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Titolo:
Circulating cell wall components derived from gram-negative, not gram-positive, bacteria cause a profound induction of the gene-encoding Toll-like receptor 2 in the CNS
Autore:
Laflamme, N; Soucy, G; Rivest, S;
Indirizzi:
Univ Laval, CHUL, Res Ctr, Mol Endocrinol Lab, Quebec City, PQ G1V 4G2, Canada Univ Laval Quebec City PQ Canada G1V 4G2 Quebec City, PQ G1V 4G2, Canada Univ Laval, Dept Anat & Physiol, Quebec City, PQ G1V 4G2, Canada Univ Laval Quebec City PQ Canada G1V 4G2 Quebec City, PQ G1V 4G2, Canada
Titolo Testata:
JOURNAL OF NEUROCHEMISTRY
fascicolo: 3, volume: 79, anno: 2001,
pagine: 648 - 657
SICI:
0022-3042(200111)79:3<648:CCWCDF>2.0.ZU;2-E
Fonte:
ISI
Lingua:
ENG
Soggetto:
KAPPA-B-ALPHA; LIPOPOLYSACCHARIDE; BRAIN; TLR4; TRANSCRIPTION; POPULATIONS; RECOGNITION; ACTIVATION; EXPRESSION; SYSTEM;
Keywords:
innate immune response; lipopolysaccharide; lipoteichoic acid; microglia; NF-kappa B; peptidoglycan;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
23
Recensione:
Indirizzi per estratti:
Indirizzo: Rivest, S Univ Laval, CHUL, Res Ctr, Mol Endocrinol Lab, 2705 Boul Laurier, Quebec City, PQ G1V 4G2, Canada Univ Laval 2705 Boul Laurier Quebec City PQ Canada G1V 4G2 anada
Citazione:
N. Laflamme et al., "Circulating cell wall components derived from gram-negative, not gram-positive, bacteria cause a profound induction of the gene-encoding Toll-like receptor 2 in the CNS", J NEUROCHEM, 79(3), 2001, pp. 648-657

Abstract

The recent characterization of human homologs of Toll may be the missing link for the transduction events leading to nuclear factor-KB (NF-KB) activity and proinflammatory gene transcription during innate immune response. Mammalian cells may express as many as 10 distinct Toll-like receptors (TLRs), although TLR2 is a key receptor for recognizing cell wall components of Gram-positive bacteria. The present study investigated the effects of circulating bacterial cell wall components on the expression of the gene-encodingTLR2 across the mouse brain. Surprisingly, while Gram-negative components caused a robust increase in TLR2 transcription within the cerebral tissue, peptidoglycan (PGN) and lipoteichoic acid (LTA), either alone or combined, failed to modulate the receptor transcript. Indeed, the mRNA levels for TLR2 in the choroid plexus and few other regions of the brain remained similarbetween vehicle-, LTA-, PGN-, and LTA/PGN-administered mice at all the times evaluated (i.e. 30 min to 24 h post-intraperitoneal injection). This contrasts with the profound de novo expression of TLR2 following a single systemic injection of the lipopolysaccharide (LPS). The signal was first detected in regions devoid of blood-brain barrier and few blood vessels and microcapillaries. A second wave of TLR2 expression was also detected from these structures to their surrounding parenchymal cells that stained for a microglial marker iba 1. The rapid induction of I kappaB alpha (index of NF-KB activity) and up-regulation of the adaptor protein MyD88 suggest that LPS-induced TLR2 transcription may be dependent on the NF-kappaB pathway. These data provide the evidence that TLR2 is not only present in the brain, but itsencoding gene is regulated by cell wall components derived from Gram-negative, not Gram-positive, bacteria. The robust wave of TLR2-expressing microglial cells may have a determinant impact on the innate immune response thatoccurs in the brain during systemic infection by Gram-negative, not Gram-positive, bacteria.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 28/11/20 alle ore 17:13:40