Effect of capsaicin on phagocytic activity of peripheral blood monocytes in patients with chronic obstructive pulmonary disease

   Introduction. Chronic obstructive pulmonary disease (COPD) is a common disorder and the third leading cause of death globally. It may be characterized by impaired phagocytosis and efferocytosis, which contributes to chronic nflammation and increases the risk of bacterial respiratory infections. Previously, we established hyperexpression of TRPV1 channels in monocytes and macrophages of patients with COPD.

   Aim. To study the phagocytic activity of monocytes in patients with COPD and to evaluate the effect of the TRPV1 agonist capsaicin on the efficiency of phagocytosis in vitro.

   Materials and methods. The study included 42 patients with COPD of varying severity and 11 control subjects. Phagocytic activity of monocytes was tested by flow cytometry using competent E. coli XL1-Blue cells transformed with pTurboGFP-B plasmid.

   Results. The results of the study showed no statistically significant differences in the initial phagocytic activity of monocytes between patients with COPD and healthy volunteers (78.6 (73.4–87.4) % vs. 84.8 (65.6–88.3) %, p = 0.77). Exposure to capsaicin caused significant inhibition of E. coli phagocytosis in both groups: in COPD patients (from 78.6 (73.4–87.4) % to 64.4 (55.9–71.8) %, p < 0.001) and in the control group (from 84.8 (65.6–88.3) % to 71.4 (65.7–74.0) %, p < 0.01). Moreover, the degree of phagocytosis suppression under the influence of capsaicin was higher in COPD patients compared to the control (–17.5 (–24.9; –13.1)% vs. –9.4 (–16.4; –3.3)%, p = 0.03). However, after exposure to capsaicin, there were also no significant differences in the level of phagocytosis between the study groups.

   Conclusion. Thus, our data indicate that monocytes from COPD patients do not exhibit significant abnormalities in phagocytic activity in vitro. Stimulation of TRPV1 with capsaicin results in statistically significant inhibition of E. coli phagocytosis in both groups, with a more pronounced decrease observed in COPD, which confirms the role of this receptor in modulating the immune functions of monocytes, given the increased expression of TRPV1 and the presence of endogenous activating stimuli..

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