Murdoch University Research Repository

Welcome to the Murdoch University Research Repository

The Murdoch University Research Repository is an open access digital collection of research
created by Murdoch University staff, researchers and postgraduate students.

Learn more

Preterm infants have deficient monocyte and lymphocyte cytokine responses to Group B Streptococcus

Currie, A.J., Curtis, S., Strunk, T., Riley, K., Liyanage, K., Prescott, S., Doherty, D., Simmer, K., Richmond, P. and Burgner, D. (2011) Preterm infants have deficient monocyte and lymphocyte cytokine responses to Group B Streptococcus. Infection and Immunity, 79 (4). pp. 1588-1596.

PDF - Published Version
Download (2MB)
Link to Published Version:
*Subscription may be required


Group B streptococcus GBS) is an important cause of early-and late-onset sepsis in the newborn. Preterm infants have markedly increased susceptibility and worse outcomes, but their immunological responses to GBS are poorly defined. We compared mononuclear cell and whole-blood cytokine responses to heat-killed GBS HKGBS) of preterm infants gestational age [GA], 26 to 33 weeks), term infants, and healthy adults. We investigated the kinetics and cell source of induced cytokines and quantified HKGBS phagocytosis. HKGBS-induced tumor necrosis factor TNF) and interleukin 6 (IL-6) secretion was significantly impaired in preterm infants compared to that in term infants and adults. These cytokines were predominantly monocytic in origin, and production was intrinsically linked to HKGBS phagocytosis. Very preterm infants GA, < 30 weeks) had fewer cytokine-producing monocytes, but nonopsonic phagocytosis ability was comparable to that for term infants and adults. Exogenous complement supplementation increased phagocytosis in all groups, as well as the proportion of preterm monocytes producing IL-6, but for very preterm infants, responses were still deficient. Similar defective preterm monocyte responses were observed in fresh whole cord blood stimulated with live GBS. Lymphocyte-associated cytokines were significantly deficient for both preterm and term infants compared to levels for adults. These findings indicate that a subset of preterm monocytes do not respond to GBS, a defect compounded by generalized weaker lymphocyte responses in newborns. Together these deficient responses may increase the susceptibility of preterm infants to GBS infection.

Item Type: Journal Article
Murdoch Affiliation(s): School of Veterinary and Biomedical Sciences
Publisher: American Society for Microbiology
Item Control Page Item Control Page


Downloads per month over past year