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6.2.2 Agrimoniin-mouse and hPBMC studies - IL-1 β release
Miyamoto and Okuda examined some immune system components in
their search for biological mediators of tannin-induced anti-tumor
activity. Specifically, treatment of mice with agrimoniin ( 61 ) stimulated
growth of peritoneal exudate cells (PECs) with a peak of about 14 × 10 6
cells/mouse produced after 4 days, while control was approximately 4 ×
10 6 cells/mouse (Miyamoto et al. , 1987a). Of these cells, 58% were
monocytes, 23% were polymorphonuclear (PMN) leukocytes, and 20%
were lymphocytes. Administration of agrimoniin to isolated murine
PECs resulted in increased natural killer (NK) cell activity that peaked
after 2 days (Miyamoto et al. , 1988). The NK cells were not, however,
cytotoxic to MM2 and MH134 tumor cells. In contrast, the adherent
PECs (presumably macrophages) did appear to inhibit tumor cell growth
(MM2 and MH134). Removal of serum from mice treated with both
MM2 tumor cells and agrimoniin, and addition of that serum to a culture
of only adherent PEC and MM2 cells, led to complete tumor lysis. The
serum was assumed to contain immunostimulatory factors such as
cytokines. The cell lytic activity of the serum peaked after 6 days
following intraperitoneal injection.
Analysis with an enzyme-linked immunosorbent assay (ELISA) of
the supernatant above hPBMC's treated with agrimoniin led to the
identification of significant quantities (average of 1203 pg/mL) of the
cytokine IL-1β compared to the untreated cells (300 pg/mL) (Murayama
et al. , 1992). Following the same experimental procedure, treatment of
hPBMC's with E. coli LPS at 10 μg/mL led to the release of an average
of 1350 pg/mL of IL-1β. The supernatant also was examined for the
cytokine IL-2, but this species could not be detected by a proliferation
assay of IL-2-dependent CTLL2 cells.
6.2.2.1 Immunostimulation - IL-1 β secretion
Interleukin-1 (IL-1, also known by hemopoietin-1, catabolin, osteoclast-
activating factor, and B-cell stimulatory factor), is another pluripotent
cytokine that has been identified as a mediator of septic shock. IL-1 was
first described in the literature in 1972 and was named in 1979 at the 2nd
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