Effects of the recombinant allergen rDer f 2 on neuro-endocrino-immune network in asthmatic mice.

Severe and life-threatening side effects can occur in patients receiving allergen-specific immunotherapy (SIT), and recombinant allergens made from cDNA have been used in clinical trials for ten years and appear promising for SIT. The aim of this study is to explore the effects of the recombinant allergen Der f 2 (the group 2 allergen from Dermatophagoides farinae) on the neuro-endocrino-immune network in asthmatic mice. Twenty-eight mice were divided into four groups - A, B, C and D. To induce asthma, a crude extract of D. farinae was injected intraperitoneally into the mice in groups B, C and D. Later, the crude extract or recombinant allergen rDer f 2 was given to groups C and D, respectively. Normal saline was given to groups A and B. Serum corticotropin-releasing hormone (CRH), adrenocorticotropic hormone (ACTH), corticosterone (CORT), interleukin 4 (IL-4), and interferon γ (IFN-γ) were detected by immunoassay and the pathological change of lung tissue was observed by hematoxylin and eosin (HE) staining. Serum CRH, ACTH, CORT, and IFN-γ were highest in healthy group A but lowest in asthma group B. Treatment with the crude extract or recombinant allergen rDer f 2 significantly attenuated this response in asthmatic mice, but there was no difference between the two treatments (p > 0.05). Serum IL-4 was elevated in asthma group B but lowest in healthy group A. Treatment with the crude extract or recombinant allergen rDer f 2 significantly attenuated this response in asthmatic mice, but there was no significant difference between the two treatments (p > 0.05). However, lung pathology as measured histologically (Underwood Score) showed that rDer f 2-treatment was significantly better than crude extract treatment (p < 0.05). In brief, recombinant allergen Der f 2 can strengthen the function of hypothalamus-pituitary-adrenal (HPA) axis, affect the balance of Th1 and Th2 cytokines, and reduce pulmonary inflammation in asthmatic mice.

[Effect of Bizhongxiao decoction on proteomics of peripheral blood mononuclear cells in patients with rheumatoid arthritis].

OBJECTIVE: To probe in the possible acting mechanism of Bizhongxiao Decoction (BZXD) for treatment of early active rheumatoid arthritis (RA) by way of observing the two-dimensional gel electrophoresis map of proteins in peripheral blood mononuclear cells (PBMCs) of healthy persons and RA patients (intervened or un-intervened with BZXD), analyzing the differential proteins and seeking out the RA associated proteins. METHODS: Eighteen patients with early active RA were randomized into the BZXD group and the methotrexate (MTX) group, nine in each group, they were treated with BZXD (contained 15 Chinese herbs, as Herba Hedyotis diffusae, Herba Sarcandrae glabrae, Radix Salviae miltiorrhizae, Caulis Trachelosperi, Rhizoma Drynariae, Semen Coicis, etc.) and MTX combined with nimesulide Tablets respectively, three months as a treatment course, and their blood samples were collected for observation. Besides, blood samples from 9 healthy persons were taken as normal controls. PBMCs were isolated from blood using lymphozytes separation medium, and total protein in the cells was extracted through immobilized pH gradient two-dimensional gel electrophoresis. After Coomassie brilliant blue G250 staining, gel-image analysis was performed using PDQuest software. The differentially expressed proteins were identified by matrix-assisted laser desorption ionization-time-of-flight mass spectrometry (MALDI-TOF-MS). Then partial proteins were validated by reverse transcription polymerase chain reaction (RT-PCR). RESULTS: The 2-DE protein profile of PBMCs from healthy persons and RA patients before and 3 months after treatment were obtained, and 23 differential protein spots were found, 14 from 18 differential protein spots were successfully identified, of which 8 proteins were up-regulated and 6 proteins were down-regulated in RA patients as compared with control. After 3-month treatment, 5 differentially expressed proteins showed more obvious in the BZXD group than in the MTX group. RT-PCR verified that the expression of ApoA-I in all the three groups was consistent with the outcomes of 2-DE. CONCLUSIONS: Some differentially expressed proteins exist in the PBMCs of RA patients, which may play a potential role in the pathogenesis of RA; BZXD may treat RA by way of regulating the expression of some differential proteins in patients.

Efficacy of continuous positive airway pressure treatment in treating obstructive sleep apnea hypopnea syndrome associated with carotid arteriosclerosis.

Sleep apnea negatively impacts patients' ability to oxygenate the bloodstream during sleep and has far-reaching, deleterious effects. The present study sought to assess the correlation between obstructive sleep apnea hypopnea syndrome (OSAHS), carotid atherosclerosis, and blood pressure variability (BPV), and to evaluate the therapeutic effects of continuous positive airway pressure (CPAP). Patients with OSAHS were classified as mild, moderate, or severe according to their condition and compared with healthy control participants. CPAP treatment was used to treat patients with OSAHS for 6 months. Prior to CPAP treatment, the apnea-hypopnea index (AHI), lowest blood oxygen saturation (LSaO2), carotid intima media thickness (IMT), and plasma levels of endothelin-1 (ET-1), nitric oxide (NO), and tumor necrosis factor-α (TNF-α) were measured in all participants, along with the low frequency components of BPV (BPV LF). The results demonstrated that carotid IMT, AHI, plasma ET-1, and plasma TNF-α were significantly higher in patients with OSAHS than those in the control group (P<0.05); whereas LSaO2 and plasma NO levels were significantly higher in the control group (P<0.05). The degree to which these indices differed was associated with the severity of OSAHS. Furthermore, the carotid IMT of patients with OSAHS was significantly correlated with AHI (P=0.037), plasma ET-1 (P=0.001), plasma NO (P<0.001), BPV LF before retiring (P<0.001). Following CPAP treatment, the observation indices of patients with moderate or severe OSAHS improved significantly (P<0.01). These results support the use of CPAP to improve the significant vascular endothelial dysfunction, increased inflammatory response, and high blood pressure variability correlated with carotid atherosclerosis observed in patients with OSAHS.

Suppression of EGFR-STAT3 signaling inhibits tumorigenesis in a lung cancer cell line.

Overactive epidermal growth factor receptor (EGFR) signaling often underlies the rapid expansion of cancerous tissue. EGFR signaling is mediated by transcription factor signal transducer and activator of transcription 3, or STAT3. This study sought to investigate the effects of altered EGFR/STAT3 signal transduction on lung cancer cells in vitro. Lung cancer cells from the cell line A549 were divided into test and control groups. Test group cells were treated with an EGFR monoclonal antibody, Nimotuzumab, while control cells received no treatment. EGFR and STAT3 protein expression, cell apoptosis rate, cell proliferation, cell invasion, and cell division were analyzed and compared. Compared to cells in the control group, lung cancer cells treated with Nimotuzumab showed slowed proliferation rates, accelerated apoptosis, decreased invasion, and arrested cell division (P < 0.05). In conclusion, altered EGFR/STAT3 signaling results in significant changes in the biology of lung cancer cells.

HMGB1 and RAGE levels in induced sputum correlate with asthma severity and neutrophil percentage.

Previous work indicated that high mobility group box-1 (HMGB1) protein may be involved in neutrophilic asthma. Here, we sought to investigate the correlation between HMGB1 and one of its receptors, receptor for advanced glycosylation end products (RAGE), with the severity of bronchial asthma. Compared to the control group (30 healthy individuals), patients in the asthma group (n=72) exhibited a higher percentage of neutrophils and higher HMGB1 and RAGE levels in induced sputum samples (P<0.05). Concurrently, FEV(1)% was significantly lower in the asthma group (P<0.05). Further, compared to mild and moderate asthma, in patients with severe asthma ACQ scores, the percentage of neutrophils, and HMGB1 levels were significantly higher, while FEV(1)% was significantly lower (P<0.05). The percentage of neutrophils and HMGB1 and RAGE levels were lower after treatment than before treatment (P<0.05). Finally, negative correlations were observed between HMGB1 or RAGE levels and FEV(1)% (r=-0.777 and r=-0.291, P<0.05), and positive correlations were detected between HMGB1 or RAGE levels and percentage of neutrophils (r=0.803 and r=0.326, P<0.05). Additionally, positive correlations were observed between HMGB1 and RAGE levels within the asthma group (r=0.306, P<0.05). Therefore, HMGB1 protein levels correlate with the severity of asthma, and HMGB1 may contribute to the inflammatory process of asthma.