- Poster presentation
- Open Access
Early bacterial spreading and inflammatory profile in a pneumosepsis model
© de Carvalho Gonçalves et al.; licensee BioMed Central Ltd. 2014
Published: 3 December 2014
Pneumonia is the major cause of sepsis, responsible for almost one-half of all sources of infection . Sepsis and septic shock lead to organ failure and death. Spreading of microorganisms and their toxins through the blood could contribute to the organ dysfunction. The heart, liver and kidney are examples of organs damaged during the systemic infection and organ failure predicts poor prognosis in patients with sepsis . However the correlation, if any, between bacterial spreading and organ injury is unclear. Thus, the aim of this study was to study the bacterial systemic spreading from a localized infection along with time and the target organ inflammatory profile using proinflammatory cytokines as surrogate markers.
Pneumosepsis was induced by Klebsiella pneumoniae as described in . The number of viable bacteria inoculated was 109 colony-forming units to achieve a mortality rate of ~50% by 48 hours. Blood, lung, heart, liver, spleen, kidney and brain were aseptically harvested, homogenized and plated on Müeller-Hinton agar dishes, for 18 hours at 37°C. Plasma and the tissues homogenates were assayed for interleukin-6 (IL-6) and interleukin-1β (IL-1β) using commercially available enzyme-linked immunosorbent assay kits according to the manufacturer's recommendations (PeproTech Inc., Rocky Hills, NJ, USA).
Lung inoculation with K. pneumoniae evolved to systemic spreading of bacteria to all organs, mostly the liver and kidney. Surprisingly, bacteria were found as early as 30 minutes in vital organs such as the brain and heart. The infection in the organs rose steadily up to 24 to 48 hours. Significant increases in IL-6 and IL-1β were found in the plasma, 24 hours after infection. However, cytokine levels in the organs were as high as fivefold the plasma levels.
Our data show that the early bacterial dissemination may be important for the onset of organ inflammation. Assuming that the higher organ cytokine level is a marker of an ongoing inflammation, this may explain organ dysfunction during sepsis. Thus, our study suggests that systemic (meaning blood) parameters may not reflect the severity of inflammation/dysfunction in target organs, and that might be the determinant to sepsis outcome.
Brazilian financial support from CNPq, CAPES, FAPESC and FINEP.
- Angus DC, Linde-Zwirble WT, Lidicker J, Clermont G, Carcillo J, Pinsky MR: Epidemiology of severe sepsis in the United States: analysis of incidence, outcome, and associated costs of care. Crit Care Med 2001, 29: 1303-1310. 10.1097/00003246-200107000-00002View ArticlePubMedGoogle Scholar
- Martin GS, Mannino DM, Eaton S, Moss M: The epidemiology of sepsis in the United States from 1979 through 2000. N Engl J Med 2003, 348: 1546-1554. 10.1056/NEJMoa022139View ArticlePubMedGoogle Scholar
- Sordi R, Menezes-de-Lima O, Della-Justina AM, Rezende E, Assreuy J: Pneumonia induced sepsis in mice: temporal study of inflammatory and cardiovascular parameters. Int J Exp Pathol 2013, 94: 144-155. 10.1111/iep.12016View ArticlePubMedPubMed CentralGoogle Scholar
This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.