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.

Bacterial clearance in septic mice is modulated by MCP-1/CCL2 and nitric oxide.

Bacterial clearance is one of the most important beneficial consequences of the innate immune response. Chemokines are important mediators controlling leukocyte trafficking and activation, whereas reactive oxygen and nitrogen species are effectors in bacterial killing. In the present work, we used in vivo and in vitro models of infections to study the role of monocyte chemoattractant protein 1 (MCP-1)/CCL2 and nitric oxide (NO) in the bacterial clearance in sepsis.