Klegeris A, McGeer P L
Kinsmen Laboratory of Neurological Research, University of British Columbia, 2255 Wesbrook Mall, Vancouver, BC V6T 1Z3, Canada.
Neurosci Lett. 2001 Nov 2;313(1-2):41-4. doi: 10.1016/s0304-3940(01)02251-0.
We measured the secretion of interleukin (IL)1beta, IL-6 and tumor necrosis factor-alpha (TNF-alpha) from human monocytic (THP-1), astrocytic (U-373 MG) and neuronal (SH-SY5Y) cell lines alone and in co-culture, with and without stimulation by a combination of lipopolysaccharide (LPS) plus interferon-gamma (IFN-gamma) or amyloid beta peptide 1-40 (Abeta). LPS+IFN-gamma stimulation increased IL-1beta secretion 16-fold from THP-1 cells. It increased IL-6 secretion 23-fold from THP-1 cells and 2.5-fold from U-373 MG cells. It increased TNF-alpha secretion 3.4-fold from THP-1 cells, but did not influence its secretion from U-373 MG cells. It did not affect the secretion of any of the cytokines from SH-SY5Y cells. Abeta stimulation increased IL-6 secretion 2.3-fold from U-373 MG cells but did not influence secretion of IL-1beta or TNF-alpha. Abeta stimulation also failed to influence secretion of any of the cytokines from THP-1 or SH-SY5Y cells. When THP-1 and U-373 MG cells were cocultured, IL-1beta and IL-6 secretion, but not TNF-alpha secretion, were significantly reduced from the levels obtained in independent cultures, suggesting that a mutual suppressive action may occur between microglia and astrocytes.
我们单独及共培养了人单核细胞系(THP - 1)、星形胶质细胞系(U - 373 MG)和神经元细胞系(SH - SY5Y),并在有或无脂多糖(LPS)加干扰素 - γ(IFN - γ)或β淀粉样肽1 - 40(Aβ)刺激的情况下,测量了白细胞介素(IL)1β、IL - 6和肿瘤坏死因子 - α(TNF - α)的分泌情况。LPS + IFN - γ刺激使THP - 1细胞的IL - 1β分泌增加了16倍。它使THP - 1细胞的IL - 6分泌增加了23倍,使U - 373 MG细胞的IL - 6分泌增加了2.5倍。它使THP - 1细胞的TNF - α分泌增加了3.4倍,但不影响U - 373 MG细胞的TNF - α分泌。它对SH - SY5Y细胞的任何一种细胞因子分泌均无影响。Aβ刺激使U - 373 MG细胞的IL - 6分泌增加了2.3倍,但不影响IL - 1β或TNF - α的分泌。Aβ刺激也未能影响THP - 1或SH - SY5Y细胞的任何一种细胞因子分泌。当THP - 1和U - 373 MG细胞共培养时,IL - 1β和IL - 6的分泌,但不包括TNF - α的分泌,与独立培养时相比显著降低,这表明小胶质细胞和星形胶质细胞之间可能发生相互抑制作用。