Endogenous interleukin 10 prevents apoptosis in macrophages during Salmonella infection
T Arai, K Hiromatsu, H Nishimura, Y Kimura… - Biochemical and …, 1995 - Elsevier
T Arai, K Hiromatsu, H Nishimura, Y Kimura, N Kobayashi, H Ishida, Y Nimura, Y Yoshikai
Biochemical and biophysical research communications, 1995•ElsevierTo elucidate the biological roles of endogenous interleukin 10 (IL-10) in macrophage
responses during bacterial infection, we examined in vitro effects of neutralizing IL-10 by anti-
IL-10 monoclonal antibodies (mAb) on apoptosis of the peritoneal macrophages following
Salmonella choleraesuis infection. Marked increments of TNF-α production were observed
in the culture supernatant later than 6 h after in vitro culture with anti-IL-10 mAb. These
macrophages succumbed to apoptosis at this stage accompanied by marked increment of IL …
responses during bacterial infection, we examined in vitro effects of neutralizing IL-10 by anti-
IL-10 monoclonal antibodies (mAb) on apoptosis of the peritoneal macrophages following
Salmonella choleraesuis infection. Marked increments of TNF-α production were observed
in the culture supernatant later than 6 h after in vitro culture with anti-IL-10 mAb. These
macrophages succumbed to apoptosis at this stage accompanied by marked increment of IL …
To elucidate the biological roles of endogenous interleukin 10 (IL-10) in macrophage responses during bacterial infection, we examined in vitro effects of neutralizing IL-10 by anti-IL-10 monoclonal antibodies (mAb) on apoptosis of the peritoneal macrophages following Salmonella choleraesuis infection. Marked increments of TNF-α production were observed in the culture supernatant later than 6 h after in vitro culture with anti-IL-10 mAb. These macrophages succumbed to apoptosis at this stage accompanied by marked increment of IL-1 release, despite the expression of higher amount of endogenous heat shock protein 70, an inhibitor of TNF-α-mediated apoptosis. These results suggest that endogenous IL-10 plays an essential role in protection of Salmonella-infected macrophages from autocrine suicide caused by excessive production of TNF-α after killing of Salmonella.
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