ObjectiveTo explore the effects of Aspergillus fumigatus (A. fumigatus) on airway inflammation, airway responsiveness and total serum IgE in asthmatic rats. MethodsEighteen male Wistar rats were divided into three groups randomly, ie. a normal control group, an asthmatic model group, and an A. fumigatus group. The rats in the model group and the A.fumigatus group were sensititized and challenged with ovalbumin to establish asthmatic model. After establishment of asthmatic model, the rats in the A. fumigatus group were treated with chronic A. fumigatus spores inhalation. Subsequently, airway responsiveness/sensitivity to methacholine(Ach), levels of serum IgE and airway inflammation were assessed and compared among three groups. ResultsCompared with the asthmatic rats, the rats treated with A. fumigatus showed higher airway responsiveness (Penh/baselin value was significantly increased at the Mch concentration of 12.5, 25 and 50 mg/mL), increased inflammatory cells infiltration in pulmonary tissue slices and increased serum IgE level (P < 0.05). Most importantly, serum IgE level was detected in close relationship with PC100 which was defined as the dose of Mch causing 100% increase of enhance pause (Penh) value without Mch challenge (r=-0.873, P < 0.01). Serum IgE level was also closely related to the percentage of eosinophils in bronchoalveolar lavage fluid (r=0.937, P < 0.01). ConclusionsChronic A. fumigatus inhalation aggravates airway inflammation, bronchial hyperresponsiveness and serum IgE level in asthma. IgE may play an important role in facilitating the development of bronchial responsiveness and eosinophilic inflammation.
ObjectiveTo investigate the role of interleukin-25 (IL-25) and its receptor during allergen challenge test in allergic asthmatics as well as its underlining mechanism.MethodsFifteen allergic asthmatic patients with dual response in allergen challenge test were enrolled and blood samples were collected before and after challenge test. The expression levels of IL-25 receptor on the surface of eosinophils, plasma and intracellular IL-25 levels were measured by flow cytometry and enzyme-linked immunosorbent assay. Besides, the function of eosinophils from these patients was evaluated through the expression of type 2 cytokines, degranulation and chemotaxis after stimulation with IL-25.ResultsUpon allergen challenge, the expression of IL-17RB on the surface of eosinophils were increased from (7 426±2 824)/106 white blood cells to (19 446±5 593)/106 white blood cells (P<0.001). The expression of IL-17RA/RB on eosinophils were significantly increased from (4 508±1 360)/106 white blood cells to (9 025±3 166)/106 white blood cells (P<0.001). The plasma level of IL-25 increased from (650±45) pg/ml to (851±43) pg/ml (7 hours after allergen challenge) and (813±56) pg/ml (24 hours after allergen challenge) (P<0.001). The intracellular IL-25 expression of eosinophils was also upregulated from (10 398±1 909)/106 white blood cells to (147 684±46 222)/106 white blood cells (P<0.05). In vitro study, IL-25 (1 ng/ml) stimulated eosinophils for 2 hours promoted its expression of peroxidase [(12.5±4.2) ng/ml compared to control (1.26±0.4) ng/ml, P<0.05). The intracellular expression of IL-5 and IL-13 in eosinophils were also increased after stimulated by IL-25. IL-25 (1 pg/ml) stimulation compared to control could increase eosinophil migration in eotaxin [(36±3) vs. (69±5), P<0.05).ConclusionIL-25 and its receptor play a critical role in eosinophilic aggregation, activation and mobilization during allergic inflammation in allergic asthmatics.
Objective To study the effect of glucocorticoid-containing triple therapy on the acute exacerbation frequency of patients with moderate to severe chronic obstructive pulmonary disease (COPD) with different blood eosinophil percentage (EOS%). Methods One hundred and twenty-four patients who were admitted to the hospital with moderate to severe COPD from January 2020 to March 2020 in the Department of Respiratory and Critical Care Medicine in this hospital were selected as the research subjects, and the patients were divided into group A according to EOS% (EOS%<2%) and B group (EOS%≥2%). Then the A and B groups were randomly divided into four subgroups A1, A2 and B1, B2, and the patients in groups A1 and B1 were treated with dual long-acting bronchodilation. The medication for the patients in groups A2 and B2 was a triple preparation containing glucocorticoids. Namely A1 group (EOS%<2%, dual therapy), A2 group (EOS%<2%, triple therapy), B1 group (EOS%≥2%, dual therapy), B2 group (EOS%≥2%, triple therapy). The patients were instructed to take medication regularly as in hospital after discharge. After discharge, patients were followed up by telephone every two weeks for a period of one year. The number of acute exacerbations, the change of forced expiratory volume in the first second as a percentage of the expected value (FEV1%pred) and the incidence of pneumonia were compared between group A and group B during the follow-up period of one year. Results In the patients with EOS%≥2%, triple therapy reduced the number of acute attacks by 40% during treatment compared with dual therapy patients (average 0.875 vs. 1.471 times per patient per year, P=0.0278). While in the patients with EOS%<2%, it was reduced by 4% (1.080 vs. 1.125 times, P=0.3527). In the same use of glucocorticoid-containing triple preparations, the number of acute exacerbations in the patients with EOS%≥2% during medication was 19% less than that of the patients with EOS%<2% (an average of 0.875 to 1.080 times per patient per year, P=0.0462). Regardless of EOS%≥2% or <2%, there was no significant difference in the changes of FEV1%pred between triple therapy and double therapy patients before and after treatment (P>0.05). Regardless of EOS%≥2% or <2%, there was no statistically significant difference in the incidence of pneumonia between patients with triple therapy and double therapy during medication (P>0.05). Conclusion Inhaled glucocorticoid triple therapy is suitable for moderate to severe COPD patients with high percentages of blood eosinophils.