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1994 ; 85
(11
): 1137-43
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Improvement of macrophage dysfunction by administration of anti-transforming
growth factor-beta antibody in EL4-bearing hosts
#MMPMID7829399
Maeda H
; Tsuru S
; Shiraishi A
Jpn J Cancer Res
1994[Nov]; 85
(11
): 1137-43
PMID7829399
show ga
An experimental therapy for improvement of macrophage dysfunction caused by
transforming growth factor-beta (TGF-beta) was tried in EL4 tumor-bearing mice.
TGF-beta was detected in cell-free ascitic fluid from EL4-bearers, but not in
that from normal mice, by western blot analysis. The ascites also showed
growth-suppressive activity against Mv1Lu cells, and the suppressive activity was
potentiated by transient acidification. To investigate whether the functions of
peritoneal macrophages were suppressed in EL4-bearers, the abilities to produce
nitric oxide and tumor necrosis factor-alpha (TNF-alpha) upon lipopolysaccharide
(LPS) stimulation were measured. Both abilities of macrophages in EL4-bearing
mice were suppressed remarkably on day 9, and decreased further by day 14,
compared with non-tumor-bearing controls. TGF-beta activity was abrogated by
administration of anti-TGF-beta antibody to EL4-bearing mice. While a large
amount of TGF-beta was detected in ascitic fluid from control EL4-bearers, little
TGF-beta was detectable in ascites from EL4-bearers given anti-TGF-beta antibody.
Furthermore, while control macrophages exhibited little or no production of
nitric oxide and TNF-alpha on LPS stimulation in vitro, macrophages from
EL4-bearers administered with anti-TGF-beta antibody showed the same ability as
normal macrophages. These results clearly indicate that TGF-beta contributes to
macrophage dysfunction and that the administration of specific antibody for
TGF-beta reverses macrophage dysfunction in EL4-bearing hosts.
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