Publication: Aberrant neutrophil function among heavy smokers and chronic obstructive pulmonary disease patients
Issued Date
2016-12-01
Resource Type
ISSN
22288694
0125877X
0125877X
DOI
Other identifier(s)
2-s2.0-85008474199
Rights
Mahidol University
Rights Holder(s)
SCOPUS
Bibliographic Citation
Asian Pacific Journal of Allergy and Immunology. Vol.34, No.4 (2016), 278-283
Suggested Citation
Jiraporn Jaroenpool, Kovit Pattanapanyasat, Naiyana Noonin, Issara Prachongsai Aberrant neutrophil function among heavy smokers and chronic obstructive pulmonary disease patients. Asian Pacific Journal of Allergy and Immunology. Vol.34, No.4 (2016), 278-283. doi:10.12932/AP0724 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/40785
Research Projects
Organizational Units
Authors
Journal Issue
Thesis
Title
Aberrant neutrophil function among heavy smokers and chronic obstructive pulmonary disease patients
Other Contributor(s)
Abstract
© 2016, Allergy and Immunology Society of Thailand. All rights reserved. Background: Chronic Obstructive Pulmonary Disease (COPD) is a chronic inflammation disease of the respiratory tract. The aberrant functions of neutrophils has been reported in COPD patients including respiratory burst and phagocytosis. Unfortunately, there is little evidence of neutrophil functions in healthy smokers who are considered a high risk group for COPD. Objective: To determine the alteration of leukocytic parameters, intracellular reactive oxygen species (ROS) levels and phagocytosis percentages among smokers and COPD. Method: Sixteen smokers, 17 COPD patients and 10 healthy controls were recruited. The informed consent and recruitment process were ethically approved by the WU-IRB committee. Leukocyte percentages were analyzed by automated cell counter. Polymorphonuclear cells were purified by gradient centrifugation. The cell suspensions were incubated with FITC-conjugated bacteria to allow phagocytosis. Dichlorofluorescin diacetate was loaded to the cells followed by porbol-12-myristyl acetate stimulation to generate ROS. The percentages of phagocytosis and intracellularROS levels were analyzed using flow cytometry. Mean of leukocyte numbers, mean fluorescence intensities and phagocytosis percentages were compared by t-test using SPSS (version 17). Results: An increased ROS level of circulating neutrophils was observed among heavy smokers and COPD (p<0.05) compared to healthy controls. There was concordance to neutrophil percentages. However, the function on phagocytosis of neutrophils was not abolished in any group of smokers except COPD. Conclusions: Our findings suggested that the elevation of intracellular ROS generated by circulating neutrophils resulted in pools of inflammatory mediators among heavy smokers, which was suspected as one of the factors causing COPD in high risk people.