PMID- 11160006
OWN - NLM
STAT- MEDLINE
DCOM- 20010315
LR  - 20231213
IS  - 0019-9567 (Print)
IS  - 1098-5522 (Electronic)
IS  - 0019-9567 (Linking)
VI  - 69
IP  - 2
DP  - 2001 Feb
TI  - Neural route of cerebral Listeria monocytogenes murine infection: role of immune 
      response mechanisms in controlling bacterial neuroinvasion.
PG  - 1093-100
AB  - The pathologic features of cerebral Listeria monocytogenes infection strongly 
      suggest that besides hematogenous spread, bacteria might also spread via a neural 
      route. We propose that after snout infection of recombination activating gene 1 
      (RAG-1)-deficient mice, L. monocytogenes spreads to the brain via a neural route. 
      The neural route of invasion is suggested by (i) the immunostaining of L. 
      monocytogenes in the trigeminal ganglia (TG) and brain stem but not in other 
      areas of the brain; (ii) the kinetics of bacterial loads in snout, TG, and brain; 
      and (iii) the increased resistance of mice infected with a plcB bacterial mutant 
      (unable to spread from cell to cell). Gamma interferon (IFN-gamma) plays a 
      protective role in neuroinvasion; inducible nitric oxide synthase (iNOS) accounts 
      only partially for the protection, as shown by a comparison of the 
      susceptibilities of IFN-gamma receptor (IFN-gamma R)-deficient, iNOS-deficient, 
      and wild-type mice to snout infection with L. monocytogenes. The dramatically 
      enhanced susceptibility of RAG-1-deficient, IFN-gamma R gene-deficient mice 
      indicated the overall importance of innate immune cells in the release of 
      protective levels of IFN-gamma. The source of IFN-gamma appeared to be NK cells, 
      as shown by use of RAG-1-deficient, gamma-chain receptor gene-deficient mice; NK 
      cells played a relevant protective role in neuroinvasion through a 
      perforin-independent mechanism. In vitro evidence indicated that IFN-gamma can 
      directly induce bacteriostatic mechanisms in neural tissue.
FAU - Jin, Y
AU  - Jin Y
AD  - Department of Neuroscience, Karolinska Institutet, Stockholm, Sweden. 
      Martin.Rottenberg@mtc.ki.se
FAU - Dons, L
AU  - Dons L
FAU - Kristensson, K
AU  - Kristensson K
FAU - Rottenberg, M E
AU  - Rottenberg ME
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Infect Immun
JT  - Infection and immunity
JID - 0246127
RN  - 0 (Receptors, Interferon)
RN  - 82115-62-6 (Interferon-gamma)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase Type II)
RN  - EC 1.14.13.39 (Nos2 protein, mouse)
RN  - EC 3.1.- (Phospholipases)
SB  - IM
MH  - Animals
MH  - Brain/*microbiology
MH  - Cytotoxicity, Immunologic
MH  - Interferon-gamma/physiology
MH  - Killer Cells, Natural/immunology
MH  - Listeria monocytogenes/*immunology
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Nitric Oxide Synthase/physiology
MH  - Nitric Oxide Synthase Type II
MH  - Phospholipases/physiology
MH  - Receptors, Interferon/physiology
MH  - Trigeminal Ganglion/microbiology
MH  - Interferon gamma Receptor
PMC - PMC97990
EDAT- 2001/02/13 11:00
MHDA- 2001/03/17 10:01
PMCR- 2001/02/01
CRDT- 2001/02/13 11:00
PHST- 2001/02/13 11:00 [pubmed]
PHST- 2001/03/17 10:01 [medline]
PHST- 2001/02/13 11:00 [entrez]
PHST- 2001/02/01 00:00 [pmc-release]
AID - 1016 [pii]
AID - 10.1128/IAI.69.2.1093-1100.2001 [doi]
PST - ppublish
SO  - Infect Immun. 2001 Feb;69(2):1093-100. doi: 10.1128/IAI.69.2.1093-1100.2001.