Team:Ciencias-UNAM/Project

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<i>Helicobacter pylori</i> colonizes the stomach of 50% of the world's human population throughout their lifetimes. Colonization with this organism is the main risk factor for peptic ulceration as well as for gastric adenocarcinoma and gastric MALT (mucosa-associated lymphoid tissue) lymphoma. Treatment for <i>H. pylori</i> has revolutionized the management of peptic ulcer disease, providing a permanent cure in most cases. Such treatment also represents first-line therapy for patients with low-grade gastric MALT lymphoma. Treatment of <i>H. pylori</i> is of no benefit in the treatment of gastric adenocarcinoma, but prevention of <i>H. pylori</i> colonization could potentially prevent gastric malignancy and peptic ulceration [1,2].
<i>Helicobacter pylori</i> colonizes the stomach of 50% of the world's human population throughout their lifetimes. Colonization with this organism is the main risk factor for peptic ulceration as well as for gastric adenocarcinoma and gastric MALT (mucosa-associated lymphoid tissue) lymphoma. Treatment for <i>H. pylori</i> has revolutionized the management of peptic ulcer disease, providing a permanent cure in most cases. Such treatment also represents first-line therapy for patients with low-grade gastric MALT lymphoma. Treatment of <i>H. pylori</i> is of no benefit in the treatment of gastric adenocarcinoma, but prevention of <i>H. pylori</i> colonization could potentially prevent gastric malignancy and peptic ulceration [1,2].
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A very small proportion of gastric <i>Helicobacter</i> infections are due to species other than <i>H. pylori</i>, possibly acquired as zoonoses. Whether these non-<i>pylori</i> gastric helicobacters cause disease remains controversial. In immunocompromised hosts, several nongastric (intestinal) <i>Helicobacter</i> species can cause disease with clinical features resembling those of <i>Campylobacter</i> infections. </span></p></div>
A very small proportion of gastric <i>Helicobacter</i> infections are due to species other than <i>H. pylori</i>, possibly acquired as zoonoses. Whether these non-<i>pylori</i> gastric helicobacters cause disease remains controversial. In immunocompromised hosts, several nongastric (intestinal) <i>Helicobacter</i> species can cause disease with clinical features resembling those of <i>Campylobacter</i> infections. </span></p></div>
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<div id="u54_rtf"><p style="text-align:left;"><span style="font-family:Museo Slab;font-size:16px;font-weight:normal;font-style:normal;text-decoration:none;color:#666666;">PROJECT MENU</span></p></div>
<div id="u54_rtf"><p style="text-align:left;"><span style="font-family:Museo Slab;font-size:16px;font-weight:normal;font-style:normal;text-decoration:none;color:#666666;">PROJECT MENU</span></p></div>

Revision as of 03:35, 26 September 2013

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ABSTRACT

 

The human peptide LL-37 is a cationic peptide with antimicrobial activity against both Gram-positive and Gram-negative microorganisms. It has been shown to protect against gastritis caused by Helicobacter pylori infection. Most of the current synthetic expression systems for LL-37 depend on the construction of soluble fusion partners to avoid cytotoxic effects of the antimicrobial peptide in the E. coli host strain. However, the fusion systems require additional cleavage steps using enzymatic or chemical methods, which makes them impossible to express an active LL-37 peptide in vivo. In order to create a resistant host that can export LL-37 to the media, we intend to overexpress the E. coli marRAB operon, which activates the AcrAB-TolC efflux pump, a mechanism that has been related with resistance to this and similar antimicrobial peptides by expulsion. Our aim is to create a system in which E. coli expels LL-37 only when H. pylori and other pathogenic bacteria are present. In order to do this, we are using the LsrA promoter, which allows transcription in presence of AI-2, a molecule produced by bacteria to communicate via quorum-sensing.

THE PROBLEM

Helicobacter pylori colonizes the stomach of 50% of the world's human population throughout their lifetimes. Colonization with this organism is the main risk factor for peptic ulceration as well as for gastric adenocarcinoma and gastric MALT (mucosa-associated lymphoid tissue) lymphoma. Treatment for H. pylori has revolutionized the management of peptic ulcer disease, providing a permanent cure in most cases. Such treatment also represents first-line therapy for patients with low-grade gastric MALT lymphoma. Treatment of H. pylori is of no benefit in the treatment of gastric adenocarcinoma, but prevention of H. pylori colonization could potentially prevent gastric malignancy and peptic ulceration [1,2].

 

Etiologic Agent

H. pylori is a gram-negative bacillus that has naturally colonized humans for at least 50,000 years—and probably throughout human evolution. It lives in gastric mucus, with a small proportion of the bacteria adherent to the mucosa and possibly a very small number of the organisms entering cells or penetrating the mucosa; its distribution is never systemic. Its spiral shape and flagella render H. pylori motile in the mucus environment. The organism has several acid-resistance mechanisms, most notably a highly expressed urease that catalyzes urea hydrolysis to produce buffering ammonia. H. pylori is microaerophilic (requiring low levels of oxygen), is slow-growing, and requires complex growth media in vitro. Publication of several complete genomic sequences of H. pylori since 1997 has led to significant advances in the understanding of the organism's biology [3]. A very small proportion of gastric Helicobacter infections are due to species other than H. pylori, possibly acquired as zoonoses. Whether these non-pylori gastric helicobacters cause disease remains controversial. In immunocompromised hosts, several nongastric (intestinal) Helicobacter species can cause disease with clinical features resembling those of Campylobacter infections.

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