Journal of Applied Physiology Ad Instruments
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


J Appl Physiol 103: 948-958, 2007. First published June 21, 2007; doi:10.1152/japplphysiol.00606.2006
8750-7587/07 $8.00
This Article
Right arrow Full Text Free
Right arrow Full Text (PDF) Free
Right arrow All Versions of this Article:
103/3/948    most recent
00606.2006v1
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
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 Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Horton, J. W.
Right arrow Articles by Minei, J. P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Horton, J. W.
Right arrow Articles by Minei, J. P.

Bactericidal/permeability increasing protein attenuates the myocardial inflammation/dysfunction that occurs with burn complicated by subsequent infection

Jureta W. Horton, David L. Maass, D. Jean White, and Joseph P. Minei

Department of Surgery, University of Texas Southwestern Medical Center, Dallas, Texas

Submitted 31 May 2006 ; accepted in final form 18 June 2007

Intubation and mechanical ventilation after burn contribute to pneumonia-related infection. Although postburn presence or absence of endotoxin has been described, inactivation of Toll-like receptor 4 signaling has been shown to improve postburn organ function, suggesting that LPS participates in burn-related susceptibility to infection. We hypothesized that bactericidal/permeability-increasing protein (rBPI) given postburn would attenuate myocardial inflammation/dysfunction associated with postburn septic challenge given 7 days postburn. Rats were given burn over 40% total body surface area, lactated Ringer 4 ml·kg–1·% burn–1; burns received either vehicle or rBPI, 1 mg·kg–1·h–1 for 48 h postburn. Postburn day 7, subgroups of burns and shams were given intratracheal Klebsiella pneumoniae, 4 x 106 CFU to produce burn complicated by sepsis; additional sham and burn subgroups received intratracheal vehicle to produce sham sepsis. Vehicle-treated groups: 1) sham burn + sham sepsis 2) sham burn + sepsis, 3) burn + sham sepsis, 4) burn + sepsis. rBPI-treated groups: 5) sham burn + sham sepsis, 6) sham burn + sepsis, 7) burn + sham sepsis, 8) burn + sepsis. Cardiomyocyte cytokine secretion and myocardial function were studied 24 h after septic challenge, postburn day 8. Pneumonia-related infection 8 days after vehicle-treated burn produced myocyte cytokine secretion (pg/ml), indicated by increased myocyte TNF-{alpha}, 549 ± 46; IL-1beta, 50 ± 8; IL-6, 286 ± 3 levels compared with levels in sham myocytes (TNF-{alpha}, 88 ± 11; IL-1beta, 7 ± 1; IL-6, 74 ± 10; P < 0.05). Contractile dysfunction was evident from lower left ventricular pressure ±dP/dt values in this group compared with sham. rBPI attenuated myocyte cytokine responses to septic challenge and improved contractile function, suggesting that burn-related mobilization of microbial-like products contribute to postburn susceptibility to infection.

TNF-{alpha}; IL-1beta; IL-6 cytokines; left ventricular function; primary cardiomyocytes; intratracheal Klebsiella pneumoniae challenge



Address for reprint requests and other correspondence: J. W. Horton, Dept. of Surgery, Univ. of Texas Southwestern Medical Center, 5323 Harry Hines Blvd., Dallas, TX 75235-9136 (e-mail: jureta.horton{at}utsouthwestern.edu)







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online
Copyright © 2007 by the American Physiological Society.