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Table of Contents
Vol. 101, No. 2, 2012
Issue release date: February 2012
Section title: Original Paper
Free Access
Neonatology 2012;101:140–146

Toll-Like Receptor 1/2 Stimulation Induces Elevated Interleukin-8 Secretion in Polymorphonuclear Leukocytes Isolated from Preterm and Term Newborn Infants

Thornton N.L. · Cody M.J. · Yost C.C.
Department of Pediatrics and Program in Human Molecular Biology and Genetics, University of Utah, Salt Lake City, Utah, USA
email Corresponding Author

Christian Con Yost, MD

Department of Pediatrics/Neonatology, University of Utah

Williams Building, 295 Chipeta Way

Salt Lake City, UT 84108 (USA)

Tel. +1 801 581 7052, E-Mail christian.yost@u2m2.utah.edu

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Background: Neonatal neutrophil dysfunction contributes to inflammatory tissue damage in newborn infants. Toll-like receptors (TLRs) activate the innate immune response through recognition of pathogen-associated molecular patterns. Expression and function of TLRs by neonatal neutrophils has not well been characterized. Objective: We hypothesized that, compared to polymorphonuclear leukocytes (PMNs) isolated from adults, neonatal PMNs isolated from either term or preterm infants express and release different levels of inflammatory cytokines and chemokines in response to stimulation with TLR1–9 agonists. Methods: We stimulated PMNs isolated from preterm (n = 12) and term (n = 10) infants as well as adults (n = 10) with agonists recognized by TLRs1–9 and quantified chemokine and cytokine expression and secretion by ELISA and Luminex® multiplex quantification assay. Results: Neonatal and adult PMNs stimulated with agonists recognized by TLRs1–9 differentially secrete inflammatory products. Signaling via TLR2 heterodimers is a potent mechanism for release of interleukin-8, a critical proinflammatory chemokine, by neonatal PMNs – a previously unrecognized facet of neonatal inflammation. Following TLR1/2 (PAM3CSK4) stimulation, interleukin-8 secretion by neonatal PMNs, whether term or preterm, substantially exceeds that of adult PMNs assayed in parallel. Conclusions: These studies provide new insights relevant to the inflammatory biology of neonates, both term and preterm, and implicate exaggerated PMN recruitment in neonatal syndromes of dysregulated inflammation such as necrotizing enterocolitis or neonatal chronic lung disease.

© 2011 S. Karger AG, Basel

Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: April 19, 2011
Accepted: July 01, 2011
Published online: September 23, 2011
Issue release date: February 2012

Number of Print Pages: 7
Number of Figures: 2
Number of Tables: 4

ISSN: 1661-7800 (Print)
eISSN: 1661-7819 (Online)

For additional information: http://www.karger.com/NEO

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