Interrelated role of cigarette smoking, oxidative stress, and immune response in COPD and corresponding treatments

Li Zuo, Feng He, Georgianna G. Sergakis, Majid S. Koozehchian, Julia N. Stimpfl, Yi Rong, Philip T. Diaz, Thomas M. Best

Research output: Contribution to journalReview article

95 Citations (Scopus)

Abstract

Cigarette smoking (CS) can impact the immune system and induce pulmonary disorders such as chronic obstructive pulmonary disease (COPD), which is currently the fourth leading cause of chronic morbidity and mortality worldwide. Accordingly, the most significant risk factor associated with COPD is exposure to cigarette smoke. The purpose of the present study is to provide an updated overview of the literature regarding the effect of CS on the immune system and lungs, the mechanism of CS-induced COPD and oxidative stress, as well as the available and potential treatment options for CS-induced COPD. An extensive literature search was conducted on the PubMed/Medline databases to review current COPD treatment research, available in the English language, dating from 1976 to 2014. Studies have investigated the mechanism by which CS elicits detrimental effects on the immune system and pulmonary function through the use of human and animal subjects. A strong relationship among continued tobacco use, oxidative stress, and exacerbation of COPD symptoms is frequently observed in COPD subjects. In addition, therapeutic approaches emphasizing smoking cessation have been developed, incorporating counseling and nicotine replacement therapy. However, the inability to reverse COPD progression establishes the need for improved preventative and therapeutic strategies, such as a combination of intensive smoking cessation treatment and pharmaceutical therapy, focusing on immune homeostasis and redox balance. CS initiates a complex interplay between oxidative stress and the immune response in COPD. Therefore, multiple approaches such as smoking cessation, counseling, and pharmaceutical therapies targeting inflammation and oxidative stress are recommended for COPD treatment.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Volume307
Issue number3
DOIs
StatePublished - Jan 1 2014
Externally publishedYes

Fingerprint

Chronic Obstructive Pulmonary Disease
Oxidative Stress
Smoking
Smoking Cessation
Therapeutics
Immune System
Lung
Counseling
Withholding Treatment
Tobacco Use
Nicotine
PubMed
Smoke
Tobacco Products
Pharmaceutical Preparations
Oxidation-Reduction
Disease Progression
Homeostasis
Language
Databases

Keywords

  • Antioxidant
  • Inflammation
  • Reactive oxygen species
  • Smoking cessation

ASJC Scopus subject areas

  • Physiology
  • Pulmonary and Respiratory Medicine
  • Cell Biology
  • Physiology (medical)

Cite this

Interrelated role of cigarette smoking, oxidative stress, and immune response in COPD and corresponding treatments. / Zuo, Li; He, Feng; Sergakis, Georgianna G.; Koozehchian, Majid S.; Stimpfl, Julia N.; Rong, Yi; Diaz, Philip T.; Best, Thomas M.

In: American Journal of Physiology - Lung Cellular and Molecular Physiology, Vol. 307, No. 3, 01.01.2014.

Research output: Contribution to journalReview article

Zuo, Li ; He, Feng ; Sergakis, Georgianna G. ; Koozehchian, Majid S. ; Stimpfl, Julia N. ; Rong, Yi ; Diaz, Philip T. ; Best, Thomas M. / Interrelated role of cigarette smoking, oxidative stress, and immune response in COPD and corresponding treatments. In: American Journal of Physiology - Lung Cellular and Molecular Physiology. 2014 ; Vol. 307, No. 3.
@article{296be80dfd3c4748971997e5abb7d79a,
title = "Interrelated role of cigarette smoking, oxidative stress, and immune response in COPD and corresponding treatments",
abstract = "Cigarette smoking (CS) can impact the immune system and induce pulmonary disorders such as chronic obstructive pulmonary disease (COPD), which is currently the fourth leading cause of chronic morbidity and mortality worldwide. Accordingly, the most significant risk factor associated with COPD is exposure to cigarette smoke. The purpose of the present study is to provide an updated overview of the literature regarding the effect of CS on the immune system and lungs, the mechanism of CS-induced COPD and oxidative stress, as well as the available and potential treatment options for CS-induced COPD. An extensive literature search was conducted on the PubMed/Medline databases to review current COPD treatment research, available in the English language, dating from 1976 to 2014. Studies have investigated the mechanism by which CS elicits detrimental effects on the immune system and pulmonary function through the use of human and animal subjects. A strong relationship among continued tobacco use, oxidative stress, and exacerbation of COPD symptoms is frequently observed in COPD subjects. In addition, therapeutic approaches emphasizing smoking cessation have been developed, incorporating counseling and nicotine replacement therapy. However, the inability to reverse COPD progression establishes the need for improved preventative and therapeutic strategies, such as a combination of intensive smoking cessation treatment and pharmaceutical therapy, focusing on immune homeostasis and redox balance. CS initiates a complex interplay between oxidative stress and the immune response in COPD. Therefore, multiple approaches such as smoking cessation, counseling, and pharmaceutical therapies targeting inflammation and oxidative stress are recommended for COPD treatment.",
keywords = "Antioxidant, Inflammation, Reactive oxygen species, Smoking cessation",
author = "Li Zuo and Feng He and Sergakis, {Georgianna G.} and Koozehchian, {Majid S.} and Stimpfl, {Julia N.} and Yi Rong and Diaz, {Philip T.} and Best, {Thomas M.}",
year = "2014",
month = "1",
day = "1",
doi = "10.1152/ajplung.00330.2013",
language = "English (US)",
volume = "307",
journal = "American Journal of Physiology",
issn = "1040-0605",
publisher = "American Physiological Society",
number = "3",

}

TY - JOUR

T1 - Interrelated role of cigarette smoking, oxidative stress, and immune response in COPD and corresponding treatments

AU - Zuo, Li

AU - He, Feng

AU - Sergakis, Georgianna G.

AU - Koozehchian, Majid S.

AU - Stimpfl, Julia N.

AU - Rong, Yi

AU - Diaz, Philip T.

AU - Best, Thomas M.

PY - 2014/1/1

Y1 - 2014/1/1

N2 - Cigarette smoking (CS) can impact the immune system and induce pulmonary disorders such as chronic obstructive pulmonary disease (COPD), which is currently the fourth leading cause of chronic morbidity and mortality worldwide. Accordingly, the most significant risk factor associated with COPD is exposure to cigarette smoke. The purpose of the present study is to provide an updated overview of the literature regarding the effect of CS on the immune system and lungs, the mechanism of CS-induced COPD and oxidative stress, as well as the available and potential treatment options for CS-induced COPD. An extensive literature search was conducted on the PubMed/Medline databases to review current COPD treatment research, available in the English language, dating from 1976 to 2014. Studies have investigated the mechanism by which CS elicits detrimental effects on the immune system and pulmonary function through the use of human and animal subjects. A strong relationship among continued tobacco use, oxidative stress, and exacerbation of COPD symptoms is frequently observed in COPD subjects. In addition, therapeutic approaches emphasizing smoking cessation have been developed, incorporating counseling and nicotine replacement therapy. However, the inability to reverse COPD progression establishes the need for improved preventative and therapeutic strategies, such as a combination of intensive smoking cessation treatment and pharmaceutical therapy, focusing on immune homeostasis and redox balance. CS initiates a complex interplay between oxidative stress and the immune response in COPD. Therefore, multiple approaches such as smoking cessation, counseling, and pharmaceutical therapies targeting inflammation and oxidative stress are recommended for COPD treatment.

AB - Cigarette smoking (CS) can impact the immune system and induce pulmonary disorders such as chronic obstructive pulmonary disease (COPD), which is currently the fourth leading cause of chronic morbidity and mortality worldwide. Accordingly, the most significant risk factor associated with COPD is exposure to cigarette smoke. The purpose of the present study is to provide an updated overview of the literature regarding the effect of CS on the immune system and lungs, the mechanism of CS-induced COPD and oxidative stress, as well as the available and potential treatment options for CS-induced COPD. An extensive literature search was conducted on the PubMed/Medline databases to review current COPD treatment research, available in the English language, dating from 1976 to 2014. Studies have investigated the mechanism by which CS elicits detrimental effects on the immune system and pulmonary function through the use of human and animal subjects. A strong relationship among continued tobacco use, oxidative stress, and exacerbation of COPD symptoms is frequently observed in COPD subjects. In addition, therapeutic approaches emphasizing smoking cessation have been developed, incorporating counseling and nicotine replacement therapy. However, the inability to reverse COPD progression establishes the need for improved preventative and therapeutic strategies, such as a combination of intensive smoking cessation treatment and pharmaceutical therapy, focusing on immune homeostasis and redox balance. CS initiates a complex interplay between oxidative stress and the immune response in COPD. Therefore, multiple approaches such as smoking cessation, counseling, and pharmaceutical therapies targeting inflammation and oxidative stress are recommended for COPD treatment.

KW - Antioxidant

KW - Inflammation

KW - Reactive oxygen species

KW - Smoking cessation

UR - http://www.scopus.com/inward/record.url?scp=84905274836&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84905274836&partnerID=8YFLogxK

U2 - 10.1152/ajplung.00330.2013

DO - 10.1152/ajplung.00330.2013

M3 - Review article

C2 - 24879054

AN - SCOPUS:84905274836

VL - 307

JO - American Journal of Physiology

JF - American Journal of Physiology

SN - 1040-0605

IS - 3

ER -