Chest
Original Research: COPDTreatment With AM3 Restores Defective T-Cell Function in COPD Patients
Section snippets
Study Subjects
Seventy patients with COPD were randomized to receive AM3 (n = 35) or an indistinguishable placebo (n = 35). Subject characteristics are shown in Table 1. All subjects received extensive information about the study and gave informed, witnessed consent to participate. Neither patients nor control subjects were unavailable for follow-up.
Two groups of age- and sex-matched control subjects were included for immunologic comparison: one group was comprised of 36 healthy nonsmokers (mean age, 61 ± 8
PBMCs From COPD Patients Show Defects in Proliferation and IFN-γ Production in Response to T-Lymphocyte Mitogens
The proliferative response of PBMCs from COPD patients, as well as those of nonsmoker and ex-smoker healthy control subjects, to stimulation with phytohemagglutinin and anti-CD3 monoclonal antibodies was investigated. The kinetics of the proliferative response of PBMCs to the mitogens were analyzed at 3 days, 5 days, and 7 days of culture. The maximum response was found at 5 days of culture for both sets of control subjects and patients (data not shown); this culture period was therefore used
Discussion
This article shows that COPD patients have a defective PBMC proliferative response to polyclonal T-lymphocyte mitogens and that the percentage of CD4 and CD8 T-lymphocytes producing IFN-γ is reduced compared to nonsmoker and ex-smoker healthy subjects. The treatment with the immunomodulator AM3 is able to restore these defects.
We and others8, 11, 16 have previously reported decreased natural killer cell activity and impaired monocyte and polymorphonuclear chemotactic and phagocytic activities
ACKNOWLEDGMENT
The placebo and AM3 used in this study were provided by the manufacturer (I. F. Cantabria; Madrid, Spain). The authors thank the Immune System Involvement in Respiratory Disease Research Group (J. Jareño, Hospital Del Aire, Madrid; J. M. Rodriguez, Hospital Universitario Gregorio Marañon, Madrid; M. Calle, Hospital Universitario Clinico San Carlos, Madrid; J.L. Izquierdo, Pulmonary Unit, Hospital General Universitario, Guadalajara; and E. Sanz, Department of Medicine, University of Alcalá,
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2021, Experimental GerontologyCitation Excerpt :Regarding the proliferation of lymphocytes, a typical activity of the acquired immunity, in response to the T cell stimulator PHA, its values were lower in both groups of patients in comparison to controls. In this respect, an increased propensity to undergo apoptosis of T cells has been described in COPD patients (Hodge et al., 2003), which could affect the proliferation capacity of these cells (Reyes et al., 2006). The higher values of adhesion, and lower phagocytosis, proliferation capacity, and Natural Killer cytotoxic activity of leukocytes in COPD patients, especially those at severe stage, could be indicative of accelerated immunosenescence in comparison to the age-matched control group.
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2008, Respiratory MedicineCitation Excerpt :CD8 T-cells also use IFN-γ as an antiviral effector moiety.15–17 It has been documented that percentage of T-cells secreting IFN-γ is reduced in both CD4 and CD8 subsets in COPD patients, compared to non-smoker and ex-smoker healthy control subjects.18 In vitro bacterial extracts exert immunomodulatory action via modulation of the signal transducer gp130 and gp130 binding cytokines, including IL-6 and IL-11.19
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All of the data acquisition and analyses were completed in the Department of Medicine, Alcal´ University.
This work was partially supported by grants from the Ministerio de Ciencía y Tecnología (FIT-2003–090000–0105, SAF-2004–08138), the Instituto de Salud Carlos III (PI021909 and GO3/075) and the Chronic Inflammatory Disease Group of Castilla-La Mancha, Spain.
Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestjournal.org/misc/reprints.shtml).