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Matrix metalloproteinases (MMPs) and A disintegrin and metalloproteinases (ADAMs) are enzymes able to degrade a variety of protein components of the extracellular matrix. Due to the diverse role of MMPs and ADAMs, they are involved in the pathogenesis of many diseases, including chronic inflammatory lung diseases. In this review, the objective is to summarize the current knowledge about the role of the two enzymes from the respective families, namely MMP-8 and ADAM-33, in Bronchial asthma in order to explore the possibility for their expression, polymorphisms or serum/BAL (Bronchoalveolar Lavage) concentration to be used as biomarkers or targets for future target therapy. Considering the key functions of MMP-8 and ADAM-33 in many pathologic conditions, development of proper inhibitors of their action might be useful tools in the treatment approaches. However, a lot of knowledge has yet to be gained about these enzymes and their role in bronchial asthma, since some of the mechanisms are unknown or not discovered yet. [ABSTRACT FROM AUTHOR]

Background and Objectives: One of the members of the neurotrophin (NT) family is the brain-derived neurotrophic factor (BDNF). In addition to its role in the nerve system, it has been found to play a role in lung health and diseases. Materials and Methods: The serum concentrations of BDNF were assessed in 57 patients with COPD and in 19 control individuals and the possible associations of BDNF with the spirometric indexes and disease stages were explored. Results: We did not find a significant difference between the serum concentrations of BDNF of patients and controls (p = 0.521). A significant negative correlation of the serum BDNF levels with the age of the patients (Rho = −0.279, p = 0.036) was observed. In addition, a borderline negative correlation with the age of disease onset (Rho= −0.244, p = 0.063) was also found. When analyzing these correlations in different genders, we found stronger statistical significance in male patients (Rho = −0.398, p = 0.009; and Rho = −0.419, p = 0.006), while no such significance was found in females (p = 0.574 and p = 0.342). The analyses of the possible relations of serum BDNF concentration with the spirometric parameters in the whole group of patients did not reveal any significance (p = 0.231 for FEV1%pr. and p = 0.271 for FEV1/FVC%). However, when the patients were dichotomized on the basis of smoking habits, we obtained a strong positive correlation between BDNF and FEV1%pr. (Rho = 0.501, p = 0.048) in non-smokers, but strong negative correlations with FEV1%pr. (Rho = −0.468, p = 0.003) and with FEV1/FVC% (Rho = −0.331, p = 0.040) in ex/current smokers. Non-smokers with moderate disease (GOLD II) had higher BDNF serum concentrations than patients with GOLD stage III/IV (p = 0.031). In ex/current smokers, there was an opposite association (p = 0.045). Conclusions: The results of our study suggest that the expression and secretion of BDNF are changed in COPD, but its effects and functions may differ according to the smoking history of the patients. [ABSTRACT FROM AUTHOR]