Chronic obstructive pulmonary disease (COPD) is one of the leading causes of death in the world and represents a major public health challenge. Cigarette smoking is the most common environmental risk factor for developing COPD. Given the fact that it is diagnosed at a relatively late stage of the disease, the question of potential earlier markers of the disease arises. Cigarette smoke can cause damage to resident cells in the lungs, leading to the release of various damage associated molecular patterns (DAMP molecules or alarmins) in the extracellular space, which can be measured in body fluids. It has been shown that the release of a DAMP molecules by cigarette smoke can lead to inappropriate inflammatory reactions such as those expressed in COPD patients. This diploma thesis provides an overview of the latest findings on DAMP molecules as inflammatory mediators in patients with COPD, and their values in serum / plasma / BAL fluid / sputum / urine were found significantly different from those in a healthy smokers, or non-smokers. Some of these alarmins (HSP27, HSP70, S100 proteins, galectins, LL-37, uric acid, HMGB1, mtDNA and eATP) show correlation with different lung function parameters and disease severity, as well as with serum biomarkers for the assessment of COPD exacerbations and comorbidities. Furthermore, calprotectin may serve as a valuable biomarker for differentiating COPD and asthma, while S100A8 is a biomarker for differentiating COPD and asthma-COPD overlap syndrome. In the future, patient classification could be facilitated as some DAMP molecules can differentiate each group of patients according to GOLD ABCD classification (severity of symptoms and history of exacerbation) as well as only according to GOLD stages (grade 2-4), but further studies are needed to validate these findings.