Inhibition of Intracellular Cathepsin Activities and Suppression of Immune Responses Mediated by Helper T Lymphocyte Type-2 by Peroral or Intraperitoneal Administration of Vitamin B6

We reported that pyridoxal phosphate (PAP), a coenzyme form of vitamin B6, strongly inhibits activities of cathepsin B and weakly inhibits those of cathepsins S, K, and C in vitro. Either intraperitoneal injection or peroral administration of medication doses of vitamin B6 in the diet caused dose-de...

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Published in:Biochemical and biophysical research communications Vol. 272; no. 1; pp. 151 - 155
Main Authors: Katunuma, N., Matsui, A., Endo, K., Hanba, J., Sato, A., Nakano, M., Yuto, Y., Tada, Y., Asao, T., Himeno, K., Maekawa, Y., Inubushi, T.
Format: Journal Article
Language:English
Published: United States Elsevier Inc 27-05-2000
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Summary:We reported that pyridoxal phosphate (PAP), a coenzyme form of vitamin B6, strongly inhibits activities of cathepsin B and weakly inhibits those of cathepsins S, K, and C in vitro. Either intraperitoneal injection or peroral administration of medication doses of vitamin B6 in the diet caused dose-dependent inhibition of hepatic cathepsins B, L, S, and C, and the inhibition was exhibited much more significantly in the case of a high protein diet than in a low protein diet. Administration of vitamin B6 induced the suppression of immune responses against ovalbumin (OVA) mediated by helper T lymphocyte type-2, based on the suppression of antigen processing by cathepsin B inhibition, as in the case of CA-074 administration, a cathepsin B specific inhibitor. Ovalbumin-dependent production of immunoglobulins IgE, IgG1 and interleukin IL-4 was suppressed by administration of medication doses of pyridoxal (PA) or pyridoxine (PI), while the production of IgG2a and interferon (INF)-γ mediated by helper T lymphocyte type 1 was not changed. Administration of medication doses of vitamin B6 caused the inhibition of intracellular cathepsin B activity due to suppression of the functions of helper T lymphocyte type-2.
Bibliography:http://www.academicpress.com/bbrc
http://www.sciencedirect.com/science/journal/0006291X
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content type line 23
ISSN:0006-291X
1090-2104
DOI:10.1006/bbrc.2000.2738