Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory disease that causes obstruction of air flow in the lungs. One of the main causes of COPD is cigarette smoke. Molecular mechanisms in the background are a classic combination of innate immunity and adaptive immunity. Pro-inflammatory cytokines and oxidative stress also play an important role. Such response can lead to cell death. Different types of cell death can be differentiated, but in this case the most relevant ones are apoptosis, necrosis and necroptosis. Heath shock proteins play an important role in modifying cell death. LPS (lipopolysaccharides) and LTA (lipoteicoic acid), as structural components of bacteria, behave as PAMPs (pathogen associated molecular patterns) and may modulate cell death via TLRs (Toll-like receptors). The aim of this study was to establish if the treatment of 16HBE cells with extracellular Hsp70, CSE (cigarette smoke extract), LPS, LTA or their combinations leads to cell death, that was quantified by the measurement of caspases activities. The measurement of the activities of caspases -3/-7 , -8 and -9 was done with the use of commercial kits that contain specific luminogenic substrats for these caspases. The measured luminescence is proportional to the activity of caspases. The activity was measured after a two hour treatment and after an eight hour treatment. The results imply that after the treatment of 16HBE cells with eHsp70, CSE, LPS, LTA and their combinations after 2 hours or 8 hours there were no significant increases of cells in apoptosis when compared to untreated cells. The only result that was statistically significantly different was that after a two hour treatment, a combination of 15% CSE and 1 μg/mL Hsp70 significantly increased an activity of caspases-3/7 in 16HBE cells when compared to the treatment with 15% CSE only. However, in the samples of 16HBE cells treated with 15% CSE during 2 hours, there was a significant drop in the activity of caspase-8 and caspase-9 when compared to untreated cells. The drop in the activity of caspaze-8 can implicate that exposure to high concentrations of CSE lead to an alternative type of cell death (inactivation of caspase-8 may lead to necroptosis). From the results of this study, we can conclude that exposure of bronchial epithelial cells 16HBE to extracellular Hsp70, CSE, LPS, LTA or their combinations mostly does not lead to activation of caspases-3/7, -8 or -9 and apoptosis in general. The results of this work could be completed by measuring the markers of other types of cell death (such as necrosis or necroptosis). That would make even better comparison to results of the already conducted experiments. Better comparisons are crucial for making new, more appropriate conclusions about what might be the cause of lung structure loss in COPD patients, and possibly even a discovery of new drug targets.