Several clinical conditions, such as trauma, burn, severe acute illness and major postoperative surgery generate a series of organic response reactions in response to these injuries, called the systemic inflammatory response syndrome (SIRS). When SIRS is associated with an infection, it is defined as sepsis [1–3]. Epidemiological studies worldwide [4–6] and in Brazil [7, 8] indicate that sepsis is a prevalent condition with a high mortality rate that is associated with the emergence of multidrug-resistant pathogens [9, 10] while also generating high social and financial costs . Thiamine (vitamin B1) is a water soluble vitamin that does not accumulate in the body; therefore, it has to be ingested daily . Thiamine pyrophosphate (TPP; the biologically active form of vitamin B1) is an important mitochondrial enzyme cofactor  with a key role in energy balance. In addition, TPP participates as a transketolase cofactor in the pentose phosphate pathway, a pathway that replenishes NADPH, which is necessary for the recovery of the reduced form of glutathione (GSH) from its oxidized form. TPP is also a cofactor of the α-ketoglutarate dehydrogenase complex , theoretically participating in the recovery of cellular reducing power .
The prevalence of TD in critically ill patients has been described [14–16] and was associated with increased morbidity and mortality . Recent studies have demonstrated that additional attention is needed in the identification of thiamine deficiency (TD) and that thiamine supplementation is necessary not only in intensive care unit patients but also in patients with heart failure [15, 17, 18].
Evidence that TD may cause heart failure has been demonstrated [12, 19, 20], whereby an increase in oxidative stress due to TD led to the apoptosis of cardiomyocytes  and produced cardiac remodeling [20, 22]. Structural remodeling and the destruction of cardiomyocyte mitochondria were also observed with TD . A similar finding was observed in a study with human neuroblastoma cells cultured under TD conditions .
Several neurological disorders have been associated with TD, including acute confusion and changes in eye movement and gait (Wernicke’s encephalopathy). These findings may be associated with chronic memory impairment (Korsakoff’s syndrome) [12, 24, 25]. Thiamine deficiency may also be associated with brain degenerative conditions such as Parkinson’s disease and Alzheimer’s disease [24–27]. Thiamine deficiency is also associated with lesions of the endoplasmic reticulum of neurons . The influence of TPP in an experimental model of sepsis in dogs has recently been performed , and the following outcomes were analyzed: blood pH, oxygen consumption, base excess, mean arterial pressure and the cardiac index. The authors observed recovery of all of these parameters in the animals treated with TPP, suggesting the involvement of thiamine as a possible protective agent against the onset of sepsis.
Sepsis is associated with an intense inflammatory response . In response to an injury, the initial inflammatory response is the activation of the innate immunity pathways. The innate inflammatory response is a series of “primitive” non-specific reactions that occur in the early hours after the interaction with a pathogen and involve acute phase proteins, the complement system, dendritic cells, macrophages and natural killer cells (NK), with the end result being inflammation [31–34]. When an activated macrophage comes into contact with a pathogen, it begins to produce TNF-α, which is responsible for an increase in vascular permeability. In addition, pathogen stimulation of macrophages leads to the production of IL-1β and IL-6, which have decisive roles in the genesis of fever by acting on the central hypothalamic temperature control system . The chemotactic factors KC and MCP-1 are involved in the recruitment of neutrophils and monocytes, respectively, and are involved in the perpetuation of the cellular response to injury. In parallel, IL-10 secretion is a self-regulatory mechanism of the inflammatory response, acting as an anti-inflammatory cytokine [30, 31].
The cellular injury observed in sepsis produces highly reactive biochemical intermediates from nitrogen and oxygen . Following an injury, we now know that the increased production of reactive oxygen species (ROS) and the increased activity of clearance mechanisms do not necessarily indicate cell damage [35, 36]. ROS have the ability to react with proteins, lipids, and genetic material. The products of these reactions are known today and include 4-hydroxy 2-nonenal (4-HNE), an aldehyde that results from the lipid peroxidation of the cell membrane . 4-HNE plays a key role in cell signaling and redox balance [38, 39], but in high concentrations, it can be harmful to cells [37–39].
Experimental sepsis models are necessary to evaluate some aspects of this clinical condition, due to ethical constraints [40–42]. Many methods are used to simulate hemodynamic, immunological and clinical sepsis events, including surgical manipulation of organs (such as ligation or perforation of the bowel loops)  and injection of bacteria or their components (e.g., endotoxins, such as gram-negative lipopolysaccharides) into the bloodstream , organs and anatomical cavities. These methods are not free of criticisms from both a methodological standpoint [43, 44] and from technical and ethical standpoints, with regard to animal handling . These experimental models, however, represent important tools for sepsis investigation.
This study analyzed the possible effect of thiamine deficiency on changes in sepsis markers of inflammation (cytokines), the balance of the oxidation-reduction system (based on the presence of a marker of lipid peroxidation), and the leukocyte recruitment profile. The hypothesis in question was that thiamine deficiency in experimental sepsis conditions could result in a pro-inflammatory profile, with greater oxidative stress and cellular migration.