Defective macrophage function in neonates and its impact on unresponsiveness of neonates to polysaccharide antigens (original) (raw)

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Department of Microbiology & Immunology and University of Kentucky

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Lexington

Sanders Brown Center on Aging, University of Kentucky

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Lexington

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Sanders Brown Center on Aging, University of Kentucky

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Lexington

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Sanders Brown Center on Aging, University of Kentucky

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Lexington

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Department of Microbiology & Immunology and University of Kentucky

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Lexington

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Sanders Brown Center on Aging, University of Kentucky

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Lexington

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Department of Microbiology & Immunology and University of Kentucky

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Lexington

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Department of Internal Medicine and University of Kentucky

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Lexington

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Department of Internal Medicine and University of Kentucky

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Lexington

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Department of Microbiology & Immunology and University of Kentucky

,

Lexington

Sanders Brown Center on Aging, University of Kentucky

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Lexington

Correspondence: 329A Sanders-Brown Building, University of Kentucky, Lexington, KY 40536-0230. E-mail: bondada@uky.edu

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Revision received:

20 December 2003

Accepted:

22 January 2004

Published:

24 February 2004

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R L Chelvarajan, S M Collins, I E Doubinskaia, S Goes, J Van Willigen, D Flanagan, W J S de Villiers, J S Bryson, S Bondada, Defective macrophage function in neonates and its impact on unresponsiveness of neonates to polysaccharide antigens, Journal of Leukocyte Biology, Volume 75, Issue 6, June 2004, Pages 982–994, https://doi.org/10.1189/jlb.0403179
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Abstract

Neonates do not respond to thymus-independent (TI) antigens (Ag), making them vulnerable to infection with encapsulated bacteria. The antibody (Ab) response of adult and neonatal B cells to TI Ag requires certain cytokines, which are provided by T cells or macrophages (MΦ). Lipopolysaccharide (LPS) failed to induce neonatal MΦ to produce interleukin (IL)-1β and tumor necrosis factor α (TNF-α) mRNA and to secrete IL-1β, IL-12, and TNF-α. However, LPS induced neonates to secrete some IL-6 and three- to fivefold more IL-10 than adults. Accordingly, adding adult but not neonatal MΦ could restore the response of purified adult B cells to trinitrophenol (TNP)–LPS, a TI Ag. Increased IL-10 is causally related to decreased IL-1β and IL-6 production, as IL-10−/− neonatal MΦ responded to LPS by secreting more IL-1β and IL-6 than wild-type (WT) neonatal MΦ. When cultures were supplemented with a neutralizing Ab to IL-10, WT neonatal MΦ secreted increased amounts of IL-6 and allowed neonatal MΦ to promote adult B cells to mount an Ab response against TNP–LPS. Thus, neonates do not respond to TI Ag as a result of the inability of neonatal MΦ to secrete cytokines, such as IL-1β and IL-6, probably as a result of an excess production of IL-10. This dysregulated cytokine secretion by neonatal MΦ may be a result of a reduction in expression of Toll-like receptor-2 (TLR-2) and TLR-4 and CD14.

© 2004 Society for Leukocyte Biology

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