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Cited by 193Respiratory Support and MechanismsInflammation biomarkers and pathwaysTrauma, Hemostasis, Coagulopathy, Resuscitation

The DOI matches its Crossref record; 39 of the 41 references it cites were found in a registry or an index.

Hemorrhagic shock primes for increased expression of cytokine‐induced neutrophil chemoattractant in the lung: role in pulmonary inflammation following lipopolysaccharide

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Fan, Jie, Marshall, John C, Jimenez, Maria, Shek, Pang N, Zagorski, John, Rotstein, Ori D·1998·The Journal of Immunology
DOI 10.4049/jimmunol.161.1.440
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Abstract

Recent studies have suggested that hemorrhagic shock followed by resuscitation renders patients more susceptible to lung injury by priming for an exaggerated response to a second stimulus, the so-called "two-hit" hypothesis. We investigated the role of C-X-C chemokines in mediating the augmented lung inflammation in response to LPS following resuscitated shock. In a rodent model, animals exposed to antecedent shock exhibited enhanced lung neutrophil sequestration and transpulmonary albumin flux in response to intratracheal LPS. This effect correlated with an exaggerated expression of cytokine-induced neutrophil chemoattractant (CINC) protein and mRNA, but not macrophage-inflammatory protein 2. Strategies designed to inhibit CINC, both anti-CINC Ab and supplementation with the antioxidant N-acetyl-cysteine, prevented the enhanced neutrophil sequestration, suggesting that CINC played a central role in the enhanced leukocyte accumulation following shock plus LPS treatment. Shock alone increased lung nuclear factor-kappaB expression and augmented the response to LPS. Prevention of this effect by N-acetylcysteine supplementation of the resuscitation fluid implicates a role for oxidant stress in the priming for lung inflammation following shock. Finally, alveolar macrophages recovered from shock-resuscitated animals released more CINC protein in vitro in response to LPS than macrophages from sham animals. Considered together, these findings show that augmented release of CINC, in part from primed alveolar macrophages, contributes significantly to the enhanced lung leukosequestration and transpulmonary albumin flux in response to LPS following resuscitated shock.

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Metadata

Authors
Fan, J., Marshall, J. C., Jimenez, M., Shek, P. N., Zagorski, J., & Rotstein, O. D.
Affiliations
  • University of Toronto (CA)
  • Defense and Civil Institute of Environmental Medicine , Toronto, Ontario ,
  • National Institutes of Health (US)
Corresponding author
  • Fan, Jie
  • Jimenez, Maria
ORCID
Venue
The Journal of Immunology
Publisher
Oxford University Press (OUP)
Published
1998-07-01
Volume
161
Issue
1
Pages
440-447
ISSN
  • 0022-1767 (ISSN-L)
  • 1550-6606
DOI
10.4049/jimmunol.161.1.440
OpenAlex
W1902960727
Cited by
193
References
41
Citations by year
2024: 1 · 2023: 1 · 2022: 1 · 2021: 2 · 2020: 2 · 2019: 4 · 2018: 5 · 2017: 1 · 2016: 2 · 2015: 8 · 2014: 7 · 2013: 7 · 2012: 12
FWCI
10.40
Type
journal article
Language
en
Open access
Licence
Locations
  • The Journal of Immunology (publishedVersion)
  • PubMed (publishedVersion)
  • Repositorio Institucional (Pontificia Universidad Javeriana) (submittedVersion, cc-by-nc)
Topics
  • Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Respiratory Support and Mechanisms
  • Life Sciences › Immunology and Microbiology › Immunology › Inflammation biomarkers and pathways
  • Health Sciences › Medicine › Critical Care and Intensive Care Medicine › Trauma, Hemostasis, Coagulopathy, Resuscitation
Keywords
hemorrhagic shock, resuscitation, two-hit hypothesis, CXC chemokines, cytokine-induced neutrophil chemoattractant, lipopolysaccharide, lung inflammation, neutrophil sequestration, alveolar macrophages, oxidative stress, N-acetylcysteine, NF-κB, neutrophil recruitment
MeSH terms
Acetylcysteine, Albumins, Animals, Biological Transport, Chemotactic Factors, Growth Substances, Immune Sera, Lipopolysaccharides, Lung, Male, Neutrophils, Shock, Hemorrhagic, Cytokines, NF-kappa B, Macrophages, Alveolar, Oxidants, Rats, Sprague-Dawley, Chemokines, CXC, Intercellular Signaling Peptides and Proteins, Rats, Chemokine CXCL2

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