PMID- 17760509
OWN - NLM
STAT- MEDLINE
DCOM- 20071207
LR  - 20220309
IS  - 1523-0864 (Print)
IS  - 1523-0864 (Linking)
VI  - 9
IP  - 11
DP  - 2007 Nov
TI  - Role of oxidants in lung injury during sepsis.
PG  - 1991-2002
AB  - The role of oxidative stress has been well appreciated in the development of 
      sepsis-induced acute lung injury (ALI). Oxidative stress in sepsis-induced ALI is 
      believed to be initiated by products of activated lung macrophages and 
      infiltrated neutrophils, promptly propagating to lung epithelial and endothelial 
      cells. This leads to tissue damage and organ dysfunction. On stimulation, 
      neutrophils (PMNs) enable their migration machinery. The lung undergoes changes 
      favoring adhesion and transmigration of PMNs, resulting in PMN accumulation in 
      lung, which is a characteristic of sepsis-induced ALI. Oxidative stress turns on 
      the redox-sensitive transcription factors (NF-kappaB, AP-1), resulting in a large 
      output of proinflammatory cytokines and chemokines, which further aggravate 
      inflammation and oxidative stress. During the process, transcription factor 
      nuclear factor-erythroid 2-p45-related factor 2 (Nrf2) and heme oxygenase (HO) 
      appear to play the counterbalancing roles to limit the propagation of oxidative 
      stress and inflammatory responses in lung. Many antioxidants have been tested to 
      treat sepsis-induced ALI in animal models and in patients with sepsis. However, 
      the results are inconclusive. In this article, we focus on the current 
      understanding of the pathogenesis of sepsis-induced ALI and novel antioxidant 
      strategies for therapeutic purposes.
FAU - Guo, Ren-Feng
AU  - Guo RF
AD  - Department of Pathology, University of Michigan Medical School, Ann Arbor, 
      Michigan 48109-0602, USA. grf@med.umich.edu
FAU - Ward, Peter A
AU  - Ward PA
LA  - eng
GR  - GM-02507/GM/NIGMS NIH HHS/United States
GR  - GM-61656/GM/NIGMS NIH HHS/United States
GR  - HL-31963/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Review
PL  - United States
TA  - Antioxid Redox Signal
JT  - Antioxidants & redox signaling
JID - 100888899
RN  - 0 (Antioxidants)
RN  - 0 (Inflammation Mediators)
RN  - 0 (NF-E2-Related Factor 2)
RN  - 0 (NF-kappa B)
RN  - 0 (NFE2L2 protein, human)
RN  - 0 (Oxidants)
RN  - 0 (Transcription Factor AP-1)
RN  - EC 1.14.14.18 (Heme Oxygenase (Decyclizing))
SB  - IM
MH  - Acute Disease
MH  - Animals
MH  - Antioxidants/therapeutic use
MH  - Heme Oxygenase (Decyclizing)/physiology
MH  - Humans
MH  - Inflammation
MH  - Inflammation Mediators
MH  - Lung Diseases/chemically induced
MH  - *Lung Injury
MH  - Macrophage Activation
MH  - Macrophages/metabolism
MH  - Models, Biological
MH  - NF-E2-Related Factor 2/physiology
MH  - NF-kappa B/physiology
MH  - Neutrophil Activation
MH  - Neutrophils/metabolism
MH  - Oxidants/*metabolism
MH  - Oxidation-Reduction
MH  - Oxidative Stress/*physiology
MH  - Sepsis/*complications
MH  - Transcription Factor AP-1/physiology
RF  - 104
EDAT- 2007/09/01 09:00
MHDA- 2007/12/08 09:00
CRDT- 2007/09/01 09:00
PHST- 2007/09/01 09:00 [pubmed]
PHST- 2007/12/08 09:00 [medline]
PHST- 2007/09/01 09:00 [entrez]
AID - 10.1089/ars.2007.1785 [doi]
PST - ppublish
SO  - Antioxid Redox Signal. 2007 Nov;9(11):1991-2002. doi: 10.1089/ars.2007.1785.