PMID- 10814786 OWN - NLM STAT- MEDLINE DCOM- 20000626 LR - 20220310 IS - 0165-5728 (Print) IS - 0165-5728 (Linking) VI - 106 IP - 1-2 DP - 2000 Jul 1 TI - Inducible expression of the long pentraxin PTX3 in the central nervous system. PG - 87-94 AB - PTX3 is a prototypic long pentraxin consisting of a C terminal 203-amino acid pentraxin-like domain coupled with an N-terminal 178-amino acid unrelated portion. PTX3 is induced by primary proinflammatory signals in various cell types, most prominently macrophages and endothelial cells. Other long pentraxins, such as murine or rat neuronal pentraxin 1 (NP1) and human neuronal pentraxin 2 (NPTX2), are expressed in the central nervous system (CNS). The present study was designed to investigate whether PTX3 is expressed in the brain and to define the structures and cells involved. Intracerebroventricular (i.c.v.), but not i.v., injection of LPS induced high levels of PTX3 mRNA in the mouse brain. In contrast NP1 is constitutively expressed in the murine CNS and is not modulated by LPS administration. I.c.v. IL-1beta was also a potent inducer of PTX3 expression in the CNS, whereas TNFalpha was substantially less effective and IL-6 induced a barely detectable signal. Central administration of LPS and IL-1 induced PTX3 also in the periphery (heart), whereas the reverse did not occur. Expression of PTX3 was also observed in the brain of mice infected with Candida albicans (C. albicans) or Cryptococcus neoformans. (C. neoformans). The kinetics of PTX3 gene induction were consistently different between C. albicans- and C. neoformans-infected mice, according to the diverse outcome of the CNS immune reaction. In situ hybridization revealed that i.c.v. injection of LPS induced a strong PTX3 expression in presumptive glial cells, in the white matter (corpus callosum, fimbria) and meningeal pia mater as well as in dentate gyrus hilus and granule cells. No constitutive expression of PTX3 was detected. Central expression of PTX3 may amplify mechanisms of innate resistance and damage in the CNS. The possibility of a direct interaction of PTX3 with neuronal cells, as suggested for NPTX2, remains to be explored. FAU - Polentarutti, N AU - Polentarutti N AD - Istituto di Ricerche Farmacologiche 'Mario Negri', Via Eritrea 62, 20157, Milano, Italy. FAU - Bottazzi, B AU - Bottazzi B FAU - Di Santo, E AU - Di Santo E FAU - Blasi, E AU - Blasi E FAU - Agnello, D AU - Agnello D FAU - Ghezzi, P AU - Ghezzi P FAU - Introna, M AU - Introna M FAU - Bartfai, T AU - Bartfai T FAU - Richards, G AU - Richards G FAU - Mantovani, A AU - Mantovani A LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - Netherlands TA - J Neuroimmunol JT - Journal of neuroimmunology JID - 8109498 RN - 0 (Interleukin-1) RN - 0 (Lipopolysaccharides) RN - 0 (Nerve Tissue Proteins) RN - 0 (RNA, Messenger) RN - 0 (Recombinant Proteins) RN - 0 (Serum Amyloid P-Component) RN - 0 (Tumor Necrosis Factor-alpha) RN - 0 (neuronal pentraxin) RN - 148591-49-5 (PTX3 protein) RN - 9007-41-4 (C-Reactive Protein) SB - IM MH - Animals MH - Brain/cytology/drug effects/*metabolism MH - C-Reactive Protein/genetics/*metabolism MH - Candidiasis/metabolism MH - Cryptococcosis/metabolism MH - Gene Expression Regulation MH - Humans MH - Injections, Intraventricular MH - Interleukin-1/pharmacology MH - Lipopolysaccharides/pharmacology MH - Male MH - Mice MH - Mice, Inbred Strains MH - Myocardium/metabolism MH - Nerve Tissue Proteins/metabolism MH - RNA, Messenger/metabolism MH - Recombinant Proteins/pharmacology MH - Serum Amyloid P-Component/genetics/*metabolism MH - Transcriptional Activation MH - Tumor Necrosis Factor-alpha/pharmacology EDAT- 2000/05/18 09:00 MHDA- 2000/07/06 11:00 CRDT- 2000/05/18 09:00 PHST- 2000/05/18 09:00 [pubmed] PHST- 2000/07/06 11:00 [medline] PHST- 2000/05/18 09:00 [entrez] AID - S0165572800002149 [pii] AID - 10.1016/s0165-5728(00)00214-9 [doi] PST - ppublish SO - J Neuroimmunol. 2000 Jul 1;106(1-2):87-94. doi: 10.1016/s0165-5728(00)00214-9.