ABSTRACT
Objective:To analyze the correlation between body mass index (BMI) and lung function in patients with bronchial asthma (asthma).Methods:This study was a retrospective study. A total of 828 patients with asthma were included from March 2013 to November 2022 in the first affiliated Hospital of Guangxi Medical University, including 292 males and 536 females, aged 21-82 years, with a median age of 47 years. According to BMI, these asthma patients were divided into high BMI group (BMI≥24 kg/m 2), normal BMI group (18.5 kg/m 2≤BMI<24 kg/m 2) and low BMI group (BMI<18.5 kg/m 2). Forced vital capacity (FVC), forced expiratory volume in first second (FEV 1), FEV 1/FVC, maximum mid-expiratory flow (MMEF), forced expiratory flow at 25%, 50% and 75% of FVC (FEF 25%, FEF 50%, FEF 75%), peak expiratory flow (PEF), absolute increases in measured values of FVC and FEV 1 and percentage increases in FVC%pred (“%pred” represents the percentage of related indicators to expected value) and FEV 1%pred after inhalation of bronchodilator (salbutamol) were measured by pulmonary function meter. The correlation between BMI and the above indexes was analyzed. Results:In the high BMI group, FEV 1%pred, MMEF, FEF 25%, FEF 50% and FEF 75% were significantly lower than those in the normal BMI group and the low BMI group (all P<0.05), FVC% pred was significantly lower than those in the normal BMI group( P<0.05), and the percentage increase of FEV 1%pred was significantly lower than those in low BMI group ( P<0.05). FVC% pred in the normal BMI group was significantly higher than that in the low BMI group ( P<0.05). In male patients, BMI was negatively correlated with the absolute increase of FEV 1 ( r=-0.148, P<0.05); In female patients, BMI was negatively correlated with FEV 1%, FEV 1/FVC, MMEF, FEF 25%, FEF 50%, FEF 75% and the percentage increase of FEV 1%pred ( r=-0.124, -0.127, -0.165, -0.138, -0.156, -0.162, -0.106, all P<0.05). Conclusion:There is a significant correlation between BMI and lung function in patients with asthma, and the lung function in patients with high BMI is relatively worse; and in female patients, the effect of BMI on lung function is more significant; the increase of BMI can lead to the decrease of lung function and airway reversibility, suggesting that attention should be paid to the management of BMI in asthma management.
ABSTRACT
T lymphocyte immune dysfunction plays an important role in the occurrence and development of chronic obstructive pulmonary disease (COPD), but the specific mechanism is not fully understood. Programmed cell death 1 (PD-1) negatively regulates the activation and effector function of T lymphocytes by binding to its ligand PD-L1, thus participating in the maintenance of immune tolerance. Recent studies have found that blocking the PD-1/PD-L1 signaling pathway can improve T-cell depletion and enhance the ability of anti-infection in COPD patients. Therefore, understanding the regulatory effects of PD-1 on T lymphocytes is of great significance to studying the pathogenesis and clinical treatment of COPD. This article briefly reviewed the research progress in PD-1 in terms of structure, function, T cell regulation and relationship with COPD.
ABSTRACT
Objective To evaluate the expression of Tc17 in a cigarette smoke-induced mice model of emphysema.To explore the probable mechanisms about how Tc17 cells to elevate in lungs of mice.Methods Forty male Balb/c mice were randomly divided into four groups,including control group ( 12 weeks,C12),control group (24 weeks,C24),smoke-exposure group (12 weeks,S12) and smoke-exposure group (24 weeks,S24 ),10 mice each group,Emphysema of mice was observed by HE pigmentation.Morphological changes were evaluated by mean linear intercepts (Lm) and destructive index (DI).The proportion of CD8+ IL-17 + Tc17,CD8+ IL-17 + CC chemokine receptor type 6 ( CCR6 ) + and 6CCR6 + Tc17 cells in lungs of mice was determined by flow cytometry.The mRNA expressions of retinoidrelated orphan nuclear receptor(RORγt) and IL-17 were evaluated by real-time PCR.The levels of IL-1 β,IL-6,IL-23,transforming growth factor β (TGFβ) and CC chemokine ligand 20 (CCL20) were tested by ELISA.Correlations among these indexes were analyzed.Results Lm and DI were significantly higher in S12 and S24 than in C12 and C24,S24 in particular (t value 4.378-15.188,all P ＜ 0.05).The percentages of Tc17 in S12 and S24[(9.28 ± 1.12)%,( 13.13 ±3.56)%]was significantly increased as compared with that in C12 and C24[(2.40 ±0.60 )%,(2.64 ±0.96 )%],S24 in particular.The mRNA levels of RORγt and IL-17 in S12 and S24 were higher than in C12 and C24,S12 and S24 in particular.There was significant difference (all P ＜0.05 ).The frequency of Tc17 cells had a positive correlation with Lm and DI ( r value were 0.734 and 0.884 respectively,P ＜ 0.01 ).The percentages of CD8+ IL-17 + CCR6 +T cells and CCR6 + Tc17 were significantly elevated in S12 and S24 compared to C12 and C24,S24 in particular (all P ＜ 0.05 ).There was positive correlation between Tc17 cell ratio and CCL20 levels( r =0.899,P ＜0.01 ).The levels of IL-1 β,IL-6,IL-23 and TGFβ in S12 and S24 were significantly increased as compared with that in C12 and C24.There was significant difference (all P ＜0.05).Meanwhile,the frequency of Tc17 cells had a positive correlation with IL-1β,IL-6,IL-23,and TGFβ.Conclusions An up-regulation of proportions Tc17 in lungs of cigarette smoke-induced emphysema mice were detected.The CCR6/CCL20 axis and the increased IL-1β,IL-6,IL-23 and TGFβ probably contributed to this up-regulation.
ABSTRACT
Objective To investigate the effect of cigarette smoke exposure on the interleukin-17-producing CD4+T helper lymphocyte( Th17 ) in peripheral blood and lungs of cigarette smoke-induced emphysema mice. MethodsForty male BALB/c mice were randomly divided into 4 groups, including a control group C12, a control group C24, a smoke-exposure group S12 and a smoke-exposure group S24, 10 mice each group. Morphological changes were evaluated by mean linear intercepts (Lm) and destructive index (DI). The concentration of IL-17, IFN-γ and TNF-α in bronchoalveolar lavage fluid(BALF) and the concentration of IFN-γ and TNF-α in lung homogenates were measured by enzyme-linked immunosorbent assay (ELISA). The proportion of CD4+IL-17+ Th17 cells in peripheral blood and lungs of mice was determined by flow cytometry. The mRNA expressions of RORγt and IL-17 in peripheral blood and lungs were evaluated by real-time PCR. ResultsLm and DI were significantly higher in S12 and S24 groups [(39.19±3.51)μm vs (46.87±7.16) μm, 39.13±1.57 vs 45.16±3.13]than that in C12 and C24 groups [(32.60± 3.21 ) μm vs (32.38±3.73) μm, 28.23± 1.62 vs 28.86±2.07], all P＜0.05. IL-17, IFN-γand TNF-α in BALF of S12 and S24 groups [(119.72±10.72) ng/L vs (296.40±14.00) ng/L,(129.7±22.2) ng/L vs(251. 1±62.4) ng/L, (17.35±1.60) ng/L, (36.35±1.43) ng/L]were higher than those in C12 and C24 groups [(52.06±4.70) ng/L vs (51.89 ±6.82) ng/L, ( 85.8 ±26.8) ng/L vs ( 88.9 ± 11.5 ) ng/L,(6.41 ±0.90) ng/L vs (5.85±0.92) ng/L], IFN-γ and TNF-α in lungs of S12 and S24 groups [( 1124.3±174.4) ng/L vs (1342.7±206.1) ng/L, (77.2±13.7) ng/L vs (101.7±19.0) ng/L, (129.7±22.2)ng/L vs (251.1 ±62.4) ng/L]were higher than those in C12 and C24 groups[(946.2±81.9) ng/L vs (1027.2±188.3) ng/L, (62.1±16.1) ng/L vs(64.4±15. 1) ng/L], all P＜0.05. The percentage of Th17 cells in lungs of S12 and S24 groups [(3.27±1.12)％ vs (7.19±2.24)％, ( 1.96±0.61 )％ vs (3.82±1.26)％]was significantly increased as compared with that of C12 and C24 groups [(1.80± 0.75)％ vs (1.99±0.59)％], all P＜0.05. And the percentage of Th17 cells in peripheral blood of S12 and S24 groups [(1.96±0.61)％ vs ( 3.82± 1.26)％]was also significantly higher than those in C12 and C24 groups [(0.90±0.37)％ vs (0.97±0.32)％], all P＜0.05. In peripheral blood and lungs,the mRNA levels of RORγt and IL-17 in S12 and S24 groups were higher than in C12 and C24 groups, all P＜0.05.Moreover, the frequency of Th17 cells in peripheral blood and lungs had a positive correlation with Lm and DI( r=0.706-0.772 ,all P＜0.05 ). ConclusionAn up-regulation of proportions Th17 in peripheral blood and lungs of cigarette smoke-inducsed emphysema mice were detected. It may be involved in the amplified and persistent inflammation.