Cytokine profile in severe gram-positive and gram-negative abdominal sepsis

Abstract

Sepsis is a principal cause of death in critical care units worldwide and consumes considerable healthcare resources. The aim of our study was to determine whether the early cytokine profile can discriminate between Gram-positive and Gram-negative bacteraemia (GPB and GNB, respectively) and to assess the prognostic value regarding outcome in critically ill patients with severe abdominal sepsis. The outcome measure was hospital mortality. Blood samples were obtained from 165 adult patients with confirmed severe abdominal sepsis. Levels of the proinflammatory mediators TNF-α, IL-8, IL-12 and IFN-γ and the anti-inflammatory mediators IL-1ra, IL-4, IL-10 and TGF-β1 were determined and correlated with the nature of the bacteria isolated from the blood culture and outcome. The cytokine profile in our study indicated that the TNF-α levels were 2-fold, IL-8 were 3.3-fold, IFN-γ were 13-fold, IL-1ra were 1.05-fold, IL-4 were 1.4-fold and IL-10 were 1.83-fold higher in the GNB group compared with the GPB group. The TNF-α levels were 4.7-fold, IL-8 were 4.6-fold, IL-1ra were 1.5-fold and IL-10 were 3.3-fold higher in the non-survivors compared with the survivors.

Chronic Heart Failure and Inflammation

“…[5][6][7][8] The magnitude in the elevation of proinflammatory cytokines in chronic HF is significantly less than what would be observed in cases of autoimmune diseases or acute infections, suggesting that low-grade chronic inflammation may be an important contributor to the maintenance or clinical deterioration of patients with established chronic HF. [9][10][11] Here, we will review what is known about the role of chronic inflammation in established HF. Importantly, we will highlight that although we have come to understand some of the intricate and contextdependent mechanisms in which inflammatory cells and pathways contribute to the development of HF in the acute setting, few of those insights have been extended to assessing the role of inflammation once chronic HF has been established.…”

Fisiopatología de la sepsis por gram positivos

“…La diferencia en la cantidad de citocinas infl amatorias inducidas por uno u otro tipo de bacterias, ha llevado a que en diversos estudios se haya encontrado que la medición rápida de éstas se plantee como un indicador que puede ayudar a discriminar si la bacteremia del paciente es por gram positivas o por gram negativas, así se ha encontrado en algunos estudios que en el caso de la sepsis por bacterias gram negativas se detectan mayores niveles de TNFα-, IL-1α, IL-1β, e IL-8, y en sepsis por gram positivas el TNFα,, IL-1β TNF β , IL-4 α, IL-18; en otros estudios se enfatiza que las mayores diferencias se observan a nivel de TNFα, Il-6, e IL-10, siendo la IL-10 un potencial marcador de la bacteremia por gram negativos en pacientes pediátricos hematológicos u oncoló-gicos. Igualmente se ha encontrado que frente al efecto sobre la producción de marcadores de sepsis como es la procalcitonina (PCT en inglés), resulta más efectivo el Lipopolisacárido de las bacterias gram negativas de ahí que la PCT se esté considerando como un agente predictor de la etiopatogenia de la sepsis (42)(43)(44)(45)(46).…”

Pro-Inflammatory Cytokines in Sepsis: Biological Studies and Prospects From In Silico Research

“…The incidence of sepsis and the consequent fatality risk has increased over the past years, especially in the United States [32] and the condition is considered the leading cause of death in intensive care units [1].…”

“…Sepsis is a common cause for admission and fatal outcomes in intensive care units (ICU) [1]. Most of these hospital-acquired infections occur in infirmaries and ICUs [2], however, many of the patients requiring intensive treatment, acquire them outside of the hospital environment [3].…”

“…The key mediators and regulators in sepsis are the cytokines, a group of endogenous inflammatory mediators and immunomodulatory proteins. They are generally divided into two groups, anti-and pro-inflammatory [1], responsible for coordinating the host defense mechanisms against pathogens [8].…”