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Innate immune response to lipooligosaccharide: pivotal regulator of the pathobiology of invasive Neisseria meningitidis infections.

Abstract Infections due to Neisseria meningitidis afflict more than one million people worldwide annually and cause death or disability in many survivors. The clinical course of invasive infections has been well studied, but our understanding of the cause of differences in patient outcomes has been limited because these are dependent on multiple factors including the response of the host, characteristics of the bacteria and interactions between the host and the bacteria. The meningococcus is a highly inflammatory organism, and the lipooligosaccharide (LOS) on the outer membrane is the most potent inflammatory molecule it expresses due to the interactions of the lipid A moiety of LOS with receptors of the innate immune system. We previously reported that increased phosphorylation of hexaacylated neisserial lipid A is correlated with greater inflammatory potential. Here we postulate that variability in lipid A phosphorylation can tip the balance of innate immune responses towards homeostatic tolerance or proinflammatory signaling that affects adaptive immune responses, causing disease with meningitis only, or septicemia with or without meningitis, respectively. Furthermore, we propose that studies of the relationship between bacterial virulence and gene expression should consider whether genetic variation could affect properties of biosynthetic enzymes resulting in LOS structural differences that alter disease pathobiology.
PMID
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Authors

Mayor MeshTerms
Keywords

Neisseria meningitidis

adaptive immunity

endotoxin tolerance

innate immunity

lipooligosaccharide

proinflammatory

Journal Title pathogens and disease
Publication Year Start




PMID- 28423169
OWN - NLM
STAT- In-Process
DA  - 20170419
LR  - 20170421
IS  - 2049-632X (Electronic)
IS  - 2049-632X (Linking)
VI  - 75
IP  - 3
DP  - 2017 Apr 01
TI  - Innate immune response to lipooligosaccharide: pivotal regulator of the
      pathobiology of invasive Neisseria meningitidis infections.
LID - 10.1093/femspd/ftx030 [doi]
AB  - Infections due to Neisseria meningitidis afflict more than one million people
      worldwide annually and cause death or disability in many survivors. The clinical 
      course of invasive infections has been well studied, but our understanding of the
      cause of differences in patient outcomes has been limited because these are
      dependent on multiple factors including the response of the host, characteristics
      of the bacteria and interactions between the host and the bacteria. The
      meningococcus is a highly inflammatory organism, and the lipooligosaccharide
      (LOS) on the outer membrane is the most potent inflammatory molecule it expresses
      due to the interactions of the lipid A moiety of LOS with receptors of the innate
      immune system. We previously reported that increased phosphorylation of
      hexaacylated neisserial lipid A is correlated with greater inflammatory
      potential. Here we postulate that variability in lipid A phosphorylation can tip 
      the balance of innate immune responses towards homeostatic tolerance or
      proinflammatory signaling that affects adaptive immune responses, causing disease
      with meningitis only, or septicemia with or without meningitis, respectively.
      Furthermore, we propose that studies of the relationship between bacterial
      virulence and gene expression should consider whether genetic variation could
      affect properties of biosynthetic enzymes resulting in LOS structural differences
      that alter disease pathobiology.
CI  - Published by Oxford University Press on behalf of FEMS 2017. This work is written
      by (a) US Government employee(s) and is in the public domain in the US.
FAU - John, Constance M
AU  - John CM
AD  - Center for Immunochemistry, Veterans Affairs Medical Center, 4150 Clement Street,
      San Francisco, CA 94121, USA.
AD  - Department of Laboratory Medicine, University of California, San Francisco, CA
      94143, USA.
FAU - Phillips, Nancy J
AU  - Phillips NJ
AD  - Department of Pharmaceutical Chemistry, University of California, San Francisco, 
      CA 94143, USA.
FAU - Stein, Daniel C
AU  - Stein DC
AD  - University of Maryland, Department of Cell Biology and Molecular Genetics,
      College Park, MD 20742 USA.
FAU - Jarvis, Gary A
AU  - Jarvis GA
AD  - Center for Immunochemistry, Veterans Affairs Medical Center, 4150 Clement Street,
      San Francisco, CA 94121, USA.
AD  - Department of Laboratory Medicine, University of California, San Francisco, CA
      94143, USA.
LA  - eng
GR  - I01 BX000727/BX/BLRD VA/United States
PT  - Journal Article
PL  - United States
TA  - Pathog Dis
JT  - Pathogens and disease
JID - 101595366
OTO - NOTNLM
OT  - Neisseria meningitidis
OT  - adaptive immunity
OT  - endotoxin tolerance
OT  - innate immunity
OT  - lipooligosaccharide
OT  - proinflammatory
EDAT- 2017/04/20 06:00
MHDA- 2017/04/20 06:00
CRDT- 2017/04/20 06:00
PHST- 2017/01/04 [received]
PHST- 2017/03/11 [accepted]
AID - 3569603 [pii]
AID - 10.1093/femspd/ftx030 [doi]
PST - ppublish
SO  - Pathog Dis. 2017 Apr 1;75(3). doi: 10.1093/femspd/ftx030.

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