Effects Of Inhaled Inactivated-Mycobacterium Phlei On Airway Hyperresponsiveness And Nuclear Factor-kappa B With Adhesion Molecule In Asthmatic Mice

Part OneEffects of inhaled inactivated-Mycobacterium phlei onairway hyperresponsiveness and expression of IL-18in asthmaticmiceObjective To study the effects of inhaled inactivated-Mycobacterium phleion the expression of IL-18and airway hyperresponsiveness in asthmatic mice,and to explore the relationships between airway hyperresponsiveness andsecretion of IL-18.Methods Male Bal b/c mice (n=24) were randomly divided into normalcontrol group (A), asthmatic model group (B), and inhaledinactivated-Mycobacterium phlei group (C). Asthmatic model were made byinhalation of Ovalbumin (OVA). The mice in group C were treated withinactivated-Mycobacterium phlei for5d. The serum, bronchoalveolar lavagefluid and lung tissue were extracted after the determination of lung resistance.Pathological HE staining was used to measure lung inflammation, ELISA wasused to detect the expression of IL-18in serum and BALF.Result There were statistically signigicant positive correlation betweenlung resistance and IL-18in serum and BALF of asthmatic mice (P <0.05, P <0.05).The RLin group B mice were statistically signigicant higher than group A(P <0.05); while group C were statistically signigicant reduced after inhalationof inactivated mycobacterium phlei (P <0.05). Levels of IL-18in serum andBALF of group B were sharply increased than group A (P <0.01, P <0.01), andcompared with group B, IL-18of group C were statistically signigicantdecreased in serum and BALF (P <0.01, P <0.01).Conclusion IL-18and airway hyperresponsiveness was significantlyrelated in bronchial asthma. Inhalation of inactivated-Mycobacterium phlei canreduce the secretion of IL-18in asthma mice’s serum and BALF, as well asreducing asthmatic airway resistance and attenuating airway inflammation. Thedecrease of IL-18may participate in the treatment process of inhalation ofinactivated-Mycobacterium phlei in asthmatic mice. Part twoEffects of inhaled inactivated-Mycobacterium phlei on airwayinflammation and nuclear factor-kappa B and adhesion moleculein asthmatic miceObjective To investigate the effects of inhaled inactivated-Mycobacteriumphlei on the mRNA expression of nuclear factor (NF)-kappa B, intercellularadhesion molecule (ICAM)-1and vascular cell adhesion molecular (VCAM)-1in the lung tissue of asthmatic mice, so as to explore the mechanism of thistherapy.Methods Male Balb/c mice (n=24) were randomly divided into normalcontrol group (A), asthmatic model group (B), and inhaledinactivated-Mycobacterium phlei group (C). Asthmatic model were builded byOvalbumin (OVA). The mice in group C were treated with inactivatedmycobacterium phlei for5d. The lung tissues and BALF were extracted. HEand PAS staining were used to measure the lung inflammation and mucusproduction. The inflammatory cells in the BALF were counted. The mRNAexpression of NF-κB, ICAM-1and VCAM-1were detected by quantitative realtime PCR.Result Mycobacterium phlei treatment alleviated lung inflammation andattenuated mucus production and reduced eosinophils percentage in the BALF(P<0.05). The mRNA levels of NF-κB and ICAM-1were decreased statisticallysignigicant in group C (P<0.05, P<0.05). While there was no significantdifference of VCAM-1mRNA was found between group B and group C. Thecorrelation between NF-κB mRNA and ICAM-1mRNA was not found, as wellas NF-κB mRNA and VCAM-1mRNA. Conclusion Inhalation of inactivated-Mycobacterium phlei alleviatedasthmatic airway inflammation and attenuated mucus production. NF-κBparticipates in the pathogenesis of asthma. Another important mechanism maybe the reduction of ICAM-1mRNA expression.