TLR-mediated inflammatory response to neonatal pathogens and co-infection in neonatal immune cells

•CD14dimCD16+ cells were increased upon stimulation with neonatal pathogens.•TLR2 and TLR4 were differentially expressed on both monocyte subpopulations.•Neonatal cells produced a powerful inflammatory response as that of adult cells.•Multiple cytokine production was impaired in neonatal cells upon...

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Published in:Cytokine (Philadelphia, Pa.) Pa.), 2014-10, Vol.69 (2), p.211-217
Main Authors: Sugitharini, V., Pavani, K., Prema, A., Berla Thangam, E.
Format: Article
Language:English
Subjects:
Chemokines - blood
Co-infection
Coinfection - immunology
Coinfection - microbiology
Cytokines
Escherichia coli - drug effects
Escherichia coli - immunology
Fetal Blood - metabolism
Humans
Infant, Newborn
Inflammation - pathology
Inflammation Mediators - metabolism
Klebsiella - drug effects
Klebsiella - immunology
Lipopolysaccharide Receptors - metabolism
Lipopolysaccharides - pharmacology
LPS
Lymphocytes - drug effects
Lymphocytes - metabolism
Lymphocytes - microbiology
Monocytes - drug effects
Monocytes - metabolism
Peptidoglycan - pharmacology
PGN
Receptors, IgG - metabolism
Staphylococcus aureus - drug effects
Staphylococcus aureus - immunology
TLR
Toll-Like Receptor 2 - metabolism
Toll-Like Receptor 4 - metabolism
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Summary:•CD14dimCD16+ cells were increased upon stimulation with neonatal pathogens.•TLR2 and TLR4 were differentially expressed on both monocyte subpopulations.•Neonatal cells produced a powerful inflammatory response as that of adult cells.•Multiple cytokine production was impaired in neonatal cells upon co-stimulation. Neonates heavily depend on the innate immune system for defence against invading pathogens. Toll-like receptors (TLRs) represent a primary line of host defence and play an important role in orchestrating the inflammatory response to invading pathogens. The most commonly infecting pathogens in neonates are E. coli, Klebsiella pneumoniae and Staphylococcus aureus. Also, co-infection with more than one organism is common in neonatal sepsis. Therefore, we aimed to study the TLR2 and TLR4 mediated neonatal inflammatory response to these pathogens. For this, we stimulated mononuclear cells from cord blood with LPS, PGN, E. coli, K. pneumoniae and S. aureus and analyzed the surface expression of TLR2 and TLR4 on CD14+CD16+ and CD14dimCD16+ and its inflammatory response in comparison with peripheral blood. We found that the TLR2 and TLR4 were differentially expressed on both monocyte subpopulations. Cytokines such as IL-6, IL-1β, IL-23, IL-10, IL-13, MCP-1 and IL-8 were measured using ELISA and we observed that although, neonatal cells were able to produce similar levels of the classical pro-inflammatory (IL-6, IL-1β) and anti-inflammatory (IL-10, IL-13) cytokines as that of adult cells, the amounts of IL-23 and MCP-1 were lower in CBMCs while the chemokine IL-8 was higher in CBMCs when compared with PBMCs. In addition, using Human Inflammation Antibody array technique we found that multiple cytokine production was impaired in cord blood when cells were co-infected with LPS and PGN. In conclusion, the TLR-mediated inflammatory response to neonatal pathogens is differentially regulated by different pathogens.
ISSN:1043-4666
1096-0023
DOI:10.1016/j.cyto.2014.06.003