An Increased Proportion of Apoptosis in CD4⁺ T Lymphocytes Isolated from the Peripheral Blood in Patients with Stable Chronic Obstructive Pulmonary Disease

Abstract

BackgroundThe pathophysiology of chronic obstructive pulmonary disease (COPD) includes inflammation, oxidative stress, an imbalance of proteases and antiproteases and apoptosis which has been focused on lately. Abnormal apoptotic events have been demonstrated in both epithelial and endothelial cells, as well as in inflammatory cells including neutrophils and lymphocytes in the lungs of COPD patients. An increased propensity of activated T lymphocytes to undergo apoptosis has been observed in the peripheral blood of COPD patients. Therefore, the apoptosis of T lymphocytes without activating them was investigated in this study.MethodsTwelve control subjects, 21 stable COPD patients and 15 exacerbated COPD patients were recruited in the study. The T lymphocytes were isolated from the peripheral blood using magnetically activated cell sorting. Apoptosis of the T lymphocytes was assessed with flow cytometry using Annexin V and 7-aminoactinomycin D. Apoptosis of T lymphocytes at 24 hours after the cell culture was measured so that the T lymphocyte apoptosis among the control and the COPD patients could be compared.ResultsStable COPD patients had increased rates of CD4+ T lymphocyte apoptosis at 24 hours after the cell culture, more than the CD4+ T lymphocyte apoptosis which appeared in the control group, while the COPD patients with acute exacerbation had an amplified response of CD4+ T lymphocyte apoptosis as well as of CD8+ T lymphocyte apoptosis at 24 hours after the cell culture.ConclusionStable COPD patients have more apoptosis of CD4+ T lymphocytes, which can be associated with the pathophysiology of COPD in stable conditions.

Defining the role of neutrophil-to-lymphocyte ratio in COPD: a systematic literature review

“… 47 On the other hand, some studies have found that CD4 + T lymphocytes participate in the amplification of the adaptive immune response. 48 In addition, they seem to play a role in the development of autoimmunity; 49 however, the clinical role of these data remains to be elucidated.…”

Serum YKL-40 Levels, Leukocyte Profiles, and Acute Exacerbations of Advanced COPD

“…Inflammation-induced recruitment/activation of inflammatory cells during AECOPDs can suppress lymphocyte activity [ 36 , 37 ], causing a decrease in lymphocyte-related blood parameters. It is also plausible that AECOPD-related systemic inflammation and oxidative stress can disrupt the normal functioning of bone marrow or accelerate lymphocyte apoptosis [ 38 , 39 ], leading to a reduction in lymphocyte production.…”

“…Selection bias occurs when the adjustment fails to address systematic differences between the adjusted groups, leading to biased estimates [ 51 ]. Since all biochemical analyses were performed for patients during the exacerbation periods, it is also plausible that their CBC profiles and YKL-40 levels were more deranged vs. stable periods [ 35 , 39 ]. As a result, the magnitude of changes in these parameters may be higher and hence more relevant to understanding the immunopathological connection between YKL-40 and CBC in COPD.…”

Cell Survival Failure in Effector T Cells From Patients With Systemic Lupus Erythematosus Following Insufficient Up‐Regulation of Cold‐Shock Y‐Box Binding Protein 1

“…Mechanisms that support T cell survival ensure efficient responsiveness to acute immune challenges and are required for the generation of T cell memory. Apoptosis, in return, serves to eliminate dysfunctional or infected T cells and is required to terminate immune response (1). Disturbed T cell homeostasis has been implicated in the pathogenesis of autoimmune diseases, such as systemic lupus erythematosus (SLE).…”