" ... there is a genetic component to this sinus disorder."

Hopkins Researchers Uncover Sinus Infection-CF Gene Link
ScienceDaily (Oct. 11, 2000)

... "In a study published in the current edition of The Journal of the
American Medical Association, the researchers found that 7 percent of
147 patients who recently visited Hopkins because of repeated bouts of
sinusitis carried a copy of the mutated gene responsible for CF,
called CFTR. The scientists predict that risk of chronic sinusitis
will likely double if you're a CF gene carrier.

"We want to be clear that these patients don't have cystic fibrosis,"
says geneticist Garry R. Cutting, M.D., of the research team. Cystic
fibrosis results from a double dose of the mutant CFTR gene-- both
parents must contribute a copy of this recessive gene for CF to
result. "But we've long wondered if having just one mutant CFTR gene
has any health effects," says Cutting. ...
http://www.sciencedaily.com/releases/2000/10/001009104808.htm

Study Lays Down Genetic Basis for Sinus Disease and Nasal Polyps
By David March Johns Hopkins Medicine
The JHU Gazette, November 8, 2004, Vol. 34 No. 11

In a three-year analysis of more than 10,500 genes, one-third of the
human genome, researchers at Johns Hopkins have found a starting point
to establishing the genetic basis for sinus disease and the growth of
nasal polyps, illnesses not well understood despite their prevalence
The findings, published Oct. 8 in the Journal of Allergy and Clinical
Immunology online, could lead to development of targeted gene
therapies or other treatments to control these conditions.

"This was a fishing expedition of sorts for sinusitis research, and a
nontraditional approach from a scientific standpoint," said study lead
author and otolaryngologist Jean Kim, assistant professor in the
School of Medicine. "The result was a host of very interesting leads
as to which genes may play a role in controlling this illness and how
we might prevent it in the future. ...

.... Of the genes studied, the researchers found that 192 were up-
regulated, or present in increased amounts, while another 156 were
down-regulated, or present in decreased amounts in the diseased tissue
samples. In the diseased tissue, a gene was determined to be "up" if
there was at least a twofold increase in its amount in samples tested,
and a gene was "down" if it had at least a 50 percent decrease in
amount.

The researchers then narrowed their initial focus to the top-four "up"
genes and the most common "down" gene to see if any proteins, as the
products of genes, were also present in significantly larger or
smaller amounts than normal. Changes in proteins and genes can be
clues to a genetic basis or origin of a disease. This may subsequently
lead to the development of new therapy for a condition (by controlling
the actions of the protein).

Three of the four "up" genes, including two proteins known to have
antibacterial activity, had their increased amounts confirmed by
specific mRNA and protein analysis. Actual increases in the amounts of
the fourth gene could not be validated.

Further analysis confirmed that one particular protein, called CC10,
was present in severely depleted quantities as the single most down-
regulated gene. CC10 is a protein, found primarily in the airways of
the lung, among other organs. This protein is thought to be a potent
anti-inflammatory molecule and one that plays an important role in the
immune response. While its precise biochemical and molecular functions
are unknown, CC10 is used as a treatment for underdeveloped lungs in
premature babies, where it suppresses inflammation.

"We were particularly surprised and excited to find low levels of this
protein CC10," said senior author Bruce Bochner, professor of medicine
and director of Hopkins' Division of Allergy and Clinical Immunology.
"This protein is usually increased by steroid therapy, yet it was
extremely low in all of our study subjects despite their use of
steroid sprays into the nose. So, it raises the possibility of one day
treating these defects with a nasal spray that is specific to raising
levels of CC10."

Kim said, "This study lays the initial groundwork for additional
studies on what has been up until now a poorly understood and
confounding illness. We now have many lead candidate genes which may
play a role in causing sinus disease. These studies may lead to new
treatments for patients with chronic rhinosinusitis and nasal polyps."
http://www.jhu.edu/~gazette/2004/08nov04/08polyps.html

Congested Sinuses Linked to 'Ghost' Parasites, Immune Response
By David March, Johns Hopkins Medicine
The JHU Gazette, September 11, 2006, Vol. 36 No. 2

"Although it's unclear why it's so, scientists at Johns Hopkins have
linked a gene that allows for the chemical breakdown of the tough,
protective casing that houses insects and worms to the severe
congestion and polyp formation typical of chronic sinusitis.

A team of Johns Hopkins sinus experts has found that the gene for the
enzyme, acidic mammalian chitinase, known as AMCase, is up to 250
times more active in people with severe sinus inflammation that
persists even after surgery when compared to patients in whom surgery
is successful. Sinus surgery is usually the treatment of last resort
for those who do not respond to drug therapy, but nearly one in 10 of
those treated see symptoms return within weeks or months after surgery
fails to keep open the nasal passages, scientists say. ...

... The Johns Hopkins report, published in the July issue of the
American Journal of Rhinology, is believed to be the first to identify
the enzyme's presence in the nose and confirm its link to sinusitis.

When researchers initially compared all the nasal tissue samples,
they found that half had the gene for AMCase turned on, or expressed,
to make the chitinase protein. During follow-up, they found that the
10 patients who had their polyps return had exceedingly higher levels
of AMCase expression than the other sinusitis patients and controls.
Gene expression of another inflammatory protein, called
interleukin-13, already known to be high in asthmatics, was also found
to be elevated in those with polyps, but the levels of interleukin-13
did not have the same predictive value as the elevated expression of
AMCase, researchers said. ..."
http://www.jhu.edu/~gazette/2006/11sep06/11sinus.html