Linked Life Data

17585043

Source:http://linkedlifedata.com/resource/pubmed/id/17585043

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2007-8-28
pubmed:abstractText
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 10(6) 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.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
8750-7587
pubmed:author
pubmed:issnType
Print
pubmed:volume
103
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
948-58
pubmed:meshHeading
pubmed-meshheading:17585043-Animals, pubmed-meshheading:17585043-Anti-Infective Agents, pubmed-meshheading:17585043-Antimicrobial Cationic Peptides, pubmed-meshheading:17585043-Bacteremia, pubmed-meshheading:17585043-Blood Proteins, pubmed-meshheading:17585043-Burns, pubmed-meshheading:17585043-Calcium, pubmed-meshheading:17585043-Cardiomyopathies, pubmed-meshheading:17585043-Cytokines, pubmed-meshheading:17585043-Hemodynamics, pubmed-meshheading:17585043-Klebsiella Infections, pubmed-meshheading:17585043-Klebsiella pneumoniae, pubmed-meshheading:17585043-Membrane Proteins, pubmed-meshheading:17585043-Myocardial Contraction, pubmed-meshheading:17585043-Myocardium, pubmed-meshheading:17585043-Myocytes, Cardiac, pubmed-meshheading:17585043-Pneumonia, pubmed-meshheading:17585043-Rats, pubmed-meshheading:17585043-Rats, Sprague-Dawley, pubmed-meshheading:17585043-Sodium
pubmed:year
2007
pubmed:articleTitle
Bactericidal/permeability increasing protein attenuates the myocardial inflammation/dysfunction that occurs with burn complicated by subsequent infection.
pubmed:affiliation
Department of Surgery, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd., Dallas, TX 75235-9136, USA. jureta.horton@utsouthwestern.edu
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural