Newly Identified Mechanism Helps Explain Why People of African
Descent Are More Vulnerable to Tuberculosis
February 27, 2006
Laptop Battery Boston, MA - A team of scientists has identified a cellular
mechanism that may help explain the puzzle of why people of African
descent are more susceptible to tuberculosis infection and why,
once infected, they develop more severe states of the disease than
whites. The team includes researchers from University of
California, Los Angeles (UCLA), and Harvard School of Public Health
(HSPH). The paper will appear online in the February 23 issue of
Science Express.
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Thinkpad Approximately eight million people worldwide are infected with
TB annually, with an estimated two million people dying from the
lung disease each year. TB is caused by the pathogen Mycobacterium
tuberculosis, but infection does not automatically result in
full-blown disease. In the U.S., minority and foreign-born
populations have significantly higher rates of TB than the overall
U.S. average, according to the Centers for Disease Control and
Prevention. In 2004, African Americans had TB case rates that were
eight times higher than whites.
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Microsoft Scientists have understood that mice - a frequently used animal
model in experiments - combat microbes such as TB by producing
nitric oxide in scavenger cells of the immune system known as
macrophages. However, this mechanism is not prominent in humans,
and the mechanism by which human macrophages kill the tubercle
bacillus has remained an additional puzzle. Innate immunity is the
rapid immune response of host scavenger cells to recognition of
certain patterns of molecules found on pathogens, which has been
retained in evolution from fruit flies to humans. A set of
receptors on macrophages in humans called Toll-like receptors
contribute to innate immune responses. The researchers describe a
novel pathway used by human macrophages that may be critical to
resisting infection with certain pathogens and that turns out to be
critically dependent on vitamin D. This description provides a
different way to think about how human immune systems battle
pathogens in general.
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Laptop Computers The research team found that when Toll-like receptors in humans
are stimulated by specific molecules of the tubercle bacillus,
vitamin D receptors and an enzyme called Cyp27B1, which converts
the vitamin from an inactive form to an active form, are
dramatically increased. The result of this dual activation is the
cleavage of a preexistent protein to a small peptide called
cathelicidin, which can kill TB bacilli in the test tube. One of
the interesting aspects of this mechanism is that production of
vitamin D in humans is dependent on exposure to UV light, generally
sunlight, and may not have evolved in mice since they are nocturnal
animals.
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Laptop Computer "These studies began with a very basic exploration of
differences in gene expression in two related human white blood
cell types known to be involved in host responses to infection, and
concluded by revealing a new and potentially important human
mechanism for killing intracellular pathogens," said Philip Liu,
postdoctoral scholar in the Department of Immunology and Molecular
Genetics at the David Geffen School of Medicine at UCLA and co-lead
author of the paper.
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Desktop Computer African Americans have significantly lower levels of vitamin D
in their blood serum than whites because higher levels of melanin -
the pigment that provides color to skin absorbs UV light and
reduces African Americans' ability to produce vitamin D. When the
macrophages were stimulated by molecules of the tubercle bacillus
that trigger Toll-like receptors, the research team found that
cells cultured in serum provided by African Americans produced 63
percent less of the microbe-killing cathelicin than when cultured
in serum from whites. Supplementing the serum from African
Americans with vitamin D precursor to a range found in serum
samples from whites boosted the induction of cathelicidin.
Notebooks Scientists have long known that African Americans have less
vitamin D than whites and that they are more vulnerable to TB. This
study helps to resolve two of the puzzles of tuberculosis, the
differences between mice and human antibacterial mechanisms, and
the susceptibility of people of African and possibly Asian descent
to tuberculosis. The researchers suggest a need for clinical trials
to investigate the effect of vitamin D supplementation.
Lenovo "Our results indicate that we have much yet to learn about human
immune responses to infections. They also emphasize the importance
of vitamin D in human immune responses, and suggest that it is now
important to learn how much vitamin D is optimal for innate
immunity, and how that can best be achieved through diet or
supplementation," said the senior investigator of these studies,
Dr. Robert Modlin, Klein Professor of Dermatology and Professor of
Microbiology, Immunology and Molecular Genetics at the David Geffen
School of Medicine at UCLA.
Hard Drive "Tuberculosis is a devastating disease that strikes vulnerable
populations particularly hard," said immunologist Barry R. Bloom,
Dean of the Faculty at HSPH and a co-author of the paper. \\\
Travelstar Harvard School of Public Health
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