Cigarette smoking is the main cause of chronic obstructive pulmonary disease (COPD) [1][2][3]. The pathogenesis of smoke-induced COPD has been evaluated in a number of studies showing the accumulation of inflammatory cells in patients' airways: predominantly polymorphonuclear leukocytes in samples representative of intraluminal infla-mmation (sputum, bronchial and bronchoalveolar lavage) and mainly mononuclear cells, lymphocytes and macrophages, in tissue specimens [4][5][6][7][8][9][10][11][12][13].While the reason (or reasons) for this discrepancy is still not completely clear, these studies have opened the field to new questions. Since the relevance of airway inflammation in COPD has been demonstrated, the next step is the characterization of the different features of airway inflammation, such as the nature of chemotactic signal(s) and the contribution of the various cell types to airway inflammation through the release of inflammatory mediators.In this regard, this study was targeted on a COPD patient population of nonatopic current smokers with airway obstruction, with the aim of investigating the characteristics of intraluminal airway inflammation in these patients. Therefore, this study evaluated the presence in bronchial lavage (BL) of: interleukin (IL)-8, a chemotactic factor for polymorphonuclear cells into the airways; myeloperoxidase (MPO), eosinophil cationic protein (ECP) and tryptase, mediators of tissue damage from polymorphonuclear cells and mast cells; and the correlations between cellular and noncellular data obtained from BL. Materials and methods Study subjectsTwelve patients with COPD entered this study. They all had chronic productive cough for >3 months for 2 consecutive yrs, in the absence of other known disorders, such as bronchiectasis, tuberculosis or lung cancer [14,15]. The patients met the following inclusion criteria: 1) history of cigarette smoking, with a minimum of 15 pack-yrs, in patients who all were current smokers at time of evaluation; 2) no occupational or other exposure to other substances known to cause lung disorders; 3) absence of atopy, i.e. with negative skin tests for common allergen These data suggest that cigarette smoke is associated with increased amounts of airway interleukin-8, a chemotactic factor for neutrophils and eosinophils. Recruited neutrophils and eosinophils are activated and they release increased amounts of inflammatory mediators capable of damaging the bronchial tissue. Eur Respir J 1998; 12: 380-386

Background-Nitric oxide (NO) plays an important role as an inflammatory mediator in the airways. Since chronic obstructive pulmonary disease (COPD) is characterised by airway inflammation, a study was undertaken to determine NO levels in the exhaled air of patients with COPD. Methods-Two groups of patients with clinically stable COPD were studied, 10 current smokers and 10 ex-smokers. Two control groups of healthy subjects consisting of 10 current smokers and 20 nonsmokers were also studied. Exhaled NO levels were measured by the collection bag technique and NO chemiluminescence analyser. Results-Mean (SE) levels of exhaled NO in ex-smokers and current smokers with COPD (25.7 (3.0) ppb and 10.2 (1.4) ppb, respectively) were significantly higher than in non-smoker and current smoker control subjects (9.4 (0.8) ppb and 4.6 (0.4) ppb, respectively). In current smokers with COPD exhaled levels of NO were significantly lower than in ex-smokers. In this latter group of patients there was a significant negative correlation between smoking history (pack years) and levels of exhaled NO (r = -0.8, p = 0.002). A positive correlation was seen between forced expiratory volume in one second (FEV 1 ) and levels of exhaled NO (r = 0.65, p = 0.001) in patients with COPD. Conclusions-These data show that exhaled NO is increased in patients with stable COPD, both current and exsmokers, compared with healthy control subjects.

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FNAC in expert hands is fairly accurate for typing NSCLC and can be regarded as an acceptable procedure for diagnostic and medical treatment planning purposes in most NSCLC cases, especially when more invasive approaches are unfeasible. In poorly differentiated and doubtful cases, the use of ancillary techniques, such as immunocytochemistry, may be required to improve the diagnostic yield.

Background: Sex-differences have been demonstrated in the acute phase of COVID-19 infection; females (F) were found to be less prone to develop a severe disease than males (M), but few studies have assessed sex-differences in Long-Covid-19 syndrome. Aim and Results:The aim of this prospective/retrospective study was to characterize the long-term consequences of this infection from a sex-perspective. For this purpose, we enrolled 223 patients (89 F and 134 M) who experienced a SARS -CoV-2 infection.In the acute phase of the illness, females reported more frequently than males: weakness, dysgeusia, anosmia, thoracic pain, palpitations, diarrhea, and myalgia without significant differences in breathlessness, cough, and sleep disturbance. After a mean follow-up time of 5 months after the acute phase, females were significantly more likely than males to report weakness, thoracic pain, palpitations, and sleep disturbance but not myalgia and cough.At the multivariate logistic regression, women were statistically significantly likely to experience persistent symptoms such as dyspnoea, fatigue, chest pain, and palpitations.On the contrary, myalgia, cough and sleep disturbance were not influenced by sex. Conclusion:We demonstrated that females were more symptomatic than males not only in the acute phase but also at follow-up. Sex was found to be an important determinant of Long-COVID syndrome because it is a significant predictor of persistent symptoms in females, such as dyspnoea, fatigue, chest pain, and palpitations.Our results suggest the need for long-term follow-up of these patients from a sexperspective in order to implement early preventive and personalized therapeutic strategies.

In order to characterize neutrophil and eosinophil presence in the airways of patients with chronic obstructive pulmonary disease (COPD), bronchoscopy with bronchial washings and bronchial biopsies was performed in 12 smoking stable COPD subjects and 18 normal non-smoking control subjects. Bronchial biopsies were examined by light microscopy using plastic embedding and histochemical techniques to identify different cell types. Bronchial washing fluid of COPD patients was characterized by a predominance of neutrophils (P = 0.001), and a slight, but significant (P = 0.03), increase of eosinophil fraction. Subjects with COPD had higher number of neutrophils in the epithelium (P = 0.01), and eosinophils in the lamina propria (P = 0.01) than did control subjects. The thickness of reticular basement membrane was increased for COPD patients in comparison to control subjects (P = 0.01). The present study provides evidence of neutrophil infiltration both in bronchial washing and bronchial epithelium of patients with COPD, suggesting that the source of neutrophils in airway lumen may be the bronchial mucosa. Although less common than in asthma, airways of COPD subjects reveal eosinophil presence and airway remodelling.

EGFR FISH can be reliably assessed on fine-needle aspirates obtained from NSCLC metastases. We found that EGFR gene copy number is discordant between primary NSCLC and the corresponding distant metastatic sites in a significant proportion of cases. These findings should be considered in future studies designed to elucidate the predictive role of EGFR FISH in NSCLC.

These data add to view that the efficacy of specific immunotherapy may be attributed to a modified cytokine secretion of CD4+ T cells.