The effect of thiamine deficiency on inflammation, oxidative stress and cellular migration in an experimental model of sepsis.
BACKGROUND
Sepsis is a prevalent condition in critically ill patients and may be associated with thiamine deficiency (TD). The aim of this study was to evaluate the effect of TD on inflammation, oxidative stress and cellular recruitment in a sepsis model.


METHODS
The experimental sepsis model, cecal ligation and puncture (CLP), was utilized on mice in comparison with a sham procedure. The following four groups were compared against each other: SHAM with AIN93G complete chow, SHAM with thiamine deficient (TD) chow, CLP with AIN93G complete chow, and CLP with TD chow. Thiamine pyrophosphate (TPP) blood concentrations were determined, and blood and peritoneal fluid were evaluated for differences in TNF-alpha, IL-1, IL-6, KC and MCP-1/CCL2 levels. In addition, the levels of 4-HNE adducts in liver proteins were evaluated by Western Blot.


RESULTS
The mean TPP blood concentration from the mice fed with the complete chow was 303.3 ± 42.6 nmol/L, and TD occurred within 10 days. TNF-α and MCP-1 concentrations in the peritoneal fluid were significantly greater in the CLP with TD chow group when compared with the other groups. The blood IL-1β level, however, was lower in the CLP with TD chow group. Liver 4-HNE levels were highest in the TD chow groups. Blood mononuclear cell numbers, as well as peritoneal total leukocyte, mononuclear cell and neutrophil numbers were greater in the CLP with TD chow group. Peritoneal bacterial colony forming units (CFU) were significantly lower in the CLP with TD chow group.


CONCLUSIONS
TD was associated with greater bacterial clearance, oxidative stress and inflammatory response changes.
Intensive Care Unit, Pedro Ernesto University Hospital, State University of Rio de Janeiro, Av. 28 de Setembro 87, Rio de Janeiro, RJ CEP 20551-030, Brazil.
José Antenor Araújo
JAA
de Andrade
Biochemistry Department, Biomedical Center, Institute of Biology, State University of Rio de Janeiro, Rio de Janeiro, Brazil.
Carlos Roberto Machado
CRM
Gayer
Biochemistry Department, Biomedical Center, Institute of Biology, State University of Rio de Janeiro, Rio de Janeiro, Brazil.
Natália Pereira de Almeida
NPA
Nogueira
Biochemistry Department, Biomedical Center, Institute of Biology, State University of Rio de Janeiro, Rio de Janeiro, Brazil.
Márcia Cristina
MC
Paes
Biochemistry Department, Biomedical Center, Institute of Biology, State University of Rio de Janeiro, Rio de Janeiro, Brazil.
Vera Lúcia Freire Cunha
VLFC
Bastos
Biochemistry Department, Biomedical Center, Institute of Biology, State University of Rio de Janeiro, Rio de Janeiro, Brazil.
Jayme da Cunha Bastos
JDCB
Neto
Immunopharmacology Laboratory, Oswaldo Cruz Institute, Rio de Janeiro, Brazil.
Sílvio Caetano
SC
Alves
Immunopharmacology Laboratory, Oswaldo Cruz Institute, Rio de Janeiro, Brazil.
Raphael Molinaro
RM
Coelho
Immunopharmacology Laboratory, Oswaldo Cruz Institute, Rio de Janeiro, Brazil.
Mariana Gysele Amarante Teixeira
MGAT
da Cunha
Immunopharmacology Laboratory, Oswaldo Cruz Institute, Rio de Janeiro, Brazil.
Rachel Novaes
RN
Gomes
Morphometry, Metabolism & Cardiovascular Laboratory; Biomedical Center, Institute of Biology, State University of Rio de Janeiro, Rio de Janeiro, Brazil.
Márcia Barbosa
MB
Águila
Morphometry, Metabolism & Cardiovascular Laboratory; Biomedical Center, Institute of Biology, State University of Rio de Janeiro, Rio de Janeiro, Brazil.
Carlos Alberto
CA
Mandarim-de-Lacerda
Immunopharmacology Laboratory, Oswaldo Cruz Institute, Rio de Janeiro, Brazil.
Patrícia Torres
PT
Bozza
Intensive Care Unit, Pedro Ernesto University Hospital, State University of Rio de Janeiro, Av. 28 de Setembro 87, Rio de Janeiro, RJ CEP 20551-030, Brazil.
Sérgio
S
da Cunha
Inflammation; Oxidative stress; Sepsis; Sepsis model; Thiamine