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Abstract Aim To evaluate the effects of montelukast in smoke-induced lung injury. Methods 28 Wistar-Albino rats were enrolled into 4 groups with 7 rats per group. The healthy control group was exposed to fresh air while all rats in the 3 experimental groups were exposed to cigarette smoke for 20 weeks for 2 hours per day. After histopathological verification of smoke induced lung injury, montelukast (0.1 mg/kg) dissolved in Na2CO3 was given in one group (MON), Na2CO3 only was given in another group (MON control) and placebo was injected in the third group (COPD control) intraperitoneally for 21 days. At the end of this period blood samples were obtained for serum TNF-α assessment and light and electron microscopy analyses were performed on the lung tissues of sacrificed rats. Results Serum TNF-α levels in the MON group were significantly lower than in the MON control and COPD control groups (38.84 ± 4.9 pg/ml, 77.5 ± 5.8 pg/ml and 79.2 ± 6.9 pg/ml respectively, p < 0.05). Furthermore there was no statistically significant difference between the MON group and healthy controls with respect to serum TNF-α levels (38.84 ± 4.9 pg/ml vs. 29.5 ± 3.6 pg/ml, p > 0.05). Light and electron microscopic evaluation of the lungs demonstrated that the total histopathological damage score of the lung samples was significantly lower in the MON group than in MON controls and COPD controls (5.14 ± 0.5, 8.4 ± 0.6 and 8.7 ± 0.4 respectively, p < 0.05), while there was no significant difference between the MON group and healthy controls (5.1 ± 0.6 vs 2.3 ± 0.2, p > 0.05). Conclusion These findings suggest that montelukast might have a protective effect on smoke-induced lung injury in rats both from a histopathological and inflammatory point of view.

Objective: To evaluate long-term effects of COVID-19, and to determine the risk factors in long-COVID in a cohort of the Turkish Thoracic Society (TTS)-TURCOVID multicenter registry. Methods: Thirteen centers participated with 831 patients; 504 patients were enrolled after exclusions. The study was designed in three-steps: (1) Phone questionnaire; (2) retrospective evaluation of the medical records; (3) face-to-face visit. Results: In the first step, 93.5% of the patients were hospitalized; 61.7% had a history of pneumonia at the time of diagnosis. A total of 27.1% reported clinical symptoms at the end of the first year. Dyspnea (17.00%), fatigue (6.30%), and weakness (5.00%) were the most prevalent long-term symptoms. The incidence of long-term symptoms was increased by 2.91 fold (95% CI 1.04-8.13, P=0.041) in the presence of chronic obstructive pulmonary disease and by 1.84 fold (95% CI 1.10-3.10, P=0.021) in the presence of pneumonia at initial diagnosis, 3.92 fold (95% CI 2.29-6.72, P=0.001) of dyspnea and 1.69 fold (95% CI 1.02-2.80, P=0.040) fatigue persists in the early-post-treatment period and 2.88 fold (95% CI 1.52-5.46, P=0.001) in the presence of emergency service admission in the post COVID period. In step 2, retrospective analysis of 231 patients revealed that 1.4% of the chest X-rays had not significantly improved at the end of the first year, while computed tomography (CT) scan detected fibrosis in 3.4%. In step 3, 138 (27.4%) patients admitted to face-to-face visit at the end of first year; at least one symptom persisted in 49.27% patients. The most common symptoms were dyspnea (27.60%), psychiatric symptoms (18.10%), and fatigue (17.40%). Thorax CT revealed fibrosis in 2.4% patients. Conclusions: COVID-19 symptoms can last for extended lengths of time, and severity of the disease as well as the presence of comorbidities might contribute to increased risk. Long-term clinical issues should be regularly evaluated after COVID-19. [ABSTRACT FROM AUTHOR]

Objective: Sildenafil is a selective and potent inhibitor of cyclic guanosine monophosphate specific phosphodiesterase-5 and has anti-inflammatory effects. The aim of the study was to evaluate the effects of sildenafil on smoke-induced lung inflammation. Material and Methods: Twenty-nine Wistar-Albino rats were enrolled into 3 groups as control, smoker and sildenafil groups. Smoker and sildenafil groups were exposed to cigarette smoke for 2 hours per day for 8 weeks. Sildenafil 10 mg/kg/day was administered to the sildenafil group by nasogastric lavage after smoke exposure. The degree of lung inflammation was scored histopathologically for each group. Results: The inflammation score was 7.25±0.93 in the control group, 8.18±1.21 in the smoker group and 7.08±1.66 in the sildenafil group. There was a non-significant decrease of inflammation score in sildenafil group with respect to control or smoker groups. While there was no significant difference of oedema, hyperemia, hemorrhage and mononuclear cell infiltration scores among the groups, it was found that the thickness of interalveolar septum and alveolar distortion was decreased in sildenafil group. However this decrease was not statistically significant. Conclusion: This study suggests that sildenafil might reduce smoke-induced inflammation in rat lungs. Future studies are needed in order to investigate the clinical effectiveness of this finding in smoking related lung diseases. [ABSTRACT FROM AUTHOR]

Abstract Aim To evaluate smoking and COPD prevalence amongst teachers working in the schools of Kocaeli City, Turkey. Method In this cross-sectional study, a questionnaire focusing on respiratory symptoms and smoking habits was administered to all participants who accepted to join the study.All subjects also underwent a physical examination and a pulmonary function test performed with portable spirometer. According to GOLD criteria, subjects who had post-bronchodilator FEV1/FVC < 70% and negative reversibility test were classified as COPD. Results A total of 685 teachers were included [female n = 307 (45%), male n = 378 (55%)] with mean age 38.9 ± 8.9 years. Smoking habit was evaluated in 660 subjects: 291 (44.1%) were smokers, 252 (38.2%) were non-smokers and 117 (17.7%) were ex-smokers. Pulmonary function test was available in 651 subjects and 510 (78.3%) were defined as normal on spirometric analysis. Small airway obstruction was found in 115 of the cases (17.7%) in whom FEF25-75 level was found to be lower than 70% predicted. FEV1/FVC level was lower than 70% in 16 subjects (2.5%). Five subjects who had positive reversibility test were excluded from the study. The remaining 11 subjects who were considered as COPD consisted of 2 (18%) females and 9 (82%) males. Six of these subjects were aged over 40 years. Conclusion Spirometry has an important role in early diagnosis of COPD. Spirometric evaluation of cases with risk factors for COPD could be helpful in diagnosing patients before the progressive decline in lung function begins. Further studies are needed to evaluate whether the interventional strategies at this stage such as smoking cessation could prevent the progression of disease.

The multisystemic effects of COVID-19 may continue for a longer time period following the acute phase, depending on the severity of the disease. However, long-term systemic transcriptomic changes associated with COVID-19 disease and the impact of disease severity are not fully understood. We aimed to investigate the impact of COVID-19 and its severity on transcriptomic alterations in peripheral blood mononuclear cells (PBMCs) following 1 year of the disease. PBMCs were isolated from the peripheral blood of healthy control donors who did not have COVID-19 (C; n = 13), from COVID-19 patients without pneumonia (NP; n = 11), and from COVID-19 patients with severe pneumonia (SP; n = 10) after 1-year of follow-up. Following RNA isolation from PBMCs, high-quality RNAs were sequenced after creating a library. Differentially expressed genes (DEGs) and differentially expressed long non-coding RNAs (DElncRNAs) were identified using Benjamini-Hochberg correction and they were analysed for hierarchical clustering and principal component analysis (PCA). Intergroup comparisons (C vs. NP, C vs. SP, and NP vs. SP) of DEGs and DElncRNAs were performed and hub genes were determined. Functional enrichment analyses of DEGs and DElncRNAs were made using Metascape (v3.5.20240101) and the first version of NCPATH. The RNA sequencing analysis revealed 4843 DEGs and 1056 DElncRNAs in "C vs. NP", 1651 DEGs and 577 DElncRNAs in "C vs. SP", and 954 DEGs and 148 DElncRNAs in "NP vs. SP", with 291 DEGs and 70 DElncRNAs shared across all groups, respectively. We identified 14 hub genes from 291 DEGs, with functional enrichment analysis showing upregulated DEGs mainly linked to inflammation and osteoclast differentiation and downregulated DEGs to viral infections and immune responses. The analysis showed that 291 common and 14 hub genes were associated with pneumonia and that these genes could be regulated by the transcription factors JUN and NFκB1 carrying the NFκB binding site. We also revealed unique immune cell signatures across DEG categories indicating that the upregulated DEGs were associated with neutrophils and monocytes, while downregulated DEGs were associated with CD4 memory effector T cells. The comparative transcriptomic analysis of NP and SP groups with 52 gene signatures suggestive of IPF risk showed a lower risk of IPF in the SP group than the NP patients. Our findings suggest that COVID-19 may cause long term pathologies by modulating the expression of various DEGs, DeLncRNAs, and hub genes at the cellular level.

We evaluated the frequency of exacerbations and hospitalizations in chronic obstructive pulmonary disease (COPD) patients who continue to smoke.: We retrospectively analyzed the medical records of the COPD patients treated in Chest Diseases Clinic of Kocaeli University School of Medicine in 2007-2013. Their demographic characteristics, smoking status (non-smoker, current smoker, ex-smoker), Charlson Comorbidity Index (CCI), and history of COPD exacerbation and hospitalizations were evaluated. The cases of 120 patients (11 females, 9.2%; 109 males, 90.8%) were analyzed. Sixteen (13.3%) of the patients were current smokers, and 104 patients were ex-smokers (n=99) or non-smokers (n=5). The mean age was 69.7±7.9 years in the ex-smokers and 62.94±6.8 years in the current smokers. There were no significant differences between the current and ex-smokers regarding smoking history, FEV1 value, frequencies of exacerbations and hospitalization per year, or duration of follow-up. The initial stage of the COPD and the frequency of exacerbations were significantly correlated (p=0.003). The CCI values were significantly higher in the ex-smokers compared to current smokers (p=0.02). A correlation analysis of age, hospitalization and CCI revealed that age was significantly correlated with the hospitalization rate (p=0.02). Older age and the presence of comorbidities in ex-smokers might explain the similar rates of exacerbation and hospitalization between these current and ex-smokers., Competing Interests: No potential conflict of interest relevant to this article was reported.