Inefficient antimicrobial functions of innate phagocytes render infant mice more susceptible to bacterial infection. Issue 5 (22nd March 2013)

• Record Type: Journal Article
• Authors: Zhang, Qi; Coveney, Andrew P.; Yu, Shenglin; Liu, Jing Hua; Li, Yiping; Blankson, Siobhan; Redmond, H. Paul; Wang, Jiang Huai; Wang, Jian
• Is Part Of: European journal of immunology. Volume 43:Issue 5(2013:May)
• Page Start: 1322
• Page End: 1332
• Publication Date: 2013-03-22
• Subjects: Immunology -- Periodicals; 616.079
• DOI: 10.1002/eji.201243077
• Languages: English
• ISSNs: 0014-2980

Abstract

<abstract abstract-type="main"> <title> <x xml:space="preserve">Abstract</x> </title> <p>Neonates and infants, due to the immaturity in their adaptive immunity, are thought to depend largely on the innate immune system for protection against bacterial infection. However, the innate immunity‐mediated antimicrobial response in neonates and infants is incompletely characterized. Here, we report that infant mice were more susceptible to microbial sepsis than adult mice, with significantly reduced bacterial clearance from the circulation and visceral organs. Infant PMNs exhibited less constitutive expression of the chemokine receptor CXCR2, and bacterial infection caused further reduction of PMN CXCR2 in infant mice compared with adult mice. This correlates with diminished in vitro chemotaxis of infant PMNs toward the chemoattractant CXCL2 and impaired in vivo recruitment of infant PMNs into the infectious site. Furthermore, consistent with the reduced antimicrobial response in vivo, infant macrophages displayed an impaired bactericidal activity with a defect in phagosome maturation after ingestion of either gram‐positive or gram‐negative bacteria. Thus, infant mice exhibit an increased vulnerability to microbial infection with delayed bacterial clearance, which is associated with the inefficiency in their innate phagocyte‐associated antimicrobial functions characterized by defects in PMN recruitment and macrophage phagosome maturation during microbial sepsis.</p> </abstract>