Objective:To investigate the effects of smoking cessation on lung function improvement in patients with chronic obstructive pulmonary disease (COPD) and the related mechanisms.Methods:A case-control study was conducted involving 184 patients with COPD admitted to the Department of Respiratory and Critical Care Medicine at Lishui Central Hospital from January 2022 to May 2023. Based on smoking behavior following 6-month smoking cessation intervention, the patients were categorized into three groups: 56 patients who continued to smoke (control group), 63 patients who completely quit smoking (observation group), and the remaining 65 patients who were partial quitters. Forced vital capacity (FVC), forced expiratory volume in 1 second (FEV 1), and peak expiratory flow rate were monitored before and after the intervention in both the control and observation groups. Additionally, serum levels of interleukin-6 (IL-6), interleukin-1 beta (IL-1β), tumor necrosis factor alpha, nuclear factor kappa B (NF-κB), malondialdehyde, superoxide dismutase, and glutathione peroxidase were measured. Western blotting was performed to detect the protein levels of phosphoinositide 3-kinase (PI3K), serine/threonine kinase (Akt), Forkhead box protein O1 (FoxO1), IL-6, IL-1β, NF-κB, nuclear factor erythroid 2-related factor 2, and heme oxygenase-1 in peripheral blood cells. FoxO1 chromatin immunoprecipitation sequencing was performed to analyze FoxO1-bound chromatin. Results:After smoking cessation intervention, the FEV 1, FVC, FEV 1/FVC ratio, and peak expiratory flow rate in the observation group were (1.29 ± 0.32) L, (1.96 ± 0.36) L, (71.81 ± 8.57)%, and (2.58 ± 0.72) L/s, respectively, which were significantly higher than those in the control group [(1.10 ± 0.37) L, (1.72 ± 0.34) L, (63.17 ± 8.82)%, (2.20 ± 0.71) L/s, t = -3.00, -3.73, -5.42, -2.89, all P < 0.01]. The serum levels of IL-6, NF-κB, IL-1β, and tumor necrosis factor alpha in the observation group were (21.67 ± 3.25) ng/L, (19.58 ± 4.02) ng/L, (24.30 ± 4.03) ng/L, and (270.14 ± 32.49) ng/L, respectively, which were significantly lower than those in the control group [(39.18 ± 4.34) ng/L, (35.48 ± 4.17) ng/L, (34.42 ± 4.05) ng/L, (445.04 ± 39.12) ng/L, t = 25.08, 21.16, 13.64, 26.63, all P < 0.001]. Additionally, the serum malondialdehyde level in the observation group was significantly lower than that in the control group ( t = 29.08, P < 0.001). In contrast, the levels of superoxide dismutase and glutathione peroxidase in the observation group were significantly higher than those in the control group ( t = -9.21, -9.59, both P < 0.001). The phosphorylation levels of PI3K, Akt, and FoxO1 in peripheral blood cells were significantly lower in the observation group compared with the control group ( t = 6.64, 9.35, 7.12, all P < 0.001). FoxO1 bound to genes involved in inflammation and oxidative stress signaling pathways. The levels of nuclear factor erythroid 2-related factor 2 and heme oxygenase-1 in the observation group were significantly higher than those in the control group ( t = -4.97, -10.49, both P < 0.05). Conclusions:Smoking cessation intervention can inhibit PI3K/Akt phosphorylation in patients with COPD, and then activate FoxO1, exert anti-inflammatory and antioxidant effects, and inhibit the deterioration of lung function in patients with COPD who smoke.

Objective:To investigate the effects of smoking cessation on lung function improvement in patients with chronic obstructive pulmonary disease (COPD) and the related mechanisms.Methods:A case-control study was conducted involving 184 patients with COPD admitted to the Department of Respiratory and Critical Care Medicine at Lishui Central Hospital from January 2022 to May 2023. Based on smoking behavior following 6-month smoking cessation intervention, the patients were categorized into three groups: 56 patients who continued to smoke (control group), 63 patients who completely quit smoking (observation group), and the remaining 65 patients who were partial quitters. Forced vital capacity (FVC), forced expiratory volume in 1 second (FEV 1), and peak expiratory flow rate were monitored before and after the intervention in both the control and observation groups. Additionally, serum levels of interleukin-6 (IL-6), interleukin-1 beta (IL-1β), tumor necrosis factor alpha, nuclear factor kappa B (NF-κB), malondialdehyde, superoxide dismutase, and glutathione peroxidase were measured. Western blotting was performed to detect the protein levels of phosphoinositide 3-kinase (PI3K), serine/threonine kinase (Akt), Forkhead box protein O1 (FoxO1), IL-6, IL-1β, NF-κB, nuclear factor erythroid 2-related factor 2, and heme oxygenase-1 in peripheral blood cells. FoxO1 chromatin immunoprecipitation sequencing was performed to analyze FoxO1-bound chromatin. Results:After smoking cessation intervention, the FEV 1, FVC, FEV 1/FVC ratio, and peak expiratory flow rate in the observation group were (1.29 ± 0.32) L, (1.96 ± 0.36) L, (71.81 ± 8.57)%, and (2.58 ± 0.72) L/s, respectively, which were significantly higher than those in the control group [(1.10 ± 0.37) L, (1.72 ± 0.34) L, (63.17 ± 8.82)%, (2.20 ± 0.71) L/s, t = -3.00, -3.73, -5.42, -2.89, all P < 0.01]. The serum levels of IL-6, NF-κB, IL-1β, and tumor necrosis factor alpha in the observation group were (21.67 ± 3.25) ng/L, (19.58 ± 4.02) ng/L, (24.30 ± 4.03) ng/L, and (270.14 ± 32.49) ng/L, respectively, which were significantly lower than those in the control group [(39.18 ± 4.34) ng/L, (35.48 ± 4.17) ng/L, (34.42 ± 4.05) ng/L, (445.04 ± 39.12) ng/L, t = 25.08, 21.16, 13.64, 26.63, all P < 0.001]. Additionally, the serum malondialdehyde level in the observation group was significantly lower than that in the control group ( t = 29.08, P < 0.001). In contrast, the levels of superoxide dismutase and glutathione peroxidase in the observation group were significantly higher than those in the control group ( t = -9.21, -9.59, both P < 0.001). The phosphorylation levels of PI3K, Akt, and FoxO1 in peripheral blood cells were significantly lower in the observation group compared with the control group ( t = 6.64, 9.35, 7.12, all P < 0.001). FoxO1 bound to genes involved in inflammation and oxidative stress signaling pathways. The levels of nuclear factor erythroid 2-related factor 2 and heme oxygenase-1 in the observation group were significantly higher than those in the control group ( t = -4.97, -10.49, both P < 0.05). Conclusions:Smoking cessation intervention can inhibit PI3K/Akt phosphorylation in patients with COPD, and then activate FoxO1, exert anti-inflammatory and antioxidant effects, and inhibit the deterioration of lung function in patients with COPD who smoke.

Objective To investigate the effects of shiga toxin ( Stx ) phage on the expression of type Ⅲsecretion system (T3SS) in E.coli O157 ∶H7.Methods A standard E.coli O157 ∶H7 strain, EDL933 and a natural Stx phage defective mutant of EDL 933 strain, TUV93-0 were used for this study .The expression of T3SS proteins was compared between EDL 933 and TUV93-0 strains.The expression of five operons ( LEE1-LEE5 ) was evaluated by measuring the green fluorescent protein ( GFP ) in five different plasmids with LEE1-LEE5 promoters, respectively.Results The expression of T3SS proteins in TUV93-0 mutant were significantly increased than those in EDL 933 strain.Moreover, the expression of LEE1, LEE2 and LEE5 were also increased in TUV93-0 mutant.Conclusion The deletion of Stx phage might enhance T3SS expression through the regulation of LEE 1.

Objective To investigate the effect of FNR on type Ⅲ secretion system (T3SS) in E.coli O157 ∶ H7.Methods fnr mutant was constructed by λRed recombineering technology promoted by Bet and Exo proteins using PCR products.Results Through bacterial infection assays and immunofluorescence microscopy,it was found that the adhesion ability was decreased insignificantly infnr mutant compared to the wild type ZAP198.However,the secreted proteins were reduced significantly in the mutant from the secretion profile.Conclusion The reason might be that high ClpXP protein caused by the deletion of fnr degraded GrlA resulting in the inhibition of LEE(locus of enterocyte effacement) and T3SS.