ピロリ菌に食道がん予防効果の可能性

 胃内によく見られるピロリ菌はある種の食道癌を防ぐ効果がある可能性があるとの研究。
 CagA遺伝子を持つピロリ菌を持つ人は食道の腺癌になるリスクがほぼ半減する。胃酸の産生を減らし食道への逆流を減らすことで悪性腺腫のリスクを減少させているのかもしれない。また、食欲を刺激するために胃から分泌されるホルモンghrelinの生産を減少させることによって作動するのかもしれない。ghrelinの減少により、悪性腺腫のための重要な危険因子である肥満を減らすことになるのかもしれない。
 世界の半分の人が胃ガンと潰瘍の原因として知られているピロリ菌を持っている。適切な衛生と抗生物質により、ピロリ菌は減少し、胃ガンと潰瘍の数はその後低下した。しかし、食道の悪性腺腫が増大し、CagA陽性のピロリ菌も低下した。かつては稀だった食道の悪性腺腫が西欧諸国のすべての食道ガンケースの半分以上を占めるに至っている。
 人と胃内細菌の長期の共存は、下痢疾患と喘息の減少を含め、いくつかの有益な効果がある可能性を示唆する。
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ピロリ菌が子どもの喘息を予防する?/米国
http://kurie.at.webry.info/200807/article_32.html
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Stomach Bacteria Might Guard Against Certain Throat Cancer
H. pylori could help prevent some esophageal adenocarcinomas, study suggests
-- Kevin McKeever
http://health.msn.com/health-topics/cancer/articlepage.aspx?cp-documentid=100218152

H. pylori could help prevent some esophageal adenocarcinomas, study suggests.

WEDNESDAY, Oct. 15 (HealthDay News) -- A common stomach bacteria may protect against a certain form of esophageal cancer, a new review suggests.

People with H. pylori strains that also had the CagA gene were almost half as likely to get adenocarcinoma of the esophagus, a cancer that develops in the tube that passes food from the throat to the stomach, according to the report published in the October issue of Cancer Prevention Research.

"CagA-positive strains of H. pylori may decrease the risk of adenocarcinoma by reducing acid production in the stomach and, therefore, reducing acid reflux to the esophagus," study co-author Dr. Farin Kamangar, a research fellow at the National Cancer Institute, said in an American Association for Cancer Research news release. "It may also work by decreasing the production of the hormone ghrelin, which is secreted from the stomach to stimulate appetite. A reduction in the level of ghrelin may lead to lower rates of obesity, an important risk factor for adenocarcinoma."

About half the world's population has H. pylori, which is a known cause of stomach cancer and ulcers. As proper sanitation and antibiotics have become more prevalent in the world, H. pylori has become less common, and the number of stomach cancers and ulcers has subsequently dropped.

However, CagA-positive H. pylori has also dropped, while esophageal adenocarcinomas have increased -- two facts the study authors suggested are linked. Esophageal adenocarcinoma, at one time a rare cancer, now makes up about half of all esophageal cancer cases in Western countries such as the United States and the United Kingdom.

Despite its deadly potential, the stomach bacteria's longtime co-existence with humans suggests it also may have some beneficial effects, including possible roles in reducing diarrheal diseases and asthma, Kamangar said.

More information
The American Cancer Society has more about esophageal cancer.
SOURCE: American Association for Cancer Research, news release, Oct. 6, 2008

Copyright (c) 2008 ScoutNews, LLC. All rights reserved.

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Cancer Prevention Research 1, 308-311, October 1, 2008. doi: 10.1158/1940-6207.CAPR-08-0170
(c) 2008 American Association for Cancer Research

Disappearing Microbiota: Helicobacter pylori Protection against Esophageal Adenocarcinoma
Martin J. Blaser

Author's Affiliation: Departments of Medicine and Microbiology, New York University Langone Medical Center, and Medical Service, New York Harbor Veterans Affairs Medical Center, New York, New York

Requests for reprints: Martin J. Blaser, Department of Medicine, New York University Langone Medical Center, 550 First Avenue, OBV A6-06, New York, NY 10016. Phone: 212-263-6394; Fax: 212-263-3969; E-mail: Martin.Blaser@med.nyu.edu.



Once rare, esophageal adenocarcinoma (EAC) is the most rapidly increasing malignancy in many developed countries, such as the United States, United Kingdom, Australia, and Norway, and now is surpassing esophageal squamous cell carcinomas in certain populations (1, 2). EAC has very specific clinical and epidemiologic characteristics: It involves the distal but not proximal esophagus, preferentially affects males and people of higher socioeconomic status, and unlike esophageal squamous cell carcinoma, is not related to drinking alcohol or smoking (3). The rapid increase in EAC is not an artifact of surveillance or classification (4); it is real and frightening. A smaller increase in adenocarcinomas involving the gastric cardia is probably related to the increase in EAC (5); however, this relationship is unclear because the origin of cardia tumors, which frequently are advanced when diagnosed, could be esophageal or gastric.

In recent years, it has become clear that EAC is a consequence of long-term gastroesophageal reflux disease, an inflammatory condition of the distal esophagus (6), often through progression to Barrett's esophagus, a metaplastic malady that may become dysplastic (7, 8). The three progressive and related conditions―gastroesophageal reflux disease, Barrett's esophagus, and EAC―have been increasing over the past several decades in developed countries; their substantial increase is a late 20th century phenomenon; and they were essentially unknown before 1900 (9).

Numerous hypotheses have been raised to explain the origins of these maladies, which are not obvious (10). Nevertheless, reports going back more than 10 years have linked the rising tide of gastroesophageal reflux disease and its consequences with Helicobacter (H.) pylori (gram-negative bacteria that colonize the human stomach), especially the cagA+ variety, but inversely (8, 11, 12). This inverse association raised an intriguing question: How could the lack of an organism predispose to a cancer?

Understanding the relationship between H. pylori and humans is necessary to begin addressing this question. Fortunately, much has been learned about H. pylori since its discovery and isolation in pure culture in 1982. It now is clear that H. pylori has colonized the human stomach probably since the beginning of the human species and certainly before prehistoric migrations out of Africa over 58,000 years ago (13). Acquired in young childhood, H. pylori persists in the stomach essentially for life unless eradicated by antibiotics (14, 15). H. pylori in humans was nearly omnipresent until recently. Clone libraries of 16S rRNA genes show that H. pylori is the most numerous organism in the human stomach (16), in contrast with most other human niches where no single organism dominates persistently. H. pylori strains can be subdivided on the basis of cagA, a marker gene for the presence of the cag island, a chromosomal region that encodes a type IV secretion system that injects H. pylori constituents (including the cagA protein) into human gastric mucosal epithelial cells (17, 18). In this and many other characteristics, cagA+ H. pylori strains are more interactive with human hosts than are cagA-negative strains (15, 17--19). On the basis of history, numbers, and intimacy, H. pylori can be considered as having been the dominant microbe colonizing the human stomach.

In developed countries, however, H. pylori has been progressively disappearing over the course of the 20th century (20-22). This secular trend allows examination of the consequences of the presence or absence of H. pylori (Fig. 1). Numerous studies have made it clear that H. pylori--positive and H. pylori--negative persons have substantial differences in gastric physiology and in tissue and immune responses (15). It also has become clear that the presence of H. pylori increases the risks for peptic ulcer disease and noncardia gastric cancer (NCGC; NCGC is used synonymously with the term "gastric cancer" throughout this Perspective) and that removing H. pylori with antibiotics reduces these risks (23, 24). Therefore, there is biological cost to humans to carry H. pylori, the removal of which may improve public health in some areas of the world (25). Not surprisingly, the cagA+ strains, which are more interactive, are associated with a greater risk of these diseases (26, 27). Nevertheless, it is important to examine whether there are disease contexts in which persistent gastric carriage of H. pylori could confer benefits.



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