Differential regulation of inflammatory mediators and granule-associated mediators in neonatal sepsis observed in cord and peripheral blood

Abstract:

Neonatal sepsis is a systemic inflammatory response to bacterial infection. The innate immune system which acts as a first line of defense in infants, mounts a powerful inflammatory response upon pathogenic stimuli marked by elevated levels of inflammatory mediators and acute phase proteins, in the absence of a proper counteracting anti-inflammatory response. However, much less is known about the role of degranulation in development of systemic inflammation and sepsis. The present study reveals differentially regulated granular contents such as neutrophil elastase, nitric oxide, and myeloperoxidase which might act as key mediators in pathogenesis of neonatal sepsis. Neutrophil elastase and nitric oxide were found to be upregulated, while myeloperoxidase was found to be downregulated in neonatal sepsis. In addition, inflammatory mediators interleukin-6, interleukin-8, C-reactive protein, and procalcitonin were elevated in both cord blood and peripheral blood of septic neonates. These findings suggest that, in addition to inflammatory mediators, granule-associated mediators are also differentially regulated in neonatal sepsis and they might be used as sensitive and rapidly responding indicators of neonatal bacterial infection.

Keywords::

• systemic inflammation
• acute phase proteins
• C-reactive protein
• neonatal spesis
• myeloperoxidase
• interleukin