Treatment of helicobacter with isothiocyanates

Drug – bio-affecting and body treating compositions – Designated organic active ingredient containing – Ester doai

Reexamination Certificate

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C514S515000, C514S024000, C424S755000

Reexamination Certificate

active

06737441

ABSTRACT:

BACKGROUND OF THE INVENTION
1. Field of the Invention
The present invention relates to methods of preventing or inhibiting the growth of Helicobacter through the use of a composition that comprises a glucosinolate, an isothiocyanate or a derivative or metabolite thereof. The present invention also relates to methods of preventing or treating persistent chronic gastritis, ulcers and/or stomach cancer in subjects at risk for, or in need of treatment thereof.
2. Background of the Invention
Stomach cancer is the second most common form of cancer worldwide.
Helicobacter pylori
is a microaerophilic, gram-negative bacterium of cosmopolitan distribution that causes persistent chronic gastritis. Carriers of
H. pylori
(in gastric mucosa) are at 3 to 6 times the risk for developing stomach cancer (gastric adenocarcinoma and mucosa-associated lymphoid tissue lymphoma) as non-carriers (J. Danesh et al.,
Cancer Surveys,
33:263-289 (1999); D. Forman et al.,
Br Med Bull,
54:71-78 (1998); S. Hansen et al.,
Scand J Gastroenterol,
34:353-360 (1999); J-Q Huang et al.,
Gastroenterology,
114:1169-1179(1998)).
H. pylori
causes inflammation of stomach tissue in carriers, resulting in increased blood flow, swelling and irritation. Inflammation of the lower part of the stomach leads to ulcers in about 10% of carriers. Inflammation of the upper part of the stomach leads to impaired acid secretion and ultimate die-off of acid-producing cells and leads to reduced stomach function and ultimately to cancer.
Helicobacter pylori
was only first described following its cultivation from human gastric biopsy specimens in 1982 (J R Warren et al., Lancet, (1983), 1:1273-1275; B J Marshall et al., Microbios Lett. (1984), 25:83-88). Since then, as many as 26 related Helicobacter species have been described colonizing the mucosal surfaces of humans and other animals (J V Solnick, D B Schauer, Clin Microbiol Rev, (2001), 14:59-97). These organisms not only colonize gastric tissues of mammals, but are found in the intestinal tract and the liver of birds, as well as in mammals including humans, mice, ferrets, gerbils, dogs and cats. They have been implicated as agents responsible for inflammation, and in malignant transformation in immunocompetent hosts as well as immunocompromised humans and animals. However,
H. pylori
is now well-documented as one of the most prevalent human pathogens worldwide (R M Genta et al.,
Virchows Arch,
425:339-347 (1994)), and the causal agent for most gastric and duodenal ulcers, as well as a risk factor for the development of gastric cancer (J Danesh,
Cancer Surveys,
33:263-289 (1999)). The human stomach is the only known natural reservoir for
H. pylori
, although many mammalian species can be infected by related species. Antibiotic therapy aimed at eradication of
H. pylori
(e.g. amoxycillin and clarithromycin plus the H
2
inhibitor omeprazol for 10-14 days) is now recommended for infected patients who have verified peptic ulcerations of the stomach or duodenum or who have gastric mucosa-associated lymphoid tissue lymphomas, and cure rates are on the order of 90% (Helicobacter Foundation, “Treatment of
Helicobacter pylori
, p. 1-5 (1998)). However, a complex antibiotic therapy as described above may not be available in developing countries, where
H. pylori
infection rates can be as high as 70% of the population.
Thus a need exists for an economical dietary supplement, food or pharmaceutical that will naturally inhibit the growth and/or infection rates of
H. pylori
, both in the lumen of the stomach and within gastric epithelial cells where
H. pylori
may serve as a low-level, chronic reservoir for re-infection. This inhibition of eradication can in turn reduce the incidence of ulcers and stomach cancer or prevent reinfection of
H. pylori.
SUMMARY OF THE INVENTION
The present invention relates to a method of treating a subject having a Helicobacter infection, comprising administering to the subject an antibacterially effective amount of a composition that comprises a glucosinolate, an isothiocyanate or a derivative thereof.
The present invention also relates to a method of preventing a Helicobacter infection in a subject, comprising treating the subject with an antibacterially effective amount of a composition that comprises a glucosinolate, an isothiocyanate or a derivative thereof.
The present invention further relates to a method for inhibiting the growth of Helicobacter, comprising administering an antibacterially effective amount of an agent selected from the group consisting of a glucosinolate, an isothiocyanate or a derivative thereof.
BRIEF DESCRIPTION OF THE DRAWINGS
N/A
DETAILED DESCRIPTION OF THE PREFERRED EMBODIMENTS
The present invention relates to a method of treating a subject having a Helicobacter infection, comprising administering to the subject an antibacterially effective amount of a composition that comprises a glucosinolate, an isothiocyanate or a derivative thereof.
Helicobacter is a gram-negative bacterium with polar flagella, using oxygen as an electron acceptor, which cannot utilize carbohydrates as an energy source. The Helicobacter genus is fully characterized in Versalovic, et al,
Manual of Clinical Microbiology,
7
th
Ed., pp. 727-738 (1999) and Perez-Perez, et al.,
Medical Microbiology,
4
th
Ed., pp. 311-322 (1996), which are incorporated herein by reference. Helicobacter is used interchangeably with “Helicobacter sp” herein.
As used herein, the terms subject or patient are used interchangeably and are used to mean any animal, preferably a mammal, including humans and non-human primates. In one embodiment of the current invention the subject having a Helicobacter infection is suffering from a peptic ulcer. Peptic ulcers, as contemplated in the current invention include, but are not limited to, circumscribed breaks in the continuity of the mucosal layer of the gastrointestinal tract. These breaks in the continuity of the mucosal layer can include breaks that extend below the epithelium, or breaks that do not extend below the epithelium, sometime referred to as “erosions.” The peptic ulcers may be acute, or chronic. Further, peptic ulcers can be located in any part of the gastrointestinal tract that is exposed to acid-pepsin gastric juice, including the esophagus, stomach, duodenum, and after gastroenterostomy, the jejunum.
In another embodiment of the current invention the subject having the Helicobacter infection is suffering from, or at risk of developing, cancer of the gastrointestinal tract. As stated previously, the portions of the gastrointestinal tract where cancer may be present are any areas where the tract is exposed to acid-pepsin gastric juice, including the esophagus, stomach, duodenum, and after gastroenterostomy, the jejunum. As used herein the term cancer is used as one of ordinary skill in the art would recognize the term. Examples of cancers include, but are not limited to, neoplasias (or neoplasms), hyperplasias, dysplasias, metaplasias, hypertrophies. The neoplasms may be benign or malignant, and they may originate from any cell type, including but not limited to epithelial cells of various origin, muscle cells and endothelial cells.
The treatment envisioned by the current invention can be used for patients with a pre-existing Helicobacter infection, or for patients pre-disposed to a Helicobacter infection. Additionally, the method of the current invention can be used to correct or compensate for cellular or physiological abnormalities involved in conferring susceptibility to Helicobacter infection in patients, and/or to alleviate symptoms of a Helicobacter infection in patients, or as a preventative measure in patients.
As used herein, the phrase Helicobacter infection is used to mean an interaction between Helicobacter and the host organism (subject). The infections may be localized, meaning that the Helicobacter grows and remains near the point of initial interaction. The infection may also be generalized, where the Helicobacter may become more widespread beyond the initial point of interaction, includi

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