Insulin modulates the inflammatory granulocyte response to streptococci via phosphatidylinositol 3-kinase.

Group B streptococci (GBS; Streptococcus agalactiae) are a major cause of invasive infections in newborn infants and in patients with type 2 diabetes. Both patient groups exhibit peripheral insulin resistance and alterations in polymorphonuclear leukocyte (PML) function. In this investigation, we studied the PML response repertoire to GBS with a focus on TLR signaling and the modulation of this response by insulin in mice and humans.

Spontaneous clearance of hepatitis C virus in vertically infected children.

Unlabelled: Spontaneous viral clearance of hepatitis C virus (HCV) has been reported to occur in children with vertical HCV infection. However, factors which are associated with or predispose for clearance are largely unknown. In this case series we retrospectively analyzed laboratory parameters associated with spontaneous clearance of HCV in vertically infected children.

Role of p38 and early growth response factor 1 in the macrophage response to group B streptococcus.

Group B streptococcus (GBS), the most frequent single isolate in neonatal sepsis and meningitis, potently activates inflammatory macrophage genes via myeloid differentiation antigen 88 (MyD88). However, events parallel to and downstream of MyD88 that instruct the macrophage response are incompletely understood. In this study, we found that only MyD88, not the Toll-like receptor (TLR) adapter proteins MAL/TIRAP, TRIF, and TRAM, essentially mediates the cytokine (tumor necrosis factor [TNF] and interleukin-6) and chemokine (RANTES) responses to whole GBS organisms, although MAL, TRIF, and TRAM have been shown to mediate the responses to substructures in other gram-positive and gram-negative bacteria.

The innate immune system and its relevance to neonatal sepsis.

Purpose Of Review: The advent of human Toll-like receptors has revolutionized our understanding of innate immunity. This review summarizes recent discoveries about the role of Toll-like receptors and innate immunity in neonatal sepsis with a particular emphasis on the paradigmatic organism S. agalactiae.

c-Jun kinase is a critical signaling molecule in a neonatal model of group B streptococcal sepsis.

Group B streptococcus (GBS) is the major cause of sepsis in newborn infants. In vitro, inactivated GBS stimulates macrophages to produce inflammatory proteins via the TLR adapter protein MyD88. Furthermore, inflammatory cytokine release in response to GBS greatly exceeds that following stimulation with pneumococci.