• Journal of Life Science
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• v.17 no.3 s.83
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• pp.396-401
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• 2007

This research investigated whether exposure of diesel exhaust particulate (DEP) and particulate metter (PM) effect on intercellular. adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) expression in asthma-induced Balb/c and IL-10 knock out (KO) mouse. Mouse was sensitized with intraperitoneal injection with ovalbumin, followed by challenges with intranasal ovalbumin. After induction of asthma mouse placed in the inhalation chamber and exposed to DEP and PM (10 $mg/m^3$). The evidences of pulmonary inflammation were assessed by immunohistochemical stain and westen blot against ICAM-1 and VCAM-1 in the lung tissue. In the immunohistochemical stain, positive reactions for ICAM-1 and VCAM-1 were much stronger in asthma-induced groups and asthma-induced group with DEP or PM than control groups. Although mild positive reactions were appeared in asthma-induced IL-10 KO mice groups, positive reactions were very strong in the asthma-induced group with DEP or PM. In Western blot, expression of VCAM-1 was increased in asthma-induced group with DEP or PM than asthma-induced groups. In the IL-10 KO mouse, ICAM-1 and VCAM-1 expression were increased in asthma-induced group with DEP or PM than asthma-induced groups. DEP and PM exposure have additive effects on the aggravation of inflammatory signs in the asthma-induced murine model. These results suggest that inhalation of DEP and PM in asthmatic patients may aggravate clinical symptoms.

• Journal of Life Science
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• v.16 no.5
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• pp.780-787
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• 2006

Asthma is a chronic inflammatory disorder of the airways, which characterized by bronchial hyperresponsiveness, reversible airflow limitation and respiratory symptoms. Internationally, the prevalence of asthma has been increased over last 3 decades. Recently, several studies of asthma have been reported with gradually increasing importance. To tesify the hypothesis that interleukin (IL)-4 and IL-10 may be an important determinant of the severity of airway inflammation, their expression was studied in mouse model of asthma. BALB/c mouse, IL-4 Knockout (KO) mouse and IL-10 KO mouse were sensitized with intraperitoneal injection of ovalbumin adsorbed to aluminum potassium sulfate, followed by challenges with intranasal ovalbumin on 3 consecutive days. The severity of pulmonary inflammation was assessed by eosinophilia in BAL fluid, number of total BAL cells, histopathological changes in lung tissues, and immunohistochemical staining against IL-4 and IL-10. In BAL fluid, the number of total cells was significantly increased in asthma induced mouse compare to the control. In asthma induced mouse, eosinophil was increased to 56% and neutrophil was 0.2%. In H &E stains, eosinophilic infiltration and epithelium hyperplasia were clearly noticed in asthma induced mouse. In immunohistochemical staining for IL-4 and IL-10, there was no positive reaction in control group. However, very strong reactions were appeared in asthma induced group. In this research, IL-4 and IL-10, which seem to play a central role in allergic asthma, KO mouse was utilized to test the causative relationship between airway inflammation and role of specific cytokine. Asthma induced IL-4 and IL-10 KO mice showed much decreased inflammatory reactions in the number of total BAL cells, in eosinophilic infiltration, and in immunohistochemical stains against diverse inflammatory proteins. These results suggest that IL-4 and IL-10 increase the asthmatic reactions in vivo mice model.

• Journal of Life Science
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• v.17 no.2 s.82
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• pp.248-253
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• 2007

This research investigated whether exposure of diesel exhaust particulate (DEP) and particulate matter (PM) effects on airway remodeling in asthma induced Balb/c and IL-10 knock out (KO) mouse. Mice were sensitized with intraperitoneal injection with ovalbumin, followed by challenges with intranasal ovalbumin. After that mice placed in inhalation chamber and exposed to DEP and $PM(10\;mg/m^3)$. The evidence of airway remodeling was assessed by masson's trichrome staining and PAS staining. The stainability of masson's trichrome and PAS reaction were increased in asthma-induced Baltic mice groups compared with control mice groups. More intensive stainability for masson's trichrome and PAS were appeared in the asthma-induced DEP and PM-exposed groups than asthama-induced groups. But, not significantly increased subepithelial fibrosis and the nember of goblet cell hyperplasia in asthma-induced IL-10 KO mice groups and asthma-induced+DEP and PM-exposed IL-10 KO mice than IL-10 KO mice groups. These results indirectly suggesting that exposure to DEP and PM in asthmatic patients might be aggravate clinical symptoms and IL-10 which seems to play a central role in allergic asthma. In conclusion, DEP and PM exposure might have additive effects on the ovalbumin- induced asthma in a murine model.