Neonatal Sepsis and Inflammatory Mediators

Abstract

Neonatal sepsis is a major cause of morbidity and mortality and its signs and symptoms are nonspecific, which makes the diagnosis difficult. The routinely used laboratory tests are not effective methods of analysis, as they are extremely nonspecific and often cause inappropriate use of antibiotics. Sepsis is the result of an infection associated with a systemic inflammatory response with production and release of a wide range of inflammatory mediators. Cytokines are potent inflammatory mediators and their serum levels are increased during infections, so changes from other inflammatory effector molecules may occur. Although proinflammatory and anti-inflammatory cytokines have been identified as probable markers of neonatal infection, in order to characterize the inflammatory response during sepsis, it is necessary to analyze a panel of cytokines and not only the measurement of individual cytokines. Measurements of inflammatory mediators bring new options for diagnosing and following up neonatal sepsis, thus enabling early treatment and, as a result, increased neonatal survival. By taking into account the magnitude of neonatal sepsis, the aim of this review is to address the role of cytokines in the pathogenesis of neonatal sepsis and its value as a diagnostic criterion.

Exercise and the cytokines-interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α): A review

“…Interleukin-6 and tumor necrosis factor- Interleukin-6 (IL-6) and Tumor necrosis factor- (TNF-) are two cytokines that are known to mediate changes in musculoskeletal and immune systems. 4 They are pro-inflammatory cytokines that mediate process of inflammation and healing. However when released in excess, they can cause unwanted exacerbation of inflammation.…”

Comparison of the Functional microRNA Expression in Immune Cell Subsets of Neonates and Adults

“…Inflammatory responses are necessary for the host to respond to components of invading organisms. At the early stages of infection, TNF-α, IL-1β, IL-6, and IL-8 pro-inflammatory cytokines are produced and stimulate immune cells leading to activation of an inflammatory cascade (47). The subsequent inflammatory cascade includes many biologically active mediators and can induce a systemic inflammatory response.…”

“…The inflammatory response is thereafter counteracted by anti-inflammatory mediators to restore immunological homeostasis. Excessive pro-inflammatory mediators or inadequate anti-inflammatory responses will lead to sepsis (47). In addition to antibiotics, other adjuvant therapies primarily target the dysregulated innate immune response.…”

The Impact of Venoarterial and Venovenous Extracorporeal Membrane Oxygenation on Cerebral Metabolism in the Newborn Brain

“…While the VV ECMO patients had higher serum creatinine levels (Table 1), post-hoc analyses demonstrated no direct correlation between serum creatinine and either GM or WM creatine (data not shown). On the other hand, systemic inflammation (e.g., elevated c-reactive protein, elevated pro-inflammatory cytokines) has been documented in neonates with ECMO [30, 31], as well as in neonates with clinical sepsis [32] and studies have demonstrated that creatine is often elevated alongside choline in the setting of cerebral inflammation [25, 27]. Taken together, the elevations in creatine and choline suggest that the systemic inflammatory response could extend to the central nervous system, as demonstrated in animal models [33].…”