Abstract
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-α (TNF-α) 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-α for maximal MCP-1 expression. In the present study, we reduced TNF-α concentrations in the PHA-sup to minimal levels using anti-TNF-α affinity columns (TNF-depleted-sup) and investigated the co-operation between TNF-α and TNF-depleted-sup. Nine hours of preincubation with TNF-depleted-sup altered the responsiveness of neutrophils to TNF-α and enabled TNF-α 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-α was clearly through TNF receptor-p55. Finally, the activity in the TNF-depleted-sup that co-operated with TNF-α 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.
| Original language | English |
|---|---|
| Pages (from-to) | 97-103 |
| Number of pages | 7 |
| Journal | Immunology |
| Volume | 101 |
| Issue number | 1 |
| DOIs | |
| Publication status | Published - 2000 |
| Externally published | Yes |
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ASJC Scopus subject areas
- Immunology
Cite this
Alteration in the responsiveness to tumour necrosis factor-α is crucial for maximal expression of monocyte chemoattractant protein-1 in human neutrophils. / Yamashiro, S.; Kamohara, H.; Yoshimura, Teizo.
In: Immunology, Vol. 101, No. 1, 2000, p. 97-103.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Alteration in the responsiveness to tumour necrosis factor-α is crucial for maximal expression of monocyte chemoattractant protein-1 in human neutrophils
AU - Yamashiro, S.
AU - Kamohara, H.
AU - Yoshimura, Teizo
PY - 2000
Y1 - 2000
N2 - 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-α (TNF-α) 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-α for maximal MCP-1 expression. In the present study, we reduced TNF-α concentrations in the PHA-sup to minimal levels using anti-TNF-α affinity columns (TNF-depleted-sup) and investigated the co-operation between TNF-α and TNF-depleted-sup. Nine hours of preincubation with TNF-depleted-sup altered the responsiveness of neutrophils to TNF-α and enabled TNF-α 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-α was clearly through TNF receptor-p55. Finally, the activity in the TNF-depleted-sup that co-operated with TNF-α 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.
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-α (TNF-α) 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-α for maximal MCP-1 expression. In the present study, we reduced TNF-α concentrations in the PHA-sup to minimal levels using anti-TNF-α affinity columns (TNF-depleted-sup) and investigated the co-operation between TNF-α and TNF-depleted-sup. Nine hours of preincubation with TNF-depleted-sup altered the responsiveness of neutrophils to TNF-α and enabled TNF-α 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-α was clearly through TNF receptor-p55. Finally, the activity in the TNF-depleted-sup that co-operated with TNF-α 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.
UR - http://www.scopus.com/inward/record.url?scp=0033797370&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0033797370&partnerID=8YFLogxK
U2 - 10.1046/j.1365-2567.2000.00085.x
DO - 10.1046/j.1365-2567.2000.00085.x
M3 - Article
C2 - 11012759
AN - SCOPUS:0033797370
VL - 101
SP - 97
EP - 103
JO - Immunology
JF - Immunology
SN - 0019-2805
IS - 1
ER -