1.3%/mg.mL-1. No significant change was observed in T/D ratio. The seasonal change in delta FVC was positively correlated with the delta FEV1,max (rs = 0.891) and the change in DRS (rs = 0.909), but not with the change in PC20, nor with changes in bronchial biopsy inflammatory features or T/D ratio.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Blood eosinophil leukotriene C4 production in asthma of different severities.

In asthma, activation and recruitment of eosinophils to the bronchial mucosa amplifies many cellular functions. The blood eosinophil count and the number of hypodense eosinophils increase with asthma severity. Eosinophils produce numerous proinflammatory mediators in response to a variety of agonists, notably the peptido-leukotriene (LT) C4, a potent bronchoconstrictor. In this study, we have evaluated blood eosinophil LTC4 release and its modulation by cytokines in normal individuals and in subjects with asthma of various severities: mild (beta 2-agonist on demand); moderate (inhaled steroids on a regular basis); and severe (inhaled and oral steroids on a regular basis). Eosinophils were isolated using a modified Percoll gradient technique, which recovers both hypodense and normodense eosinophils in a global cell population. Eosinophils released detectable amounts of LTC4 only in the presence of the stimulus (calcium ionophore A23187, 2 microM). The ionophore-induced LTC4 release was greater in moderate asthmatics (mean +/- SEM 5.7 +/- 1.3 pg x 10(3)/250,000 eosinophils) than in normal individuals (1.6 +/- 0.4 pg x 10(3)/250,000 eosinophils), mild asthmatics (1.8 +/- 0.3 pg x 10(3)/250,000 eosinophils) and severe asthmatics (2.0 +/- 0.3 pg x 10(3)/250,000 eosinophils). Granulocyte/macrophage colony-stimulating factor (GM-CSF) and interleukin-5 (IL-5) amplified the ionophore-induced LTC4 release in the four groups from 1.9 to 2.6 and 1.9 to 2.8 fold, respectively. Interleukin-3 (IL-3) did not increase LTC4 production except by the eosinophils of the severe asthmatics whose ionophore-induced LTC4 production was enhanced by 1.9 fold. These data demonstrate that the asthmatic bronchial inflammatory process may modify blood eosinophil LTC4 release and its modulation by cytokines according to asthma severity and treatment.

Adult↗
PubMed1994

Is reactive airways dysfunction syndrome a variant of occupational asthma?

BACKGROUND: Reactive airways dysfunction syndrome (RADS) or irritant-induced asthma is a syndrome that leaves subjects with asthma-like symptoms after one or more exposures to a high concentration of an irritant substance. The degree of reversibility of airway obstruction in subjects with RADS is nevertheless unknown, as is the degree of associated lesions at the airway level. METHODS: We compared the acute reversibility of forced expiratory volume in 1 second (FEV1) after inhalation of albuterol (200 micrograms) in 15 subjects with RADS (12 cases caused by chlorine inhalation) with that of 30 subjects with occupational asthma (OA) caused by various agents. They were paired according to baseline airway obstruction (61% and 63% of predicted value in the RADS and OA groups), requirement for medication (bronchodilator only--7 of 15 subjects with RADS and 14 of 30 subjects with OA--as compared with bronchodilator + inhaled steroids in 8 of 15 subjects with RADS and 16 of 30 subjects with OA, respectively), and interval since removal from exposure (means of 30 and 24 months in the RADS and OA groups). In addition, five nonsmokers with RADS who had not received inhaled steroids underwent bronchoscopy with lavage and bronchial biopsies less than 2 years after the exposure. RESULTS: The percentage increase in FEV1 over baseline after inhalation of albuterol was 10% +/- 9% in the RADS group and 19% +/- 16% in the OA group (p = 0.005). Only 2 of 15 subjects (13%) with RADS and 12 of 30 subjects (40%) with OA showed an improvement in FEV1 of 20% or greater after inhalation of albuterol. Bronchoalveolar lavage showed an increased number of cells with a predominance of lymphocytes, and biopsy specimens showed increased basement membrane thickness in the five subjects with RADS who underwent bronchoscopy. CONCLUSION: Subjects with RADS are generally left with less airway reversibility than those with OA. We suggest that this difference is secondary to distinct pathologic changes.

Adult↗
PubMed1994

Influence of lung volume on collateral resistance during methacholine-induced bronchospasm.

We tested the hypothesis that lung inflation in response to a bronchospasm could be beneficial by maintaining the lung collateral channels open. Six mild asthmatics were studied on 2 separate days. The first day we determined the methacholine dose response and measured collateral resistance (Rcoll) before and during the metacholine-induced bronchospasm and the effects of decreasing lung volumes on Rcoll. The lung volume changes were induced by applying progressively increasing positive extrathoracic pressures (PEP). The second day we measured the changes in end-expiratory lung volume (EELV) resulting from the inhaled methacholine and from the applied positive extrathoracic pressure. With the inhalation of methacholine, the FEV1 decrease ranged from 26-43% of the baseline values while Rcoll increased significantly in only three of the six subjects. EELV remained unchanged in one subject and increased by 1408, 990, 260, and 44 ml in four others. It was not measured in one subject. Decreasing EELV by PEP increased Rcoll in all subjects. By extrapolation of the lung volume-Rcoll relationship, we calculated that Rcoll would have increased by 18,227%, 6843%, 994%, 140%, and 128% if EELV had not increased in the five subjects in whom delta EELV was measured. We conclude that an increase in EELV in response to an induced bronchospasm helps maintain open and functional collateral pathways despite the bronchoconstriction.

Adult↗
PubMed1994

Experimental allergic bronchopulmonary aspergillosis in the mouse: immunological and histological features.

C57BL/6 mice treated with intranasal instillation of 100 micrograms of Aspergillus antigen three times a week developed a pulmonary eosinophilia, observed in the bronchoalveolar lavage (BAL) and on histopathological examination. At week 3, the instillation of Aspergillus antigen provoked a 10-fold increase in the BAL cell number and eosinophils were the predominant inflammatory cells (66.4%). Histopathological findings showed focal alveolar lesions with peribronchial and perivascular infiltration of lymphoid cells, numerous eosinophils, epithelioid cells, and granulomas with giant cells. Increases in total IgE and IgG1 levels in BAL fluid (33-fold and 14-fold) and serum (67-fold and 8-fold) were observed also (P < 0.05). IgG1 specific to Aspergillus fumigatus (Af) was detected only in the antigen-treated mice. At 12 weeks, there was a persistent but less intense eosinophilia both in BAL and on histopathological examination accompanied by steadily elevated total IgE and total IgG1 and a higher level of specific IgG1-Af in BAL fluids and sera. No bronchocentric granulomatosis, mucoid impaction nor bronchiectasis could be observed. Data from the study described here showed that in mice repeated exposure to Aspergillus antigen leads to a strong inflammatory pulmonary response, characterized by remarkable pulmonary eosinophilia and elevations of total IgE, total IgG1 and specific IgG1-Af in both BAL and serum, which are the hallmarks of human allergic bronchopulmonary aspergillosis also. However, this inflammation did not induce the chronic histological features of the human disease.

Animals↗