Nitric oxide prevents mucosal damage induced by NSAIDs in H. pylori infection

2001 ◽  
Vol 120 (5) ◽  
pp. A147-A147
Author(s):  
M HIROTO ◽  
H OKA ◽  
A SHIOTANI ◽  
M IGUCHI ◽  
N SHINNGAKI ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Mucosal Damage ◽  
H Pylori

Nitric oxide prevents mucosal damage induced by NSAIDs in H. pylori infection

2001 ◽  
Vol 120 (5) ◽  
pp. A147
Author(s):  
Magari Hiroto ◽  
Hisato Oka ◽  
Akiko Shiotani ◽  
Mikitaka Iguchi ◽  
Naoki Shinngaki ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Mucosal Damage ◽  
H Pylori

scholarly journals Role of Activated Protein C in Helicobacter pylori-Associated Gastritis

2000 ◽  
Vol 68 (5) ◽  
pp. 2863-2869 ◽  
Author(s):  
Satoko Oka ◽  
Esteban Cesar Gabazza ◽  
Yukiko Taguchi ◽  
Michihiko Yamaguchi ◽  
Shigehito Nakashima ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Protein C ◽  
Activated Protein C ◽  
Mucosal Damage ◽  
Gastric Mucosal Damage ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Gastric Corpus ◽  
H Pylori

ABSTRACT The protein C (PC) pathway has recently been suggested to play a role in the regulation of the inflammatory response. To further extend the anti-inflammatory effect of activated PC (APC) in vivo, particularly its biological relevance to human disease, the activity of APC in the mucosa of patients with Helicobacter pylori-associated gastritis and the effect of vacuolating cytotoxin (VacA), cytotoxin-associated antigen (CagA), andH. pylori lipopolysaccharide (LPS) on PC activation were evaluated. This study comprised 35 patients with chronic gastritis. There were 20 patients with and 15 without H. pylori infection. The levels of PC and APC-PC inhibitor (PCI) complex were measured by immunoassays. The level of PC was significantly decreased and the level of APC-PCI complex was significantly increased in biopsy specimens from gastric corpus and antrum in patients with H. pylori-associated gastritis as compared to H. pylori-negative subjects. The concentrations of VacA, CagA, and LPS were significantly correlated with those of the APC-PCI complex in biopsy mucosal specimens from the gastric corpus and antrum. H. pylori LPS, VacA, and CagA induced a dose-dependent activation of PC on the surface of monocytic cells. APC inhibited the secretion of tumor necrosis factor alpha (TNF-α) induced by H. pylori LPS. Overall, these results suggest that H. pylori infection is associated with increased APC generation in the gastric mucosa. The inhibitory activity of APC on TNF-α secretion may serve to protect H. pylori-induced gastric mucosal damage.

Roles of ET-1 in endotoxin-induced microcirculatory disturbance in rat small intestine

1996 ◽  
Vol 271 (3) ◽  
pp. G461-G469 ◽  
Author(s):  
S. Miura ◽  
D. Fukumura ◽  
I. Kurose ◽  
H. Higuchi ◽  
H. Kimura ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Intestinal Mucosa ◽  
High Speed ◽  
Platelet Activating Factor ◽  
Video Camera ◽  
Mucosal Damage ◽  
Dependent Manner ◽  
Camera System ◽  
Eta Receptor Antagonist ◽  
Leukocyte Sticking

The major objective of this study was to investigate whether endothelin-1 (ET-1) plays a significant role in endotoxin-induced microcirculatory disturbances of the intestinal mucosa. Submucosal microvessels of the rat ileum were observed by intravital microscopy with a high-speed video camera system. Preceding the apparent intestinal mucosal damage, red blood cell (RBC) velocity was significantly decreased 30 min after endotoxin treatment in both arterioles and venules. The number of leukocytes sticking to submucosal venules was significantly increased at 30 min. BQ-123, an ETA-receptor antagonist, significantly attenuated the decrease in RBC velocity and also prevented an increase in leukocyte sticking as well as the subsequent mucosal damage induced by endotoxin. The ET-1 concentrations began to be elevated in plasma at 15 min and in the mucosa at 30 min and subsequently further increased in a time-dependent manner. A significant decrease in calcium-dependent nitric oxide synthase activity and significant increases in the concentration of platelet-activating factor (PAF) were demonstrated in the intestinal mucosa after endotoxin treatment. BQ-123 also significantly attenuated these changes. We concluded that the increased ET-1 production in intestinal mucosa induced by endotoxin stimulation could lead to leukocyte sticking and decreased RBC velocity in the intestinal microcirculatory beds via ETA receptors, which are closely related to increased production of PAF and decreased synthesis of constitutive nitric oxide.

scholarly journals l-Arginine Availability Regulates Inducible Nitric Oxide Synthase-Dependent Host Defense against Helicobacter pylori

2007 ◽  
Vol 75 (9) ◽  
pp. 4305-4315 ◽  
Author(s):  
Rupesh Chaturvedi ◽  
Mohammad Asim ◽  
Nuruddeen D. Lewis ◽  
Holly M. Scott Algood ◽  
Timothy L. Cover ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Helicobacter Pylori ◽  
Protein Expression ◽  
Translation Initiation Factor ◽  
No Production ◽  
Dependent Manner ◽  
Inos Protein ◽  
Inos Protein Expression ◽  
H Pylori ◽  
Inducible Nitric Oxide

ABSTRACT Helicobacter pylori infection of the stomach causes an active immune response that includes stimulation of inducible nitric oxide (NO) synthase (iNOS) expression. Although NO can kill H. pylori, the bacterium persists indefinitely, suggesting that NO production is inadequate. We determined if the NO derived from iNOS in macrophages was dependent on the availability of its substrate, l-arginine (l-Arg). Production of NO by H. pylori-stimulated RAW 264.7 cells was dependent on the l-Arg concentration in the culture medium, and the 50% effective dose for l-Arg was 220 μM, which is above reported plasma l-Arg levels. While iNOS mRNA induction was l-Arg independent, iNOS protein increased in an l-Arg-dependent manner that did not involve changes in iNOS protein degradation. l-Lysine, an inhibitor of l-Arg uptake, attenuated H. pylori-stimulated iNOS protein expression, translation, NO levels, and killing of H. pylori. While l-Arg starvation suppressed global protein translation, at concentrations of l-Arg at which iNOS protein was only minimally expressed in response to H. pylori, global translation was fully restored and eukaryotic translation initiation factor α was dephosphorylated. H. pylori lacking the gene rocF, which codes for a bacterial arginase, induced higher levels of NO production by increasing iNOS protein levels. When murine gastric macrophages were activated with H. pylori, supraphysiologic levels of l-Arg were required to permit iNOS protein expression and NO production. These findings indicate that l-Arg is rate limiting for iNOS translation and suggest that the levels of l-Arg that occur in vivo do not permit sufficient NO generation by the host to kill H. pylori.

scholarly journals cagA positive and negative Helicobacter pyloristrains are simultaneously present in the stomach of most patients with non-ulcer dyspepsia: relevance to histological damage

Gut ◽  
1998 ◽  
Vol 42 (6) ◽  
pp. 772-778 ◽  
Author(s):  
N Figura ◽  
C Vindigni ◽  
A Covacci ◽  
L Presenti ◽  
D Burroni ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Intestinal Metaplasia ◽  
Normal Mucosa ◽  
Mucosal Damage ◽  
Gastric Mucosal Damage ◽  
Glandular Cell ◽  
Increased Risk ◽  
Molecular Masses ◽  
Non Ulcer Dyspepsia ◽  
H Pylori

Background/Aims—Infection with Helicobacter pylori strains harbouring the cagA gene (cagA+) is associated with an increased risk of developing peptic ulcer and gastric cancer. The aim of this study was to assess whether H pylori isolates with different cagA status were present in patients with non-ulcer dyspepsia, and whether a variable cagA status is relevant to histological gastric mucosal damage and glandular cell proliferation.Methods—Well separated H pyloricolonies (between 2 and 25) from primary plates, per gastric area, for each of 19 patients with non-ulcer dyspepsia were examined forcagA by hybridisation. Western blotting was used to examine both representative colonies for CagA expression and the patients’ sera for antibody response to CagA. Glandular gastric cell proliferation was assessed immunohistochemically.Results—Of the 747 colonies examined, 45.3% werecagA+. All colonies from four patients werecagA+, and all colonies from two patients werecagA−. In 13 patients (68%) both cagA+ andcagA− colonies were found. CagA expression of isolates corresponded to their cagA status. H pyloristrains with different CagA molecular masses were present in three patients. Results based on all 19 patients studied showed that the prevalence of cagA+ colonies in areas with mucosal atrophy associated or not with intestinal metaplasia (67.9%) was significantly higher than in normal mucosa (44.7%) and mucosa from patients with chronic gastritis (44.0%) (p< 0.001). High levels of cell proliferation were associated with histological atrophy with or without intestinal metaplasia, but not with the possession of cagA by organisms colonising the same mucosal sites.Conclusions—Most patients with non-ulcer dyspepsia are infected by both cagA+ and cagA−H pylori colonies. The cagA status of infecting organisms may play a role in the development of atrophy and intestinal metaplasia.

Nitric oxide and sensory afferent neurones modulate the protective effects of low-dose endotoxin on rat gastric mucosal damage

1995 ◽  
Vol 280 (3) ◽  
pp. 339-342 ◽  
Author(s):  
Ma.Dolores Barrachina ◽  
Sara Calatayud ◽  
Lucrecia Moreno ◽  
Ma.Angeles Martínez-Cuesta ◽  
Brendan J.R. Whittle ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Low Dose ◽  
Mucosal Damage ◽  
Gastric Mucosal Damage ◽  
Protective Effects

Role of nitric oxide in pathogenesis of gastric mucosal damage induced by compound in rats

1997 ◽  
Vol 91 (3-5) ◽  
pp. 131-138 ◽  
Author(s):  
T Yasuhiro ◽  
A Konaka ◽  
H Ukawa ◽  
S Kato ◽  
K Takeuchi
Keyword(s):  
Nitric Oxide ◽  
Mucosal Damage ◽  
Gastric Mucosal Damage

Gastric mucosal damage induced by compound 48/80: Roles of serotonin and nitric oxide

1998 ◽  
Vol 13 (11) ◽  
pp. 1099-1106 ◽  
Author(s):  
TETSUYA YASUHIRO ◽  
AKIRA KONAKA ◽  
SHINICHI KATO ◽  
KOJI TAKEUCHI
Keyword(s):  
Nitric Oxide ◽  
Mucosal Damage ◽  
Gastric Mucosal Damage
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