Effect of sodium butyrate on reactive oxygen species generation by human neutrophils

Q. Liu, T. Shimoyama, Katsuhiko Suzuki, T. Umeda, S. Nakaji, K. Sugawara

Research output: Contribution to journalArticle

47 Citations (Scopus)

Abstract

Background: Short-chain fatty acids enema has been shown to be effective in the treatment of ulcerative colitis (UC). However, the mechanisms that lead to this response have not been well characterized. The aims of this study were to investigate the effect sodium butyrate has on reactive oxygen species (ROS) generation by human neutrophils, which are responsible for mucosal injury. Methods: Human neutrophils incubated with or without sodium butyrate were stimulated with opsonized zymosan (OZ) or phorbol myristate acetate (PMA). ROS generation was largely differentiated with flow cytometry assays of hydroethidine oxidation and dichlorofluorescein oxidation for superoxide anion and hydrogen peroxide respectively, and luminol-dependent chemiluminescence for myeloperoxidase-mediated oxidants. Results: Sodium butyrate (up to 50 mM) did not alter hydroethidine oxidation upon stimulation of the OZ or PMA. However, sodium butyrate at a concentration of 25 mM elevated dichlorofluorescein oxidation to 125 ± 8% (P = 0.028) of control upon stimulation of OZ and to 191 ± 30% (P = 0.0016) upon stimulation of PMA. Contrary to these results, sodium butyrate greatly inhibited chemiluminescence responses in a dose-dependent manner. The inhibition by 50 mM sodium butyrate was 61 ± 6% upon OZ and 71 ± 9% upon PMA, respectively. Conclusions: These data indicate that sodium butyrate up-regulates hydrogen peroxide generation but down-regulates generation of myeloperoxidase-mediated oxidants, the latter being more potent in killing microorganisms and in inducing tissue injury. A possible mechanism is suggested whereby sodium butyrate may inhibit myeloperoxidase activity and hence attenuate the destructive activities of neutrophils in UC.

Original languageEnglish
Pages (from-to)744-750
Number of pages7
JournalScandinavian Journal of Gastroenterology
Volume36
Issue number7
Publication statusPublished - 2001
Externally publishedYes

Fingerprint

Butyric Acid
Reactive Oxygen Species
Neutrophils
Zymosan
Tetradecanoylphorbol Acetate
Peroxidase
Luminescence
Ulcerative Colitis
Oxidants
Hydrogen Peroxide
Luminol
Volatile Fatty Acids
Enema
Wounds and Injuries
Superoxides
Flow Cytometry
Up-Regulation
Down-Regulation

Keywords

  • Human neutrophils
  • Reactive oxygen species
  • Sodium butyrate
  • Ulcerative colitis

ASJC Scopus subject areas

  • Gastroenterology

Cite this

Effect of sodium butyrate on reactive oxygen species generation by human neutrophils. / Liu, Q.; Shimoyama, T.; Suzuki, Katsuhiko; Umeda, T.; Nakaji, S.; Sugawara, K.

In: Scandinavian Journal of Gastroenterology, Vol. 36, No. 7, 2001, p. 744-750.

Research output: Contribution to journalArticle

Liu, Q, Shimoyama, T, Suzuki, K, Umeda, T, Nakaji, S & Sugawara, K 2001, 'Effect of sodium butyrate on reactive oxygen species generation by human neutrophils', Scandinavian Journal of Gastroenterology, vol. 36, no. 7, pp. 744-750.
Liu, Q. ; Shimoyama, T. ; Suzuki, Katsuhiko ; Umeda, T. ; Nakaji, S. ; Sugawara, K. / Effect of sodium butyrate on reactive oxygen species generation by human neutrophils. In: Scandinavian Journal of Gastroenterology. 2001 ; Vol. 36, No. 7. pp. 744-750.
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abstract = "Background: Short-chain fatty acids enema has been shown to be effective in the treatment of ulcerative colitis (UC). However, the mechanisms that lead to this response have not been well characterized. The aims of this study were to investigate the effect sodium butyrate has on reactive oxygen species (ROS) generation by human neutrophils, which are responsible for mucosal injury. Methods: Human neutrophils incubated with or without sodium butyrate were stimulated with opsonized zymosan (OZ) or phorbol myristate acetate (PMA). ROS generation was largely differentiated with flow cytometry assays of hydroethidine oxidation and dichlorofluorescein oxidation for superoxide anion and hydrogen peroxide respectively, and luminol-dependent chemiluminescence for myeloperoxidase-mediated oxidants. Results: Sodium butyrate (up to 50 mM) did not alter hydroethidine oxidation upon stimulation of the OZ or PMA. However, sodium butyrate at a concentration of 25 mM elevated dichlorofluorescein oxidation to 125 ± 8{\%} (P = 0.028) of control upon stimulation of OZ and to 191 ± 30{\%} (P = 0.0016) upon stimulation of PMA. Contrary to these results, sodium butyrate greatly inhibited chemiluminescence responses in a dose-dependent manner. The inhibition by 50 mM sodium butyrate was 61 ± 6{\%} upon OZ and 71 ± 9{\%} upon PMA, respectively. Conclusions: These data indicate that sodium butyrate up-regulates hydrogen peroxide generation but down-regulates generation of myeloperoxidase-mediated oxidants, the latter being more potent in killing microorganisms and in inducing tissue injury. A possible mechanism is suggested whereby sodium butyrate may inhibit myeloperoxidase activity and hence attenuate the destructive activities of neutrophils in UC.",
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AU - Liu, Q.

AU - Shimoyama, T.

AU - Suzuki, Katsuhiko

AU - Umeda, T.

AU - Nakaji, S.

AU - Sugawara, K.

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N2 - Background: Short-chain fatty acids enema has been shown to be effective in the treatment of ulcerative colitis (UC). However, the mechanisms that lead to this response have not been well characterized. The aims of this study were to investigate the effect sodium butyrate has on reactive oxygen species (ROS) generation by human neutrophils, which are responsible for mucosal injury. Methods: Human neutrophils incubated with or without sodium butyrate were stimulated with opsonized zymosan (OZ) or phorbol myristate acetate (PMA). ROS generation was largely differentiated with flow cytometry assays of hydroethidine oxidation and dichlorofluorescein oxidation for superoxide anion and hydrogen peroxide respectively, and luminol-dependent chemiluminescence for myeloperoxidase-mediated oxidants. Results: Sodium butyrate (up to 50 mM) did not alter hydroethidine oxidation upon stimulation of the OZ or PMA. However, sodium butyrate at a concentration of 25 mM elevated dichlorofluorescein oxidation to 125 ± 8% (P = 0.028) of control upon stimulation of OZ and to 191 ± 30% (P = 0.0016) upon stimulation of PMA. Contrary to these results, sodium butyrate greatly inhibited chemiluminescence responses in a dose-dependent manner. The inhibition by 50 mM sodium butyrate was 61 ± 6% upon OZ and 71 ± 9% upon PMA, respectively. Conclusions: These data indicate that sodium butyrate up-regulates hydrogen peroxide generation but down-regulates generation of myeloperoxidase-mediated oxidants, the latter being more potent in killing microorganisms and in inducing tissue injury. A possible mechanism is suggested whereby sodium butyrate may inhibit myeloperoxidase activity and hence attenuate the destructive activities of neutrophils in UC.

AB - Background: Short-chain fatty acids enema has been shown to be effective in the treatment of ulcerative colitis (UC). However, the mechanisms that lead to this response have not been well characterized. The aims of this study were to investigate the effect sodium butyrate has on reactive oxygen species (ROS) generation by human neutrophils, which are responsible for mucosal injury. Methods: Human neutrophils incubated with or without sodium butyrate were stimulated with opsonized zymosan (OZ) or phorbol myristate acetate (PMA). ROS generation was largely differentiated with flow cytometry assays of hydroethidine oxidation and dichlorofluorescein oxidation for superoxide anion and hydrogen peroxide respectively, and luminol-dependent chemiluminescence for myeloperoxidase-mediated oxidants. Results: Sodium butyrate (up to 50 mM) did not alter hydroethidine oxidation upon stimulation of the OZ or PMA. However, sodium butyrate at a concentration of 25 mM elevated dichlorofluorescein oxidation to 125 ± 8% (P = 0.028) of control upon stimulation of OZ and to 191 ± 30% (P = 0.0016) upon stimulation of PMA. Contrary to these results, sodium butyrate greatly inhibited chemiluminescence responses in a dose-dependent manner. The inhibition by 50 mM sodium butyrate was 61 ± 6% upon OZ and 71 ± 9% upon PMA, respectively. Conclusions: These data indicate that sodium butyrate up-regulates hydrogen peroxide generation but down-regulates generation of myeloperoxidase-mediated oxidants, the latter being more potent in killing microorganisms and in inducing tissue injury. A possible mechanism is suggested whereby sodium butyrate may inhibit myeloperoxidase activity and hence attenuate the destructive activities of neutrophils in UC.

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