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PORTSIDE  August 2011, Week 5

PORTSIDE August 2011, Week 5

Subject:

The Janus Bug

From:

Portside Moderator <[log in to unmask]>

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Date:

Mon, 29 Aug 2011 02:22:52 -0400

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The Janus Bug
by Moselio Schaechter
Small Things Considered
The Microbe Blog
August 1, 2011
http://schaechter.asmblog.org/schaechter/

A paradox, a paradox,
A most ingenious paradox.
(The Pirates of Penzance by Gilbert and Sullivan)

If you wonder what I do with myself when I'm not
blogging, well I'll tell you. Among other things, I
participate in an ASM-sponsored podcast called This Week
In Microbiology (TWIM). It's posted every two weeks and
is easily accessible by clicking here or going to the
MicrobeWorld home page. Under the leadership of Columbia
University's podcaster extraordinaire Vincent
Racaniello, we sit before our computers and schmooze
away about a couple of papers that caught our fancy.
Recently, one of the podcasters, Margaret McFall-Ngai,
went over a paper with the puzzling title Helicobacter
pylori infection prevents allergic asthma in mouse
models through the induction of regulatory T cells. You
see why this caught Margaret's attention. Helicobacter
and asthma? A bacterium that lives in the stomach has an
effect on the respiratory tract? Makes you wonder.

To put this story in context, it is part of a broader
concern, to wit the multiple natures of members of our
"normal" microbiota. At times, our own bacteria cause
disease, while at others they help us. A most insightful
review that discusses this topic is by Martin Blaser and
Stanley Falkow, two people very much in the know. It's
entitled: What are the consequences of the disappearing
human microbiota? A must read!

In the case of H. pylori, it has been known that people
free of the bug have a greater incidence of
gastroesophageal reflux disease (popularly known as
"reflux"), and that's also true for certain cancers of
the esophagus and stomach. On the other hand, those who
carry H. pylori have a greater incidence of gastric
ulcers and, in some cases, other kinds of stomach
cancer, which is how the bug was discovered in the first
place. Sounds like you can't win. So here's a naïve
question: is H. pylori good or bad for you? Don't ask
me. The answer requires a great deal of clinical and
epidemiological (and even psychological) information
(all beyond me). Keep in mind that in about two
generations, the incidence of H. pylori has decreased in
the technological world from around 80% to a few
percent. It is still prevalent in many developing
countries and, overall, about half of the people on
Earth are still colonized by this bug. This is all a bit
peculiar. Why has the bug abandoned the stomachs of so
many of us? The reason, it is said, is better hygiene
and medical care, but I still find this puzzling. H.
pylori is said to have colonized the earliest humans
some 50,000 years ago. One would think that such a long
and steady association would not lead to such a quick
divorce.

Many other things about H. pylori are peculiar. The most
obvious is its distinction of being the major microbial
species in the stomach. In fact, it isn't clear if the
other bacteria found here are much more than transients
on their way down. H. pylori certainly knows how to make
a home in this demanding environment. It survives the
harsh acidic environment by chemotaxing towards the less
acidic surface of the gastric epithelium and making a
large amount of urease, which, by producing ammonia,
raises the pH locally. Patients infected with H. pylori
tend to have a higher pH in their stomach, but this is
not due to the action of the bug's urease. The mechanism
is more complicated. Colonization by this bug affects
the regulation of gastric hormones involved in acid
secretion, such as gastrin and somatostatin. Gastrin
stimulates acid secretion, somatostatin suppresses the
release of gastrin. It gets even thornier. Gastrin is an
H. pylori growth factor!

One could go on, but the point here is that in people
infected for many years, the level of stomach acidity
decreases, perhaps from hormone action and the shrinkage
of the gastric acid-secreting glands due to the long-
term effects of inflammation. This leads to an increase
in the risk of stomach cancer. But, as we said above,
lack of H. pylori keeps the pH low, which increases the
chance for reflux and certain esophageal and stomach
cancers. Moreover, some epidemiological studies say that
H. pylori-positive individuals have a lower risk of
childhood asthma, allergic rhinitis, and skin allergies.
Is that all? In their review, Blaser and Falkow
speculate: It is possible that the disappearance of H.
pylori might be contributing to the current epidemics of
early-life obesity, type 2 diabetes and related
metabolic syndromes. And maybe the Tea Party movement?

Conclusions such as these are based largely on
epidemiological correlations. Strong correlations,
especially between non-obvious cause and effect, are
nothing to sneeze at, but experimental results have a
greater finality. So we welcome the study we discussed
in the podcast. Asthma has achieved epidemic proportions
in the industrialized countries, making Blaser and
Falkow's "disappearing microbiome" hypothesis ("lose
members of your biota, and you lose") tenable for this
disease. The Swiss and German authors of this particular
paper used a mouse model for asthma, where neonate or
adult mice are exposed to an allergen (ovalbumin or
house dust mite allergen), then challenged later with
the same allergen. The mice came down with asthma, as
witnessed by all sorts of immunological and histological
manifestations. Infecting them with H. pylori alleviated
these symptoms considerably. Infection of neonates was
more beneficial than infection of adult mice.

What causes this effect? Because H. pylori causes
inflammation, the stomachs of infected animals have a
rich population of immune cells. Primary among these are
the regulatory T-cells (known in my days as suppressor
T-cells). Here's the clincher: The effect of the H.
pylori residents was lost when the mice were depleted of
their regulatory T-cells using a specific monoclonal
antibody. And administering such T-cells to uninfected
mice protected them from asthma. Of course, mice may
react differently than people, and H. pylori is not a
species found in mice, but the conclusions are highly
suggestive.

Now, you may have concluded that if having H. pylori may
be a good thing, why not develop a strain that can be
used as a probiotic to infect newborn humans? Not so
fast. Much of the pathogenesis due to H. pylori is
caused by a toxin called CagA. And so is the anti-asthma
effect. No toxin, no protection. So, it may take some
doing before one can come up with a strain that is
beneficial without being potentially dangerous. But the
thought has merit, it seems to me. Replacing old
partners with suitable new strains may be a worthwhile
goal. Perhaps one should find probiotics not so much by
looking for them in yoghurt and other dairy products as
by modifying members of our own microbiome.

The general point here is that we need to shift our
outlook from one that simply labels our microbes as
being good or bad to a much more nuanced view that all
of them can be either helpful, harmful, neither, or
both. H. pylori may turn out to be a relatively
tractable bug, being that it establishes a near
monoculture in infected people. Sorting out the
interactions between the hundreds or thousands of
species elsewhere in our body may well turn out to be a
formidable task, but one well worth pursuing.

Arnold IC, Dehzad N, Reuter S, Martin H, Becher B, Taube
C, & Müller A (2011). Helicobacter pylori infection
prevents allergic asthma in mouse models through the
induction of regulatory T cells. The Journal of clinical
investigation PMID: 21737881

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