PMID- 11012759
OWN - NLM
STAT- MEDLINE
DCOM- 20001016
LR  - 20190513
IS  - 0019-2805 (Print)
IS  - 1365-2567 (Electronic)
IS  - 0019-2805 (Linking)
VI  - 101
IP  - 1
DP  - 2000 Sep
TI  - Alteration in the responsiveness to tumour necrosis factor-alpha is crucial for 
      maximal expression of monocyte chemoattractant protein-1 in human neutrophils.
PG  - 97-103
AB  - We previously reported delayed expression of monocyte chemoattractant protein-1 
      (MCP-1) in human neutrophils cultured with a cytokine-rich crude supernatant of 
      phytohaemagglutinin-stimulated peripheral blood mononuclear cells (PHA-sup). 
      Tumour necrosis factor-alpha (TNF-alpha) contained in the PHA-sup played a key 
      role in this event, but there appeared to be another factor(s) in the same 
      supernatant that co-operated with TNF-alpha for maximal MCP-1 expression. In the 
      present study, we reduced TNF-alpha concentrations in the PHA-sup to minimal 
      levels using anti-TNF-alpha affinity columns (TNF-depleted-sup) and investigated 
      the co-operation between TNF-alpha and TNF-depleted-sup. Nine hours of 
      preincubation with TNF-depleted-sup altered the responsiveness of neutrophils to 
      TNF-alpha and enabled TNF-alpha to increase the level of MCP-1 expression to a 
      maximal level within 4 hr. The priming effect was not due to the increased 
      expression of cell-surface TNF receptors. However, the activation of primed cells 
      by TNF-alpha was clearly through TNF receptor-p55. Finally, the activity in the 
      TNF-depleted-sup that co-operated with TNF-alpha was eluted at 60 000 MW on 
      high-performance liquid chromatography-gel filtration. Thus, delayed neutrophil 
      expression of MCP-1 is regulated by a cytokine-dependent mechanism that induces 
      neutrophils to enter a 'mature' stage.
FAU - Yamashiro, S
AU  - Yamashiro S
AD  - Laboratory of Molecular Immunoregulation, National Cancer Institute-Frederick 
      Cancer Research and Development Center, Frederick, MD, USA.
FAU - Kamohara, H
AU  - Kamohara H
FAU - Yoshimura, T
AU  - Yoshimura T
LA  - eng
PT  - Journal Article
PL  - England
TA  - Immunology
JT  - Immunology
JID - 0374672
RN  - 0 (Antigens, CD)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Culture Media, Conditioned)
RN  - 0 (Phytohemagglutinins)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, Tumor Necrosis Factor)
RN  - 0 (Receptors, Tumor Necrosis Factor, Type I)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Antigens, CD/immunology
MH  - Cell Culture Techniques
MH  - Chemokine CCL2/genetics/*metabolism
MH  - Culture Media, Conditioned
MH  - Dose-Response Relationship, Immunologic
MH  - Gene Expression Regulation
MH  - Humans
MH  - Neutrophils/*immunology
MH  - Phytohemagglutinins/immunology
MH  - RNA, Messenger/genetics
MH  - Receptors, Tumor Necrosis Factor/immunology
MH  - Receptors, Tumor Necrosis Factor, Type I
MH  - Tumor Necrosis Factor-alpha/*immunology
PMC - PMC2327059
EDAT- 2000/09/30 11:00
MHDA- 2000/10/21 11:01
PMCR- 2001/09/01
CRDT- 2000/09/30 11:00
PHST- 2000/09/30 11:00 [pubmed]
PHST- 2000/10/21 11:01 [medline]
PHST- 2000/09/30 11:00 [entrez]
PHST- 2001/09/01 00:00 [pmc-release]
AID - imm085 [pii]
AID - 10.1046/j.1365-2567.2000.00085.x [doi]
PST - ppublish
SO  - Immunology. 2000 Sep;101(1):97-103. doi: 10.1046/j.1365-2567.2000.00085.x.