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Helicobacter pylori and gastritis
Helicobacter pylori and gastritis
Helicobacter pylori requires iron to survive and propogate in the
body. Antibiotics bind up iron and remove it from the scenario /
disease process.
Gastritis is caused by increased red blood cell production and
H.pylori has been found to be associated with gastritis as per its
association with peptic ulcers.
Sooo IS the erradication of the H.pylori due TO the sequestration /
elimination OF the .. iron ..?
The article below states .. smoking / pseudopolycythemia is associated
with decreased ability to clear the pathogen .. ?
Sooo .. does the polycythemia / increased red blood cells /
erythrocytosis .. PRECEDE .. the colonization OF the H.pylori .. ? ..
ALLOWING the H.pylori to take and proliferate .. BY .. causing
gastritis / blood loss .. iron **AVAILABILITY** / lack of iron
sequestering ABILITY .. ?
----------------------------------------------------
<<snip>>
Smoking and a short duration of treatment are predictors of
eradication failure.
<<snip>>
Treatment of Helicobacter pylori infection.
Cavallaro LG, Egan B, O'Morain C, Di Mario F
Helicobacter. 2006 Oct ; 11 Suppl 1: 36-9
In clinical practice the recommended treatment regimens achieve only
an 80%Helicobacter pylori eradication rate and this rate is lower in
patients who have failed first-line treatment. The increasing
indications for H. pylori treatment (idiopathic thrombocytopenia and
iron deficiency anemia) and an increasing trend of antibiotic
resistance (especially in southern Europe) emphasize the need for more
effective H. pylori eradication. Smoking and a short duration of
treatment, especially in patients with functional dyspepsia, are
predictors of eradication failure. In first line, the best option
remains the clarithromycin-based regimens but an extended treatment
duration is now indicated. Following first-line treatment failure, 14-
day proton pump inhibitor triple therapy employing alternative
antibiotics or quadruple therapy could be used. Levofloxacin-based 10-
day triple therapy seems to be an encouraging strategy following one
or more eradication failures.
Review Infect Immun. 2002 July; 70(7): 3923-3929.
doi: 10.1128/IAI.70.7.3923-3929.2002.
Copyright ? 2002, American Society for Microbiology
---------------------------------------------------------------------
* w w w .pubmedcentral.nih.gov/articlerender.fcgi?artid=128114
Essential Role of Ferritin Pfr in Helicobacter pylori Iron Metabolism
and Gastric Colonization
Received December 26, 2001; Revised March 19, 2002; Accepted April 2,
2002.
Abstract
The reactivity of the essential element iron necessitates a concerted
expression of ferritins, which mediate iron storage in a nonreactive
state. Here we have further established the role of the Helicobacter
pylori ferritin Pfr in iron metabolism and gastric colonization. Iron
stored in Pfr enabled H. pylori to multiply under severe iron
starvation and protected the bacteria from acid-amplified iron
toxicity, as inactivation of the pfr gene restricted growth of H.
pylori under these conditions. The lowered total iron content in the
pfr mutant, which is probably caused by decreased iron uptake rates,
was also reflected by an increased resistance to superoxide stress.
Iron induction of Pfr synthesis was clearly diminished in an H. pylori
feoB mutant, which lacked high-affinity ferrous iron transport,
confirming that Pfr expression is mediated by changes in the
cytoplasmic iron pool and not by extracellular iron. This is well in
agreement with the recent discovery that iron induces Pfr synthesis by
abolishing Fur-mediated repression of pfr transcription, which was
further confirmed here by the observation that iron inhibited the in
vitro binding of recombinant H. pylori Fur to the pfr promoter region.
The functions of H. pylori Pfr in iron metabolism are essential for
survival in the gastric mucosa, as the pfr mutant was unable to
colonize in a Mongolian gerbil-based animal model. In summary, the pfr
phenotypes observed give new insights into prokaryotic ferritin
functions and indicate that iron storage and homeostasis are of
extraordinary importance for H. pylori to survive in its hostile
natural environment.
----------------------------------------------------------------
-------------------------------------------------------------------
* jac.oxfordjournals.org/cgi/content/full/46/4/577
<<snip>>
These findings lend experimental support to the use of iron-chelating
agents in the therapy of pneumocystis infections
<<snip>>
Abstract
The in vitro activity of lactoferrins alone and in combination with
clarithromycin, minocycline and pyrimethamine was investigated against
three clinical isolates of Pneumocystis carinii. Susceptibility was
tested by inoculating isolates on to cell monolayers and determining
the parasite count after 72 h incubation at 37°C. The culture medium
was supplemented with serial dilutions of each agent. At 20 mg/L,
bovine lactoferrin, the most active agent, suppressed the growth of
cystic and trophic forms by >60%. Human lactoferrin, at the same
concentration, suppressed the growth of cystic and trophic forms by
>50%. Lactoferrins at 20 mg/L combined with clarithromycin 4 mg/L had
high anti-P. carinii activity, with a >90% decrease in cystic and
trophic form counts. Our study suggests that lactoferrins may inhibit
P. carinii growth in vitro and act synergically with other clinically
used compounds. These findings lend experimental support to the use of
iron-chelating agents in the therapy of pneumocystis infections.
Who loves ya.
Tom
Jesus Was A Vegetarian!
* jesuswasavegetarian.7h . com
Man Is A Herbivore!
* tinyurl . com /a3cc3
DEAD PEOPLE WALKING
* tinyurl . com /zk9fk
Helicobacter pylori requires iron to survive and propogate in the
body. Antibiotics bind up iron and remove it from the scenario /
disease process.
Gastritis is caused by increased red blood cell production and
H.pylori has been found to be associated with gastritis as per its
association with peptic ulcers.
Sooo IS the erradication of the H.pylori due TO the sequestration /
elimination OF the .. iron ..?
The article below states .. smoking / pseudopolycythemia is associated
with decreased ability to clear the pathogen .. ?
Sooo .. does the polycythemia / increased red blood cells /
erythrocytosis .. PRECEDE .. the colonization OF the H.pylori .. ? ..
ALLOWING the H.pylori to take and proliferate .. BY .. causing
gastritis / blood loss .. iron **AVAILABILITY** / lack of iron
sequestering ABILITY .. ?
----------------------------------------------------
<<snip>>
Smoking and a short duration of treatment are predictors of
eradication failure.
<<snip>>
Treatment of Helicobacter pylori infection.
Cavallaro LG, Egan B, O'Morain C, Di Mario F
Helicobacter. 2006 Oct ; 11 Suppl 1: 36-9
In clinical practice the recommended treatment regimens achieve only
an 80%Helicobacter pylori eradication rate and this rate is lower in
patients who have failed first-line treatment. The increasing
indications for H. pylori treatment (idiopathic thrombocytopenia and
iron deficiency anemia) and an increasing trend of antibiotic
resistance (especially in southern Europe) emphasize the need for more
effective H. pylori eradication. Smoking and a short duration of
treatment, especially in patients with functional dyspepsia, are
predictors of eradication failure. In first line, the best option
remains the clarithromycin-based regimens but an extended treatment
duration is now indicated. Following first-line treatment failure, 14-
day proton pump inhibitor triple therapy employing alternative
antibiotics or quadruple therapy could be used. Levofloxacin-based 10-
day triple therapy seems to be an encouraging strategy following one
or more eradication failures.
Review Infect Immun. 2002 July; 70(7): 3923-3929.
doi: 10.1128/IAI.70.7.3923-3929.2002.
Copyright ? 2002, American Society for Microbiology
---------------------------------------------------------------------
* w w w .pubmedcentral.nih.gov/articlerender.fcgi?artid=128114
Essential Role of Ferritin Pfr in Helicobacter pylori Iron Metabolism
and Gastric Colonization
Received December 26, 2001; Revised March 19, 2002; Accepted April 2,
2002.
Abstract
The reactivity of the essential element iron necessitates a concerted
expression of ferritins, which mediate iron storage in a nonreactive
state. Here we have further established the role of the Helicobacter
pylori ferritin Pfr in iron metabolism and gastric colonization. Iron
stored in Pfr enabled H. pylori to multiply under severe iron
starvation and protected the bacteria from acid-amplified iron
toxicity, as inactivation of the pfr gene restricted growth of H.
pylori under these conditions. The lowered total iron content in the
pfr mutant, which is probably caused by decreased iron uptake rates,
was also reflected by an increased resistance to superoxide stress.
Iron induction of Pfr synthesis was clearly diminished in an H. pylori
feoB mutant, which lacked high-affinity ferrous iron transport,
confirming that Pfr expression is mediated by changes in the
cytoplasmic iron pool and not by extracellular iron. This is well in
agreement with the recent discovery that iron induces Pfr synthesis by
abolishing Fur-mediated repression of pfr transcription, which was
further confirmed here by the observation that iron inhibited the in
vitro binding of recombinant H. pylori Fur to the pfr promoter region.
The functions of H. pylori Pfr in iron metabolism are essential for
survival in the gastric mucosa, as the pfr mutant was unable to
colonize in a Mongolian gerbil-based animal model. In summary, the pfr
phenotypes observed give new insights into prokaryotic ferritin
functions and indicate that iron storage and homeostasis are of
extraordinary importance for H. pylori to survive in its hostile
natural environment.
----------------------------------------------------------------
-------------------------------------------------------------------
* jac.oxfordjournals.org/cgi/content/full/46/4/577
<<snip>>
These findings lend experimental support to the use of iron-chelating
agents in the therapy of pneumocystis infections
<<snip>>
Abstract
The in vitro activity of lactoferrins alone and in combination with
clarithromycin, minocycline and pyrimethamine was investigated against
three clinical isolates of Pneumocystis carinii. Susceptibility was
tested by inoculating isolates on to cell monolayers and determining
the parasite count after 72 h incubation at 37°C. The culture medium
was supplemented with serial dilutions of each agent. At 20 mg/L,
bovine lactoferrin, the most active agent, suppressed the growth of
cystic and trophic forms by >60%. Human lactoferrin, at the same
concentration, suppressed the growth of cystic and trophic forms by
>50%. Lactoferrins at 20 mg/L combined with clarithromycin 4 mg/L had
high anti-P. carinii activity, with a >90% decrease in cystic and
trophic form counts. Our study suggests that lactoferrins may inhibit
P. carinii growth in vitro and act synergically with other clinically
used compounds. These findings lend experimental support to the use of
iron-chelating agents in the therapy of pneumocystis infections.
Who loves ya.
Tom
Jesus Was A Vegetarian!
* jesuswasavegetarian.7h . com
Man Is A Herbivore!
* tinyurl . com /a3cc3
DEAD PEOPLE WALKING
* tinyurl . com /zk9fk
Re: Helicobacter pylori and gastritis
"Helicobacter pylori requires iron to survive and propogate in the
body."
Intresting that life thing, humans need iron to live and propagate also.
"Helicobacter pylori requires iron to survive and propogate in the
body."
Intresting that life thing, humans need iron to live and propagate also.
