PMID- 12153519
OWN - NLM
STAT- MEDLINE
DCOM- 20021001
LR  - 20190513
IS  - 0019-2805 (Print)
IS  - 1365-2567 (Electronic)
IS  - 0019-2805 (Linking)
VI  - 106
IP  - 4
DP  - 2002 Aug
TI  - Augmented expression of tumour necrosis factor-alpha induced by 
      lipopolysaccharide in spleen of human monocyte chemoattractant protein-1 
      transgenic mouse enhances the lipopolysaccharide sensitivity of the marginal zone 
      macrophages.
PG  - 554-63
AB  - Monocyte chemoattractant protein-1 (MCP-1) is a protective cytokine in murine 
      endotoxaemia induced by lipopolysaccharide (LPS). In this study, LPS-induced 
      pathophysiology in the human (h) MCP-1 transgenic mouse (Tgm) line was 
      investigated. The hMCP-1 Tgm showed a marked increase in the mortality and weight 
      loss following LPS administration. In the Tgm spleens, disappearance of marginal 
      zone macrophages (MZMphi) and dendritic cells (DC) was induced by a smaller 
      amount of LPS than that required for the disappearance in non-transgenic 
      littermates. A significant number of apoptotic cells were seen in these areas. 
      Furthermore, expressions of tumour necrosis factor-alpha (TNF-alpha), 
      interleukin-1alpha (IL-1alpha), and IL-6 mRNA were enhanced and sustained in the 
      LPS-treated Tgm. Neutralization of TNF-alpha considerably depressed the 
      LPS-sensitivity of Tgm. These findings demonstrate that the continuous and 
      systemic presence of MCP-1 is no more protective toward endotoxaemia and suggest 
      that the high sensitivity of the MZMphi and DC to LPS is attributed to the 
      enhanced TNF-alpha production in the hMCP-1 Tgm.
FAU - Ato, Manabu
AU  - Ato M
AD  - Division of Immunobiology, Research Section of Pathophysiology, Institute for 
      Genetic Medicine, Hokkaido University; Sapporo, Japan. kazunori@imm.hokudai.ac.jp
FAU - Iwabuchi, Kazuya
AU  - Iwabuchi K
FAU - Shimada, Shigeki
AU  - Shimada S
FAU - Mukaida, Naofumi
AU  - Mukaida N
FAU - Onoe, Kazunori
AU  - Onoe K
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Immunology
JT  - Immunology
JID - 0374672
RN  - 0 (Chemokine CCL2)
RN  - 0 (Cytokines)
RN  - 0 (Interleukin-1)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (RNA, Messenger)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Animals
MH  - Apoptosis/immunology
MH  - Chemokine CCL2/genetics/*immunology
MH  - Cytokines/genetics/metabolism
MH  - Dendritic Cells/immunology
MH  - Endotoxemia/*immunology
MH  - Gene Expression
MH  - Humans
MH  - Interleukin-1/metabolism
MH  - Lipopolysaccharides/*immunology
MH  - Macrophages/*immunology
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Transgenic
MH  - RNA, Messenger/genetics
MH  - Spleen/immunology
MH  - Tumor Necrosis Factor-alpha/*metabolism
PMC - PMC1782746
EDAT- 2002/08/03 10:00
MHDA- 2002/10/03 04:00
PMCR- 2003/08/01
CRDT- 2002/08/03 10:00
PHST- 2002/08/03 10:00 [pubmed]
PHST- 2002/10/03 04:00 [medline]
PHST- 2002/08/03 10:00 [entrez]
PHST- 2003/08/01 00:00 [pmc-release]
AID - 1450 [pii]
AID - 10.1046/j.1365-2567.2002.01450.x [doi]
PST - ppublish
SO  - Immunology. 2002 Aug;106(4):554-63. doi: 10.1046/j.1365-2567.2002.01450.x.