Advanced Search

Journal Navigation

Journal Home

Subscriptions

Archive

Contact Us

Table of Contents

Sign In to gain access to subscriptions and/or personal tools.
Journal of Endotoxin Research
This Article
Right arrow Full Text (PDF)
Right arrow References
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Saved Citations
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Request Reprints
Right arrow Add to My Marked Citations
Citing Articles
Right arrow Citing Articles via Google Scholar
Right arrow Citing Articles via Scopus
Google Scholar
Right arrow Articles by Calkins, C. M.
Right arrow Articles by McIntyre, R. C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Calkins, C. M.
Right arrow Articles by McIntyre, R. C., JR
Right arrowPubmed/NCBI databases
*Substance via MeSH
Social Bookmarking
Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati   Add to Twitter  
What's this?

IL-1 regulates in vivo C—X—C chemokine induction and neutrophil sequestration following endotoxemia

Casey M. Calkins

Department of Surgery, University of Colorado Health Sciences Center and Veterans Affairs Hospital,

Denis D. Bensard

Department of Surgery, University of Colorado Health Sciences Center and Veterans Affairs Hospital,, Division of Pediatric Surgery, The Children's Hospital, and Department of Medicine,

Brian D. Shames

Department of Surgery, University of Colorado Health Sciences Center and Veterans Affairs Hospital,

Edward J. Pulido

Department of Surgery, University of Colorado Health Sciences Center and Veterans Affairs Hospital,

Edward Abraham

Division of Pulmonary and Critical Care Medicine

Nathan Fernandez

Department of Surgery, University of Colorado Health Sciences Center and Veterans Affairs Hospital,

Xianzhong Meng

Department of Surgery, University of Colorado Health Sciences Center and Veterans Affairs Hospital,

Charles A. Dinarello

Division of Infectious Diseases, University of Colorado Health Sciences Center, Denver, Colorado, USA

Robert C. McIntyre, JR

Department of Surgery, University of Colorado Health Sciences Center and Veterans Affairs Hospital, robert.mcintyre{at}uchsc.edu

The influx of neutrophils into tissues in response to inflammatory stimuli involves C—X—C chemokines. Interleukin-1 (IL-1) stimulates chemokine production in vitro , but its role in vivo on chemokine production is not as clearly understood. We hypothesized that IL-1 mediates in vivo tissue C—X—C chemokine production induced by systemic lipopolysaccharide (LPS). IL-1 activity was blockedbyIL-1 receptor antagonist (IL-1Ra). Rats were injected with Salmonella typhi LPS (0.5 mg/kg) with and without prior administration of IL-1Ra. Cytokine-induced neutrophil chemoattractant-1 (CINC-1) and macrophage inflammatory protein-2 (MIP-2) protein and mRNA levels, tissue neutrophil accumulation, and indices of organ injury were measured. LPS administration resulted in increased plasma, lung, and liver IL-1ß that was decreased by IL-1Ra. LPS also induced an increase in plasma, lung, and liver CINC-1 and MIP-2 protein and mRNA. However, IL-1Ra had no effect on LPS-induced plasma or lung tissue CINC-1 levels. In contrast, IL-1Ra pretreatment did significantly decrease CINC-1 protein expression in the liver (45% decrease) and MIP-2 protein expression in plasma (100% decrease), lung (72% decrease) and liver (100% decrease) compared to LPS-treated controls. Steady-state mRNA levels by Northern blot analysis of both CINC-1 and MIP-2 in lung and liver were similar to the protein findings. Pretreatment with IL-1Ra also resulted in a 47% and 59% decrease in lung and liver neutrophil accumulation, respectively, following LPS. In addition, indices of both lung and liver injury were decreased in animals pretreated with IL-1Ra. In summary, LPS induces IL-1ß and MIP-2 expression in the lung and liver, both of which are IL-1 dependent. Although lung neutrophil accumulation in both lung and liver after LPS is also IL-1 mediated, lung CINC-1 levels were unaffected by IL-1Ra. These data suggest that IL-1 regulates tissue chemokine expression and neutrophil accumulation after LPS.

Journal of Endotoxin Research, Vol. 8, No. 1, 59-67 (2002)
DOI: 10.1177/09680519020080010601
Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati   Add to Twitter Twitter    What's this?