Effect of tobacco smoking on tissue protein citrullination and disease progression in patients with rheumatoid arthritis

AbstractThe aim of the present work was to study the effect of tobacco smoking on disease progression in rheumatoid arthritis patients and its relation to anti-cyclical citrullinated peptide (anti-CCP) antibodies. The study included 54 patients; 20 non-smokers, 9 ex-smokers, 14 mild to moderate smokers and 11 heavy smokers. Fifteen normal volunteers were also studied as controls. Disease stage was clinically and radiologically determined, rheumatoid factor (RF) and anti-CCP antibodies were measured in serum. Higher percentage of severe disease (stage III) was seen in heavy smoker patients than mild to moderate smokers (54.6% versus 35.7%) and in moderate smokers than ex-smokers (35.7% versus 33.6%). Lowest percentage of severe disease was seen in non-smokers (15%). RF and anti-CCP were significantly higher in smoker than non-smoker and in heavy than mild to moderate smoker patients (p<0.01, p<0.05 and p<0.01, p<0.001, respectively). In smoker patients, both RF and anti-CCP antibodies correlated significantly and positively with smoking index (r=0.581, p<0.001; r=0.661, p<0.001). Also, smoking index and anti-CCP correlated significantly and positively with disease stage (r=0.424, p<0.05; r=0.523, p<0.01). It appears from our results that, tobacco smoking mostly play a role in progression of rheumatoid arthritis through tissue protein citrullination. So all rheumatoid arthritis patients must quit completely to achieve a good control

Study of serum Granzyme B in heavy cigarette smokers with and without chronic obstructive pulmonary disease

Background: Inflammation of the airways is present in COPD with increased number of inflammatory cells including killer cells that lyse their target cells by two mechanisms; membranolysis in which secreted molecules such as granzymes form pores in the membrane of target cells; and apoptosis. Granzyme B has the strongest apoptotic activity of all granzymes. Aim of this work: Aim of this work was to study the relation between Granzyme B, tobacco smoking and chronic obstructive pulmonary disease. Methods: The study included 40 clinically stable COPD patients classified according to GOLD (2013) criteria into two groups; moderate (GOLD II) and severe (GOLD III) plus 40 apparently healthy control subjects (20 smokers and 20 nonsmokers). Pulmonary function results and serum levels of Granzyme B (measured by ELISA) were recorded. Results: Granzyme B levels are elevated in COPD. Cigarette smoking appears to be a direct stimulus to Granzyme B production. Granzyme B could play a role in the pathogenesis of COPD. Aging seems to be a risk factor for Granzyme B production and pathogenesis of COPD. Conclusion: Granzyme B levels are elevated in COPD. Cigarette smoking appears to be a direct stimulus to Granzyme B production. Granzyme B could play a role in the pathogenesis of COPD. Aging seems to be a risk factor for Granzyme B production and pathogenesis of COPD

Study of effect of inhaled versus oral corticosteroids on sputum granzyme B in patients with moderate persistent bronchial asthma

Background: Asthma is a major public health problem with a high economic burden. It involves several inflammatory cells and multiple mediators. Granzyme B is an inflammatory mediator expressed and secreted by both immune and non immune cells. Recently it was found to play a role in the pathogenesis of asthma. The aim of this work: was to evaluate the effect of both inhaled and oral corticosteroids on sputum granzyme B in asthmatic patients with moderate severity. Methods: The study included 25 patients with moderate persistent asthma plus 15 healthy subjects as a control group. Granzyme B was measured before treatment with corticosteroids then after inhalation therapy and oral therapy. Results: It was found that expected pulmonary function parameters were significantly lower in asthmatic patients than in controls. Sputum granzyme B levels were significantly higher in asthmatic patients than in controls. Sputum granzyme B levels were significantly lower after treatment with inhaled corticosteroids than basal levels. Oral corticosteroids further significantly lowered granzyme B, but the lowering effect of inhaled steroids was significantly higher than that of oral drugs. There was no statistically significant correlation between granzyme B and PFTs in asthmatic patients. Conclusion: Granzyme B levels are elevated in bronchial asthma. Granzyme B could play a role in the pathogenesis of bronchial asthma. Both inhaled and oral corticosteroids lowered granzyme B levels significantly. The lowering effect of inhaled corticosteroids on sputum granzyme B is more than that of the oral corticosteroids