Allergologia et immunopathologia最新文献

Objective: The aim of the present study is to investigate the effects of auraptene on inflammation and apoptosis of pneumonia cell model and uncover the mechanism.

Methods: WI-38 cells were treated with lipopolysaccharide (LPS) to construct a pneumonia model. Cell counting kit-8 assay, enzyme-linked-immunosorbent serologic assay, and quantitative polymerase chain reaction assay were conducted to confirm the effects of auraptene on the viability and inflammation of WI-38 cells. Flow cytometry (FCM) and immunoblot assays were conducted to detect the effects of auraptene on the apoptosis of WI-38 cells. Immunoblot assay was performed to confirm the mechanism.

Results: We found that auraptene stimulated cell viability in WI-38 cells upon LPS treatment. Auraptene also inhibited cellular inflammation. Furthermore, auraptene inhibited cell apoptosis of WI-38 cells upon LPS treatment. Mechanically, auraptene inhibited the nuclear factor kappa B signaling pathway, thereby suppressing the pneumonia.

Conclusion: Auraptene alleviates inflammatory injury and cell apoptosis in pneumonia, thus has the potential to act as a pneumonia drug.

Objective: To detect serum metalloproteinase-9 (MMP-9), tissue inhibitor of metalloproteinases (TIMP-1), cyclooxygenase-2 (COX-2), and T helper cells 1-T helper cells 2 (Th1-Th2) levels in asthma patients and assess their clinical significance.

Methods: A total of 72 patients experiencing acute asthma (acute group), 66 stable asthma patients (stable group), and 60 healthy volunteers (control group) were included in this study. The levels of TIMP-1, COX-2, and Th1-Th2 in patients with acute asthma were measured following treatment with budesonide aerosol inhalation. In addition, the levels of MMP-9, TIMP-1, COX-2 and Th1-Th2 were compared in patients with different severity of acute asthma before and after treatment.

Results: The serum levels of MMP-9, TIMP-1, and COX-2 showed an increasing trend in the control, stable, and acute groups, while levels of Th1-Th2 showed a sequential decreasing trend, and the differences were statistically significant. Comparison of lung function indexes among the three groups of patients established a negative correlation between serum MMP-9 and its forced vital capacity% predicted (FEV%pred), TIMP-1, and COX-2, and FEV%pred and forced expiratory volume in 1 s-forced vital capacity (FEV₁/FVC) levels, but a positive correlation between Th1-Th2 and FEV₁/FVC levels in the acute group. A significant difference was observed on comparing the levels of serum MMP-9, TIMP-1, COX-2, and Th1-Th2 in patients with different conditions in the acute group. Specifically, as the condition worsened, a significant increase in serum MMP-9, TIMP-1, and COX-2 levels but a significant decrease in Th1-Th2 levels was observed. After treatment, we observed a significant decrease in serum MMP-9, TIMP-1, and COX-2 levels but a significant increase in Th1-Th2 levels in the acute group.

Conclusion: The serum levels of MMP-9, TIMP-1, COX-2, and Th1-Th2 are valuable indicators reflecting the condition of asthma patients and could be considered promising clinical monitoring indicators.

Background: Severe pneumonia is a kind of disease that develops from lung inflammation, and new drugs are still required to treat the same. Erythropoietin (EPO) is widely used to treat anemia in patients. However, there are fewer studies on the role of EPO in neutrophil extracellular trappings (NETs) and pneumonia, and the mechanism is unclear.

Objective: To investigate the possible effects of EPO on the formation of NETs and progression of pneumonia.

Methods: Mice pneumonia model was induced by tracheal lipopolysaccharide (LPS) administration. Hematoxylin and eosin (H&E) staining and automatic blood cell analysis were performed in this model to confirm the effects of EPO on lung injury. Flow cytometry, enzyme-linked immunosorbent serological assay, and immunostaining assay were conducted to detect the effects of EPO on the inflammation as well as formation of NETs in mice. Immunoblot was further conducted to confirm the mechanism.

Results: EPO alleviated LPS-induced lung injury. EPO reduced the release of inflammatory factors induced by LPS. In addition, EPO inhibited the formation of NETs. Mechanically, EPO inhibited tumor necrosis factor (TNF) receptor associated factor 2 (TRAF2)/nuclear factor kappa-B (NF-κB) activity in mouse models, and therefore suppressed the progression of pneumonia.

Conclusion: EPO inhibited formation of NETs to ameliorate lung injury in a pneumonia model, and could serve as a drug of pneumonia.

Oral immunotherapy (OIT) has gained popularity recently for IgE-mediated food allergy. Omalizumab (OMZ) has been used in patients (10-20%) who have too severe/frequent allergic reactions (AR) to continue OIT, to reduce these reactions. In this study, it was aimed to compare two groups of patients who completed OIT with and without OMZ and to seek determinants predicting the need of this treatment. It was also aimed to share the clinical findings regarding the long-term use of OMZ and the withdrawal process. Forty-one patients were started OIT and 93% could be desensitized. Two groups were similar in means of demographic characteristics, and clinical and laboratory findings. The patients who needed OMZ during OIT had also lower reaction doses during oral challenge (p = 0.037). Higher AR rate in this group declined after starting OMZ (p < 0.001). The injection intervals of OMZ were gradually extended. Most patients were able to discontinue OMZ (81%). There were no severe reactions during drug withdrawal attempts. The low reaction thresholds during oral food challenge may give a clue about OMZ requirement during OIT. It may be an option to start the treatment before OIT if reaction was seen in the first few steps of the oral food challenge. For the sake of safety, extension of injection intervals should be preferred instead of abruptly stopping OMZ.