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The Long-term Effects Of Diesel Exhaust Particles On Airway Inflammation And Responsiveness In A Mouse Model
S26 Abstracts
SATURDAY
97
Allergy To Cumaru (Dipterix micrantha Harms) Tropical Wood F. de la Losa, Sr.; DIATER Laboratories San Martin de la Vega
SPAIN. RATIONALE: Wood dust may produce allergic rhinitis, asthma, or contact dermatitis in sensitized patients, being tropical woods frequently implicated in occupational allergy in last years. However, the knowledge about wood allergens is still limited. Shihuahuaco (Dipterix micrantha Harms), internationally known as Cumaru, is a tropical wood very appreciate for wood floors. The aim of this study was to identify allergens involved in a case of asthma due to the tropical wood Cumaru, which has never been reported to be allergenic so far. METHODS: A 47-years-old man suffered from acute dry cough and asthma in several occasions after polishing Cumaru wood. He did not suffered any symptom when working with other woods. An in vitro study was performed to determine the presence and the possible pattern of IgE sensitization to this wood. Specific IgE to Cumaru wood dust was determined with enzymatic method. Extract proteins were separated by SDS-PAGE and SDS PAGE immunobloting was performed with serum from patient. RESULTS: Specific IgE was 2.2 IU/L (EAST: HYTEC, HYCOR Biomedical Ltd.UK). SDS-PAGE Immunoblotting showed two IgE-binding bands of 28 and 90 kDa. CONCLUSIONS: In vitro sensitisation to Cumaru wood has been demonstrated, being implicated two bands of 28 and 90 kDa, recognized by the serum of the patient. To our knowledge, this is the first case reported so far of asthma due to Shihuahuaco wood dust, where an IgE mediated mechanism has been suggested. Funding: DIATER Laboratorios
98
Impact of Absences due to Asthma on Total School Absences in Upstate New York Elementary Schools E. Simons, A. Reddy, M. Gomez, C. Kielb, S. Lin; New York State Department of Health, Center for Environmental Health, Albany, NY. RATIONALE: Asthma absenteeism may be a useful indicator of asthma morbidity, but is difficult to track with available data. We estimated the impact of asthma absences on total school absences. METHODS: In response to a survey question, 1203 elementary school nurses in upstate NY reported the number of students who missed school due to asthma. The National Asthma Survey/NY State (unpublished data) estimated that students who missed school due to asthma averaged 8.6 asthma absences per year. We estimated the impact of asthma absenteeism by calculating the ratio of asthma absences (the number of students who missed at least one day of school due to asthma multiplied by the average number of days missed due to asthma) to total school absences (NY State Education Department attendance data). RESULTS: The ratio of estimated asthma absences to total school absences was 25.6 per 1000 absences (95% CI 24.0-27.2). The ratio varied by geographic location from 9.7 to 27.3 asthma absences per 1000 absences and increased with the number of school environmental triggers reported by school nurses (test for trend, p<0.001). A higher ratio of asthma absences to total absences was correlated with physical activity limitations (r50.54) and visits to the health office (r50.50) but not with asthma management practices. CONCLUSIONS: The effect of asthma on total absenteeism may vary by school demographics and environmental conditions. Development of a model to estimate the impact of asthma absenteeism has proved challenging using existing data. Improved tracking and methods of estimating asthma absenteeism are needed.
J ALLERGY CLIN IMMUNOL JANUARY 2007
99
Effects of Cigarette Smoke Extract and Rhinovirus on Expression of B7H1 and B7H3 in Human Airway Epithelial Cells E. Schafer, S. Favoreto, J. Shen, R. Dave, P. C. Avila; Northwestern University, Chicago, IL. RATIONALE: Exposure to tobacco smoke and to rhinovirus increase the risk of developing asthma exacerbations. In infants, these exposures also independently increase the risk of wheezing in preschool years. We hypothesized that cigarette smoke and rhinovirus infection induce similar inflammatory responses in airway epithelial cells. METHODS: To determine whether cigarette smoke extract (CSE) and rhinovirus serotype 16 (RV16) exposures to human airway epithelial cells amplify expression of the co-stimulatory molecules B7H1 and B7H3, we grew cells to 80 % confluence before exposing them to 5%CSE (0-72h), RV (0-6h) or both. B7 homologs were quantified at 72h by mRNA gene expression and flow cytometry. RESULTS: Exposure to 5%CSE (p50.01) or RV16 (p50.04) alone increased B7H1 mRNA. Exposure to both increased B7H1 mRNA compared with unexposed cells (p<0.001) and against single exposures (p<0.001) showing an additive effect. Expression of B7H3 increased with 5%CSE (p50.03), and with combined exposure (p<0.001), but was not altered with RV16 alone. Similar changes were observed by flow cytometry, particularly induction of B7H1 and B7H3 by 5%CSE. CONCLUSION: Tobacco smoke and rhinovirus, both exacerbators of asthma in vivo, alter expression of the T cell co-stimulatory molecules B7H1 and B7H3 on airway epithelial cells. Changes in these B7 homologs and other co-stimulatory molecules may affect T cells, the main driver of allergic inflammation. Funding: Ernest S. Bazley Grant
100
The Long-term Effects Of Diesel Exhaust Particles On Airway Inflammation And Responsiveness In A Mouse Model A. Jang; Soonchunhyang University Hospital, Bucheon, REPUBLIC OF KOREA. RATIONALE: Diesel exhaust particles (DEP) can induce airway hyperresponsiveness and inflammation by amplifying Th2 immune response. OBJECTIVE: The aims were to investigate the effect of long-term DEP on airway hyperresponsiveness (AHR) and inflammation in a mouse model. METHODS: BALB/c mice were exposed to DEP 1 hour for 5 days a week during three month in a closed system chamber attached to an ultrasonic nebulizer (low dose: 100 mg/m3 DEP, high dose: 3 mg/m3 DEP). The control group was exposed to saline. Animals were subjected to whole-body plethysmography and then killed for performance of BAL and histology. RESULTS: AHR (Penh to methacholine) was higher in low doe and high dose DEP groups than in that of control group at 4, 8, 12 weeks. AHR was higher in high dose DEP group than in that of low dose DEP group at 4, 8, 12 weeks. The number of neutrophils and lymphocytes were higher in high dose DEP group than in that of low dose DEP group and control group at 4, 8, 12 weeks. The level of IL-5, IL-6, and IFN-g were increased in low doe DEP group than in those of control group at 12 weeks. CONCLUSION: These results suggest that long-term DEP exposure may increase AHR and inflammation. Funding: This work was supported by grant R01-2003-000-0041-0 From the Basic Research Program of the Korea Science & Engineering Foundation
SATURDAY
97
Allergy To Cumaru (Dipterix micrantha Harms) Tropical Wood F. de la Losa, Sr.; DIATER Laboratories San Martin de la Vega
SPAIN. RATIONALE: Wood dust may produce allergic rhinitis, asthma, or contact dermatitis in sensitized patients, being tropical woods frequently implicated in occupational allergy in last years. However, the knowledge about wood allergens is still limited. Shihuahuaco (Dipterix micrantha Harms), internationally known as Cumaru, is a tropical wood very appreciate for wood floors. The aim of this study was to identify allergens involved in a case of asthma due to the tropical wood Cumaru, which has never been reported to be allergenic so far. METHODS: A 47-years-old man suffered from acute dry cough and asthma in several occasions after polishing Cumaru wood. He did not suffered any symptom when working with other woods. An in vitro study was performed to determine the presence and the possible pattern of IgE sensitization to this wood. Specific IgE to Cumaru wood dust was determined with enzymatic method. Extract proteins were separated by SDS-PAGE and SDS PAGE immunobloting was performed with serum from patient. RESULTS: Specific IgE was 2.2 IU/L (EAST: HYTEC, HYCOR Biomedical Ltd.UK). SDS-PAGE Immunoblotting showed two IgE-binding bands of 28 and 90 kDa. CONCLUSIONS: In vitro sensitisation to Cumaru wood has been demonstrated, being implicated two bands of 28 and 90 kDa, recognized by the serum of the patient. To our knowledge, this is the first case reported so far of asthma due to Shihuahuaco wood dust, where an IgE mediated mechanism has been suggested. Funding: DIATER Laboratorios
98
Impact of Absences due to Asthma on Total School Absences in Upstate New York Elementary Schools E. Simons, A. Reddy, M. Gomez, C. Kielb, S. Lin; New York State Department of Health, Center for Environmental Health, Albany, NY. RATIONALE: Asthma absenteeism may be a useful indicator of asthma morbidity, but is difficult to track with available data. We estimated the impact of asthma absences on total school absences. METHODS: In response to a survey question, 1203 elementary school nurses in upstate NY reported the number of students who missed school due to asthma. The National Asthma Survey/NY State (unpublished data) estimated that students who missed school due to asthma averaged 8.6 asthma absences per year. We estimated the impact of asthma absenteeism by calculating the ratio of asthma absences (the number of students who missed at least one day of school due to asthma multiplied by the average number of days missed due to asthma) to total school absences (NY State Education Department attendance data). RESULTS: The ratio of estimated asthma absences to total school absences was 25.6 per 1000 absences (95% CI 24.0-27.2). The ratio varied by geographic location from 9.7 to 27.3 asthma absences per 1000 absences and increased with the number of school environmental triggers reported by school nurses (test for trend, p<0.001). A higher ratio of asthma absences to total absences was correlated with physical activity limitations (r50.54) and visits to the health office (r50.50) but not with asthma management practices. CONCLUSIONS: The effect of asthma on total absenteeism may vary by school demographics and environmental conditions. Development of a model to estimate the impact of asthma absenteeism has proved challenging using existing data. Improved tracking and methods of estimating asthma absenteeism are needed.
J ALLERGY CLIN IMMUNOL JANUARY 2007
99
Effects of Cigarette Smoke Extract and Rhinovirus on Expression of B7H1 and B7H3 in Human Airway Epithelial Cells E. Schafer, S. Favoreto, J. Shen, R. Dave, P. C. Avila; Northwestern University, Chicago, IL. RATIONALE: Exposure to tobacco smoke and to rhinovirus increase the risk of developing asthma exacerbations. In infants, these exposures also independently increase the risk of wheezing in preschool years. We hypothesized that cigarette smoke and rhinovirus infection induce similar inflammatory responses in airway epithelial cells. METHODS: To determine whether cigarette smoke extract (CSE) and rhinovirus serotype 16 (RV16) exposures to human airway epithelial cells amplify expression of the co-stimulatory molecules B7H1 and B7H3, we grew cells to 80 % confluence before exposing them to 5%CSE (0-72h), RV (0-6h) or both. B7 homologs were quantified at 72h by mRNA gene expression and flow cytometry. RESULTS: Exposure to 5%CSE (p50.01) or RV16 (p50.04) alone increased B7H1 mRNA. Exposure to both increased B7H1 mRNA compared with unexposed cells (p<0.001) and against single exposures (p<0.001) showing an additive effect. Expression of B7H3 increased with 5%CSE (p50.03), and with combined exposure (p<0.001), but was not altered with RV16 alone. Similar changes were observed by flow cytometry, particularly induction of B7H1 and B7H3 by 5%CSE. CONCLUSION: Tobacco smoke and rhinovirus, both exacerbators of asthma in vivo, alter expression of the T cell co-stimulatory molecules B7H1 and B7H3 on airway epithelial cells. Changes in these B7 homologs and other co-stimulatory molecules may affect T cells, the main driver of allergic inflammation. Funding: Ernest S. Bazley Grant
100
The Long-term Effects Of Diesel Exhaust Particles On Airway Inflammation And Responsiveness In A Mouse Model A. Jang; Soonchunhyang University Hospital, Bucheon, REPUBLIC OF KOREA. RATIONALE: Diesel exhaust particles (DEP) can induce airway hyperresponsiveness and inflammation by amplifying Th2 immune response. OBJECTIVE: The aims were to investigate the effect of long-term DEP on airway hyperresponsiveness (AHR) and inflammation in a mouse model. METHODS: BALB/c mice were exposed to DEP 1 hour for 5 days a week during three month in a closed system chamber attached to an ultrasonic nebulizer (low dose: 100 mg/m3 DEP, high dose: 3 mg/m3 DEP). The control group was exposed to saline. Animals were subjected to whole-body plethysmography and then killed for performance of BAL and histology. RESULTS: AHR (Penh to methacholine) was higher in low doe and high dose DEP groups than in that of control group at 4, 8, 12 weeks. AHR was higher in high dose DEP group than in that of low dose DEP group at 4, 8, 12 weeks. The number of neutrophils and lymphocytes were higher in high dose DEP group than in that of low dose DEP group and control group at 4, 8, 12 weeks. The level of IL-5, IL-6, and IFN-g were increased in low doe DEP group than in those of control group at 12 weeks. CONCLUSION: These results suggest that long-term DEP exposure may increase AHR and inflammation. Funding: This work was supported by grant R01-2003-000-0041-0 From the Basic Research Program of the Korea Science & Engineering Foundation