The strong correlation between ADAM33 expression and airway inflammation in chronic obstructive pulmonary disease and candidate for biomarker and treatment of COPD

Abstract

Airway inflammation in patients with chronic obstructive pulmonary disease (COPD) is an amplified response of the normal immune system that occurs as a result of chronic irritation by toxic substances, such as cigarette smoke. This leads to the characteristic pathological changes in the inflammatory cells of COPD patients. ADAM33 has been reported to be involved in the pathogenesis of COPD in East Asia by affecting airway inflammation and other immune responses. The aim of this study was to determine the potential role of ADAM33 (mRNA and soluble levels) as a biomarker of inflammation in COPD patients. This is a case control study using consecutive sampling. The COPD case and control (non-COPD) groups comprised 37 and 29 patients, respectively. We used univariate analysis to assess differences in the parameters between the groups and bivariate analysis to non-parametrically compare these parameters between the two groups. We observed significantly higher mRNA levels of ADAM33 in the COPD patients (10.39 ± 1.76) as compared to that in the non-COPD individuals (6.93 ± 0.39; P < 0.001). The levels of soluble ADAM33 were also significantly higher in the COPD patients (2.188 ± 1.142 ng/ml) compared to the non-COPD individuals (0.487 ± 0.105 ng/ml; P < 0.001). The mRNA and soluble ADAM33 levels were significantly higher in COPD patients compared to those in the parameter-matched non-COPD individuals. Thus, ADAM33 is a potential biomarker and treatment for inflammation in COPD patients.

Heparin for patients with coronavirus disease 2019 and hypercoagulation complications: A cohort study

“…COVID-19 can predispose patients to both venous and arterial thromboembolic disease due to the activation of coagulation caused by excessive inflammation, activation of platelets, endothelial dysfunction, and stasis of blood flow related to immobility. Indications of disease severity and the establishment of coagulopathy may vary; these indications include increased D-dimer, thrombocytopenia, elevated D-dimer levels, and prolonged PT and aPTT [ 7 , 8 , [11] , [12] , [13] ].…”

“…Typical imaging findings include bilateral ground-glass opacities, as well as bilateral multiple lobular and subsegmental areas of consolidation. In severe cases, complications include respiratory failure, septic shock, and multiple organ failure [ [4] , [5] , [6] , [7] , [8] ].…”

“…COVID-19 causes patients to enter a hypercoagulable state, but the pathophysiology behind the thrombotic complications observed in this disease is still not well understood. Several mechanisms have been proposed, such as the host immune response, which contributes to vascular endothelial cell injury, inflammation, activation of the coagulation cascade through tissue factor expression, and cessation of fibrinolysis [ [4] , [5] , [6] , [7] , [8] ].…”

“…Heparin is also known to have a suppressive effect on the expression of interleukin (IL)-6 and IL-8 in lung epithelial cells, which may help reduce the thrombotic complications associated with the host immune response to COVID-19. LMWH (fondaparinux) is an indirect factor Xa inhibitor, but LMWH (fondaparinux) does not inhibit thrombin at all, which is why LMWH (fondaparinux) is better for preventing heparin-induced thrombocytopenia [ 4 , 5 , [7] , [8] , [9] ]. The aim of this study was to compare the effectiveness of unfractionated heparin (UFH) and LMWH (fondaparinux) in hospitalised COVID-19 patients with hypercoagulable complications.…”

IL-17A Promotes Epithelial ADAM9 Expression in Cigarette Smoke-Related COPD

“…A variety of proteases, such as serine proteinases, cysteine proteinases, and matrix metalloproteases (MMPs), have been reported to participate in the development of emphysema, 3 whereas a disintegrin and metalloproteinases (ADAMs), such as ADAM8, 4 ADAM9, 5 , 6 ADAM15, 7 and ADAM33, 8 as a less studied subgroup of metalloproteinases, were found to be involved in COPD pathogenesis in recent years. ADAMs are type I transmembrane proteins containing six important domains, among which the metalloproteinase and disintegrin domains endow them with proteolytic and adhesive functions, respectively.…”