Background:
Inorganic nitrate from exogenous and endogenous sources is accumulated
in saliva, reduced to nitrite by oral bacteria and further converted to
nitric oxide (NO) and other bioactive nitrogen oxides in the acidic
gastric lumen. To further explore the role of oral microbiota in this
process we examined the gastric mucus layer in germ free (GF) and
conventional mice given different doses of nitrate and nitrite.
Methods:
Mice were given either nitrate (100 mg/kg/d) or nitrite (0.55–11
mg/kg/d) in the drinking water for 7 days, with the lowest nitrite
dose resembling the levels provided by swallowing of fasting saliva. The
gastric mucus layer was measured in vivo.
Results:
GF animals were almost devoid of the ?rmly adherent mucus layer
compared to conventional mice. Dietary nitrate increased the mucus
thickness in conventional animals but had no effect in GF mice. In
contrast, nitrite at all doses, restored the mucus thickness in GF mice
to the same levels as in conventional animals. The nitrite-mediated
increase in gastric mucus thickness was not inhibited by the soluble
guanylyl cyclase inhibitor ODQ. Mice treated with antibiotics had
signi?cantly thinner mucus than controls. Additional studies on mucin
gene expression demonstrated down regulation of Muc5ac and Muc6 in germ
free mice after nitrite treatment.
Conclusion:
Oral bacteria remotely modulate gastric mucus generation via
bioactivation of salivary nitrate. In the absence of a dietary nitrate
intake, salivary nitrate originates mainly from NO synthase. Thus,
oxidized NO from the endothelium and elsewhere is recycled to regulate
gastric mucus homeostasis.
摘要較長,我們分部分進行解讀。首先是背景部分。
Background: Inorganic nitrate from exogenous and endogenous sources is accumulated in saliva, reduced tonitrite by oral bacteria and further converted to nitric oxide (NO) and other bioactive nitrogen oxides in the acidic gastric lumen. To further explore the role of oral microbiota in this process we examined the gastric mucus layer in germ free (GF) and conventional mice given different doses of nitrate and nitrite.
首先,通過尋找主謂賓快速讀懂背景的主干,即紅色標注的部分。第一句,硝酸鹽積累、還原、轉變,顯然講的是硝酸鹽的命運,換句話說,就是解釋什么是硝酸鹽循環。第二句,“To”引出研究的目的,examined the gastric mucus layer寫出了研究的方法。把它們翻譯成自己的話,就是“硝酸鹽循環是指巴拉巴拉,為了探究口腔細菌在其中的作用,我們檢查了胃黏膜”。
Methods:Mice were given either nitrate (100 mg/kg/d) or nitrite
(0.55–11 mg/kg/d) in the drinking water for 7 days, with the lowest
nitrite dose resembling the levels provided by swallowing of fasting
saliva. The gastric mucus layer was measured in vivo.
Results: GF animals were almost devoid of the ?rmly adherent mucus layer compared to conventional mice. Dietary nitrate increased the mucus thickness in conventional animals but had no effect in GF mice. In contrast, nitrite at all doses, restored the mucus thicknessin GF mice to the same levels as in
conventional animals. The nitrite-mediated increase in gastric mucus
thickness was not inhibited by the soluble guanylyl cyclase inhibitor
ODQ. Mice treated with antibiotics had signi?cantly thinner mucus
than controls. Additional studies on mucin gene expression demonstrated
down regulation of Muc5ac and Muc6 in germ free mice after nitrite
treatment.
Conclusion:Oral bacteria remotely modulate gastric mucus generation via bioactivation of salivary nitrate.
In the absence of a dietary nitrate intake, salivary nitrate originates
mainly from NO synthase. Thus, oxidized NO from the endothelium and
elsewhere is recycled to regulate gastric mucus homeostasis.