Postnatal development of hepatic innate immune response

Inflammation. 2011 Dec;34(6):576-84. doi: 10.1007/s10753-010-9265-5.

Abstract

The liver is an immunocompetent organ that plays a key role in the immune response to infections, and the development of hepatic immune function during early postnatal stages has not been thoroughly characterized. This study analyzed the constitutive expression of complement factors, namely C3 and C9, and pattern recognition receptors, namely CD14, toll-like receptor (TLR)-4, and lipopolysaccharide binding protein (LBP), in the liver of postnatal day (P)1, P21, and P70 rats, and compared the kinetics of induction of cytokines and chemokines in the liver of P 1 and P 21 animals. Our studies found that while the mRNA expression of C3, C9, CD14, and TLR-4 was lower in P1 animals, the mRNA level of LBP was higher in P1 animals as compared to older animals, and that the kinetics of induction of cytokines and chemokines was significantly delayed in P1 as compared to P21 liver following LPS stimulation. Our data suggest that hepatic innate immunity is deficient in the neonates and undergo significant development during early postnatal life.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acute-Phase Proteins / genetics
  • Age Factors
  • Animals
  • Animals, Newborn
  • Carrier Proteins / genetics
  • Complement System Proteins / genetics
  • Immunity, Innate*
  • Kinetics
  • Lipopolysaccharide Receptors / genetics
  • Liver / immunology*
  • Membrane Glycoproteins / genetics
  • RNA, Messenger / analysis
  • Rats
  • Toll-Like Receptor 4 / genetics
  • Transcriptional Activation / immunology*

Substances

  • Acute-Phase Proteins
  • Carrier Proteins
  • Lipopolysaccharide Receptors
  • Membrane Glycoproteins
  • RNA, Messenger
  • Toll-Like Receptor 4
  • lipopolysaccharide-binding protein
  • Complement System Proteins