Differential activation of NFκB/RelA-p50 and NFκB/p50-p50 in control and alcohol-drinking rats subjected to carrageenin-induced pleurisy

Ashok K Singh, Yin Jiang

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

BACKGROUND: Carrageenin (CAR) injection into the pleural cavity causes local inflammation called carrageenin-induced pleurisy (CAR-IP). Inflammation onset is characterized by an activation of pro-inflammatory NFκB, RelA-p50, while inflammation resolution is characterized by an activation of an anti-inflammatory NFκB, p50-p50, that re-establishes homeostasis, an essential process for an organism's survival. Although chronic alcohol intake disrupts inflammation, the mechanism behind the development of inflammatory disorder in alcoholics is not yet known. Therefore, the aim of this investigation was to study the effects of ethanol intake on CAR-IP and NFκB activation in pleural fluid neutrophils in P rats. Methods: Alcohol-preferring, P rats were given free choice of alcohol (15% ethanol) and water or water alone (for control) for 15 days. Then, each rat was injected with 0.2 ml of 2% CAR into the pleural cavity under light ether anesthesia. At different time intervals after the CAR injection, rats were anesthetized and their blood and pleural fluid samples were collected. Pleural fluid inflammatory cells were identified with Turk's or Wright-Giemsa staining. Different cell types were sorted using a fluorescence-activated cell sorter. Pleural fluid neutrophils were examined for apoptosis and activation of the two NFκB subspecies. Results: In control rats, fluid began to accumulate in the pleural cavity 0.5 h after, which peaked 24 h after, CAR injection. Then, the values declined gradually. The increase in pleural fluid correlated with RelA-p50 activation, while the decline in pleural fluid correlated with p50-p50 activation and apoptosis in neutrophils. In alcohol-drinking rats, pleural fluid remained elevated for up to 6 days after CAR injection. Neutrophils from alcohol-drinking rats exhibited suppressed apoptosis, augmented RelA-p50 activation, and suppressed p50-p50 activation. Conclusions: Alcohol intake prolonged inflammation in P rats. An alcohol-induced upregulation of RelA-p50 activation and downregulation of p50-p50 activation may be causally related to the alcohol-induced inflammation dysregulation.

Original languageEnglish (US)
Pages (from-to)255-262
Number of pages8
JournalMediators of inflammation
Volume13
Issue number4
DOIs
StatePublished - Aug 1 2004

Fingerprint

Pleurisy
Carrageenan
Alcohol Drinking
Alcohols
Inflammation
Pleural Cavity
Neutrophils
Injections
Apoptosis
Ethanol
Water
Alcoholics
Ether
Homeostasis
Anti-Inflammatory Agents
Up-Regulation
Down-Regulation
Anesthesia
Fluorescence
Staining and Labeling

Keywords

  • Alcohol
  • Apoptosis, Neutrophils
  • Carrageenin
  • NFκB
  • RelA-p50
  • p50-p50

Cite this

@article{f68afe787560499ebd577ad28456b45e,
title = "Differential activation of NFκB/RelA-p50 and NFκB/p50-p50 in control and alcohol-drinking rats subjected to carrageenin-induced pleurisy",
abstract = "BACKGROUND: Carrageenin (CAR) injection into the pleural cavity causes local inflammation called carrageenin-induced pleurisy (CAR-IP). Inflammation onset is characterized by an activation of pro-inflammatory NFκB, RelA-p50, while inflammation resolution is characterized by an activation of an anti-inflammatory NFκB, p50-p50, that re-establishes homeostasis, an essential process for an organism's survival. Although chronic alcohol intake disrupts inflammation, the mechanism behind the development of inflammatory disorder in alcoholics is not yet known. Therefore, the aim of this investigation was to study the effects of ethanol intake on CAR-IP and NFκB activation in pleural fluid neutrophils in P rats. Methods: Alcohol-preferring, P rats were given free choice of alcohol (15{\%} ethanol) and water or water alone (for control) for 15 days. Then, each rat was injected with 0.2 ml of 2{\%} CAR into the pleural cavity under light ether anesthesia. At different time intervals after the CAR injection, rats were anesthetized and their blood and pleural fluid samples were collected. Pleural fluid inflammatory cells were identified with Turk's or Wright-Giemsa staining. Different cell types were sorted using a fluorescence-activated cell sorter. Pleural fluid neutrophils were examined for apoptosis and activation of the two NFκB subspecies. Results: In control rats, fluid began to accumulate in the pleural cavity 0.5 h after, which peaked 24 h after, CAR injection. Then, the values declined gradually. The increase in pleural fluid correlated with RelA-p50 activation, while the decline in pleural fluid correlated with p50-p50 activation and apoptosis in neutrophils. In alcohol-drinking rats, pleural fluid remained elevated for up to 6 days after CAR injection. Neutrophils from alcohol-drinking rats exhibited suppressed apoptosis, augmented RelA-p50 activation, and suppressed p50-p50 activation. Conclusions: Alcohol intake prolonged inflammation in P rats. An alcohol-induced upregulation of RelA-p50 activation and downregulation of p50-p50 activation may be causally related to the alcohol-induced inflammation dysregulation.",
keywords = "Alcohol, Apoptosis, Neutrophils, Carrageenin, NFκB, RelA-p50, p50-p50",
author = "Singh, {Ashok K} and Yin Jiang",
year = "2004",
month = "8",
day = "1",
doi = "10.1080/09629350400003035",
language = "English (US)",
volume = "13",
pages = "255--262",
journal = "Mediators of Inflammation",
issn = "0962-9351",
publisher = "Hindawi Publishing Corporation",
number = "4",

}

TY - JOUR

T1 - Differential activation of NFκB/RelA-p50 and NFκB/p50-p50 in control and alcohol-drinking rats subjected to carrageenin-induced pleurisy

AU - Singh, Ashok K

AU - Jiang, Yin

PY - 2004/8/1

Y1 - 2004/8/1

N2 - BACKGROUND: Carrageenin (CAR) injection into the pleural cavity causes local inflammation called carrageenin-induced pleurisy (CAR-IP). Inflammation onset is characterized by an activation of pro-inflammatory NFκB, RelA-p50, while inflammation resolution is characterized by an activation of an anti-inflammatory NFκB, p50-p50, that re-establishes homeostasis, an essential process for an organism's survival. Although chronic alcohol intake disrupts inflammation, the mechanism behind the development of inflammatory disorder in alcoholics is not yet known. Therefore, the aim of this investigation was to study the effects of ethanol intake on CAR-IP and NFκB activation in pleural fluid neutrophils in P rats. Methods: Alcohol-preferring, P rats were given free choice of alcohol (15% ethanol) and water or water alone (for control) for 15 days. Then, each rat was injected with 0.2 ml of 2% CAR into the pleural cavity under light ether anesthesia. At different time intervals after the CAR injection, rats were anesthetized and their blood and pleural fluid samples were collected. Pleural fluid inflammatory cells were identified with Turk's or Wright-Giemsa staining. Different cell types were sorted using a fluorescence-activated cell sorter. Pleural fluid neutrophils were examined for apoptosis and activation of the two NFκB subspecies. Results: In control rats, fluid began to accumulate in the pleural cavity 0.5 h after, which peaked 24 h after, CAR injection. Then, the values declined gradually. The increase in pleural fluid correlated with RelA-p50 activation, while the decline in pleural fluid correlated with p50-p50 activation and apoptosis in neutrophils. In alcohol-drinking rats, pleural fluid remained elevated for up to 6 days after CAR injection. Neutrophils from alcohol-drinking rats exhibited suppressed apoptosis, augmented RelA-p50 activation, and suppressed p50-p50 activation. Conclusions: Alcohol intake prolonged inflammation in P rats. An alcohol-induced upregulation of RelA-p50 activation and downregulation of p50-p50 activation may be causally related to the alcohol-induced inflammation dysregulation.

AB - BACKGROUND: Carrageenin (CAR) injection into the pleural cavity causes local inflammation called carrageenin-induced pleurisy (CAR-IP). Inflammation onset is characterized by an activation of pro-inflammatory NFκB, RelA-p50, while inflammation resolution is characterized by an activation of an anti-inflammatory NFκB, p50-p50, that re-establishes homeostasis, an essential process for an organism's survival. Although chronic alcohol intake disrupts inflammation, the mechanism behind the development of inflammatory disorder in alcoholics is not yet known. Therefore, the aim of this investigation was to study the effects of ethanol intake on CAR-IP and NFκB activation in pleural fluid neutrophils in P rats. Methods: Alcohol-preferring, P rats were given free choice of alcohol (15% ethanol) and water or water alone (for control) for 15 days. Then, each rat was injected with 0.2 ml of 2% CAR into the pleural cavity under light ether anesthesia. At different time intervals after the CAR injection, rats were anesthetized and their blood and pleural fluid samples were collected. Pleural fluid inflammatory cells were identified with Turk's or Wright-Giemsa staining. Different cell types were sorted using a fluorescence-activated cell sorter. Pleural fluid neutrophils were examined for apoptosis and activation of the two NFκB subspecies. Results: In control rats, fluid began to accumulate in the pleural cavity 0.5 h after, which peaked 24 h after, CAR injection. Then, the values declined gradually. The increase in pleural fluid correlated with RelA-p50 activation, while the decline in pleural fluid correlated with p50-p50 activation and apoptosis in neutrophils. In alcohol-drinking rats, pleural fluid remained elevated for up to 6 days after CAR injection. Neutrophils from alcohol-drinking rats exhibited suppressed apoptosis, augmented RelA-p50 activation, and suppressed p50-p50 activation. Conclusions: Alcohol intake prolonged inflammation in P rats. An alcohol-induced upregulation of RelA-p50 activation and downregulation of p50-p50 activation may be causally related to the alcohol-induced inflammation dysregulation.

KW - Alcohol

KW - Apoptosis, Neutrophils

KW - Carrageenin

KW - NFκB

KW - RelA-p50

KW - p50-p50

UR - http://www.scopus.com/inward/record.url?scp=9644252657&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=9644252657&partnerID=8YFLogxK

U2 - 10.1080/09629350400003035

DO - 10.1080/09629350400003035

M3 - Article

VL - 13

SP - 255

EP - 262

JO - Mediators of Inflammation

JF - Mediators of Inflammation

SN - 0962-9351

IS - 4

ER -