Abstract
Many theories have been proposed to explain pathogenesis of COPD; however, remains unclear why the majority of smokers (~80%) do not develop COPD, or only develop a mild disease. To explore if COPD has an autoimmune component, the role of T regulatory lymphocytes (Tregs) in the lung tissue of COPD patients is of crucial importance. Bronchial tissue biopsy samples were prospectively collected from 64 patients (39 COPD and 25 controls - 15 smokers and 10 non-smokers). The patients with COPD were subdivided into mild/moderate (GOLD stage I-II) and severe/very severe (GOLD stage III-IV) groups. Digital image analysis was performed to estimate densities of CD4+ CD25+ cell infiltrates in double immunohistochemistry slides of the biopsy samples. Blood samples were collected from 42 patients (23 COPD and 19 controls) and tested for CD3+ CD4+ CD25+ bright lymphocytes by flow cytometry. The number of intraepithelial CD4+ CD25+ lymphocytes mm-2 epithelium was significantly lower in the severe/very severe COPD (GOLD III-IV) group as well as in the control non-smokers (NS) group (p < 0,0001). Likewise, the absolute number of Treg (CD3+ CD4+ CD25+ bright) cells in the peripheral blood samples was significantly different between the four groups (p = 0.032). The lowest quantity of Treg cells was detected in the severe/very severe COPD and healthy non-smokers groups. Our findings suggest that severe COPD is associated with lower levels of Tregs in the blood and bronchial mucosa, while higher Tregs levels in the smokers without COPD indicate potential protective effect of Tregs against developing COPD.
Highlights
Many theories have been proposed to explain pathogenesis of Chronic obstructive pulmonary disease (COPD); remains unclear why the majority of smokers (~80%) do not develop COPD, or only develop a mild disease
The intriguing clinical and pathological observations made over the past few years have led to a new concept: in susceptible individuals, cigarette-smoke exposure may trigger long-lasting inflammatory memory T-cell responses that can persist beyond the immediate period of exposure to cigarette smoke
It has been shown that T regulatory lymphocytes (Tregs) cells are important in the control of autoimmunity
Summary
Many theories have been proposed to explain pathogenesis of COPD; remains unclear why the majority of smokers (~80%) do not develop COPD, or only develop a mild disease. Material and methods: Bronchial tissue biopsy samples were prospectively collected from 64 patients (39 COPD and 25 controls — 15 smokers and 10 non-smokers). Blood samples were collected from 42 patients (23 COPD and 19 controls) and tested for CD3+ CD4+ CD25+ bright lymphocytes by flow cytometry. Results: The number of intraepithelial CD4+ CD25+ lymphocytes mm-2 epithelium was significantly lower in the severe/very severe COPD (GOLD III-IV) group as well as in the control non-smokers (NS) group (p < 0,0001). The absolute number of Treg (CD3+ CD4+ CD25+ ) bright cells in the peripheral blood samples was significantly different between the four groups (p = 0.032). The development of an adaptive immune response to a self-antigen, along with the eventual development of autoimmunity, would depend on the level of tolerance to the antigen: when tolerance is high, no adaptive inflammation would result; when there is no tolerance, a full adaptive immune reaction and autoimmunity would develop [2]
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