Helicobacter pylori can multiply in autophagic vesicles
Helicobacter pylori, a Gram-negative, flagellated, microaerophilic
bacterium, can selectively colonize in the human stomach. Its infection is
widespread throughout the world, and is present in about 50% of the global human
population with 80% in developing countries and 20-50% in industrialized
countries. Infection of the stomach with
H. pylori induces a local immune
response with infiltration of the mucosa by macrophages, neutrophils and
lymphocytes. Although the innate and adaptive immune responses are activated,
the bacterium is rarely eliminated and infections can last for decades if left
untreated. Most infections are asymptomatic, but overt diseases can occur in
10-20 % of infected individuals. The disease spectrum ranges from gastritis to
peptic ulceration disease. A long-term chronic infection will increase the risk
to gastric adenocarcinoma and mucosa-associated lymphoid-tissue lymphoma. It has
been classified as a class I carcinogen by the WHO. Despite intensive studies,
and the award of the 2005 Nobel Prize in Physiology for the discovery of the
H. pylori by Robin Warren and Barry Marshall, our understanding
H. pylori-infection-caused disease is still limited.
has evolved several mechanisms to increase its adherence and persistence in the
host. In addition, it must also evade immune clearance. Elimination of
pyloriH. pylori exhibits
several virulence factors to evade opsonization, retard phagocytosis, and
disrupt membrane trafficking and phagosome maturation after internalization of
the microorganism. by phagocytes is inefficient because
In the February 2009 issue of
Experimental Biology and Medicine
researchers at the National Cheng Kung University, Tainan, Taiwan, have reported
a novel phenomenon involving autophagosome formation induced by
infection and subsequent adoption of these autophagic vesicles by
pylori for replication in macrophages. The fate of
H. pylori is
dependent on the strains (isolates) as well as the host macrophages used.
Several clinical isolates of
H. pylori from Taiwanese patients, but not
standard strains, can multiply in the double-layered vesicles of macrophages.
The senior author, Dr. Huan-Yao Lei stated that "The autophagy induction by
H. pylori is not only found in macrophages, but also in dendritic cells
and gastric epithelial cells". This new finding has several implications for the
life cycle of
H. pylori in the host.
H. pyloriH. pylori antibodies. In view of the
critical role of dendritic cells in presenting
H. pylori antigen to
initiate the immune response, it is possible that
dendritic cells induce an inadequate immune response to
infection that might hinder the clearance of this bacterium. Alternatively, the
various immunopathogenesis during the
H. pylori-caused diseases might be
caused by an unbalanced Th-1 or Th2-mediated response post infection. Finally,
the micro-heterogeneity of Taiwanese
H. pylori isolates used in this
study provides an important hint as to why this microorganism causes so broad a
spectrum of diseases. Dr. Steven R. Goodman, Editor-in-Chief of
Biology and Medicine stated "This study also has potential implications for
H. pylori drugs that target the enhancement of autophagy. Dr.
Lei and his co-workers have provided an important contribution to our
H. pylori infection." can be considered
as a kind of intracellular microorganism because it can invade host cells to
undergo replication within the autophagosome. The bacterium's residence inside
infected cells not only increases its resistance to antibiotic treatment, but
also avoids neutralization by anti-
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