Not a new theory, a new excuse.

Don,

  Do you not think that the new Mayo theory of the MBP in the mucus
may be an extension of the fungal theory?  It says it is the
eosinophils that are creating the MBP and the fungal theory says that
the fungi cause the release of eosinophils.  So maybe it is an
adaptation of that theory?  Just a guess;  they may have completely
changed it, but I think I saw an update on the fungal thoery as
recently as 2004.   Dr. Jens Ponikau came up with both theories.
   I haven't completely given up on that theory, but as you know,
there are so many things that cause chronic sinusitis, that is just one
of the possiblities.  

Kathyw

what does alterations in fecal microbiota mean???

This is an interesting article.  I agree that it's not good to get rid
of the "good" bacteria, but from what I've read they come back within 2
weeks after taking an antibiotic. I also agree that it creates
overgrowth of the "bad guys" and Candida. It is not good to take
antibiotics if not absolutely necessary, but sometimes that is the only
choice.  I am a perfect example of how indiscriminately taking them can
lead to "superinfections."  That's why I now think it is a good idea to
try to get cultures if at all possible.  I ran low grade fevers for
years after developing a really bad sinus infection many years ago,
that I don't think was ever completely cleared up.  I think that if I
had been given a stronger antibiotic for a longer period of time, then
maybe I wound't be in the "chronic sinusitis" group and now have
inflammation and/or infection in the bone.  So I think that just
telling people not to take antibiotics at all is just as dangerous and
taking too many of them.  I also think that one should also try to
allow the immune system to clear it up on it's own first, but if it
doesn't it needs to be treated aggressively and then maybe some of
these other problems could be eliminated and the digestive system
restored by use of probiotics, etc.

I also think that there is some validity to the Candida allergy
theory.  I think that  I have read somewhere that an allergy to Candida
can make one more susceptible to sinusitis, but an actual allergy
would be a genetic predisposition, which I must obviously have because
I've gotten bad "yeast" infections before I ever took an antibitotic.
To some extent, in women, it is also a hormonal thing.  I've also
tested positive to Candida in allergy testing.  I don't completely
understand the article that you quoted, but it sounds like it is saying
it is the overgrowth of Candida from antibiotic use that creates the
response that you are describing and has nothing to do with genetics.
That may partly be true, but I don't think it explains the whole story.

That being said,  many of us have tried the Candidia elimination diet,
topical and systemic antifungals without any help at all.

So, I think there are so many factors involved, that one has to learn
their own body's response to everything from allergies, to diet, to
immunodifficienies, genetic susceptibiltity (that's a big factor from
my research), and environmental exposure.

Now on to the mycotoxins.  I do think without a doubt, that exposure to
the toxins that some fungi create can disrupt the entire immune system
and affect the nasal mucosa also.  This is particulary true for such
molds as STachybotrys, Fusarium, Penicillium, and Aspergillus.  I had
toxic exposures to Fusarium in my workplace that I know have caused or
at least contributed to my problems.  I worked in a school that had
water leaks from a poorly constructed roof and a malfunctioning HVAC
system and these molds were abundant.  Many people at that school have
been and still are sick.  I think the reason this is happening is
because people started trying to save money and build "energy
efficient" airtight buildings that set up the conditions for higher
indoor humidity and mold growth.  Then the buildings are not maintained
and the mold grows in the dust, organic debris, etc. and will produce
mycotoxins when not in their natural environment.  At the school where
I taught, the building also had a flat roof that held water and an
algae grew in it and was growing many molds including Fusarium which
produces toxins even worse than STachybotrys.  Then the roof leaked and
mold infiltrated.

The massive flooding that has occurred after Hurricane Katrina has
saturated homes and buildings with water which makes it "ripe" for
growth of these kinds of molds.  I think it is a disgrace that people
aren't being made more aware of the potential dangers of this.

Well, that's just my "2 cents" worth.

I hope everyone has a great Thanksgiving.

Kathyw

found  the following two fairly recent articles from Mayo Cine.
Please read both before judging the first.  Perhaps this may set up the
initial response but when it persists for a long time or the immune
system goes awry, then the anitifungals don't work?  I hope everyone
had a great Thanksgiving!!

http://www.mayoclinic.org/news2004-rst/2459.html

Mayo Clinic in Rochester
Friday, October 08, 2004
Mayo Clinic Research Shows Common Airborne Fungi Cause Chronic Stuffy
Nose, Suggests New Treatment Strategy
ROCHESTER, Minn. -- A team led by Mayo Clinic researchers has
determined that over-reactive immune responses to airborne fungi could
cause the stuffy noses and airway inflammation among sufferers of
chronic rhinosinusitis. These findings could one day lead to a new,
longer-lasting treatment.
"It's time to recognize there is a greater sensitivity to airborne
fungi in some patients, and therefore we need to remove or reduce the
fungal exposure," says lead investigator Hirohito Kita, M.D.
In today's electronic edition of the Journal of Allergy and Clinical
Immunology
<http://www2.us.elsevierhealth.com/scripts/om.dll/serve?action=searchDB&searchDBf
or=home&id=ai>,
the Mayo Clinic researchers and a colleague from the University of Utah
conclude that certain species of airborne fungus produce spores and
by-products, that when inhaled, prompt irregular and damaging immune
responses. The responses, in turn, produce the congestion and
inflammation. Chronic rhinosinusitis costs society about $5.6 billion a
year. And that doesn't include an estimated $70 million in annual
lost work days, as well as a diminished quality of life.
Implications of Research
"The fungi we're talking about are very common," Dr. Kita.
"They are airborne fungi found anywhere in the United States. Now
that we know the role of the fungi, we can work toward reducing the
potential role of the fungi through such treatments as nasal
irrigations (flushing with water) that clear the fungi, or prescription
of antifungal medicines taken by mouth."
Preliminary results show that the irrigation treatment relieves
symptoms. Larger, multicenter studies are needed before this treatment
can move into general use. But the results are encouraging because they
support the idea that reducing fungal exposure in sensitive individuals
could offer a new treatment option to sufferers worldwide.
Background
Chronic rhinosinusitis is one of the most common chronic illnesses in
the United States. Its symptoms include persistent stuffy nose, thick
mucus production and loss of smell. Though chronic rhinosinusitis
causes significant discomfort and health problems, it is not well
understood. Viruses, bacteria and allergic reactions all have been
researched and debated as potential mechanisms driving the responses.
The immune system mounts different kinds of responses for different
invaders -- a bacterium gets attacked by a different cell or system
than an allergy-prompting particle, for example. That's why it's
critical to identify the key mechanisms in the immune response to
chronic rhinosinusitis, allowing researchers to design treatments to
relieve the distressing symptoms.
The Mayo Clinic work is the first to provide data for the role of
airborne fungi in chronic rhinosinusitis and to show that several
immune system branches appear to collaborate in response to the fungi
-- resulting in an abnormally enhanced response that causes troublesome
inflammation and congestion. The research team's data show that
specific cells in 90 percent of chronic rhinosinusitis patients produce
an enhanced immune-system response to one fungus in particular,
Alternaria. Another kind of common fungus, Cladosporium, also provoked
an abnormally enhanced immune response.
Mayo Clinic scientists previously used antifungal therapies to treat
patients with chronic sinusitis, which marked a new clinical approach.
These new findings serve to further support this perspective and will
prompt additional research.
The Investigation
Researchers tested blood from 18 patients with chronic rhinosinusitis
and 15 healthy persons to evaluate how specific immune system cells
responded to common airborne fungi. The immune systems of those with
chronic rhinosinusitis reacted more robustly than those of healthy
individuals. In fact, when exposed to Alternaria, one branch of the
immune system's response was five times greater in the chronic
rhinosinusitis patients than in the healthy volunteers.
The research team investigated the body's responses to this fungal
exposure by measuring components within the two branches of the
adaptive immune system. The adaptive immune system takes several days
to mount a response to foreign invaders. The two branches of the
adaptive immune system are: 1) a cell-directed branch that involves
special cells known as T lymphocytes and 2) the humoral branch, which
works primarily through cells known as B lymphocytes.
Research Team Members and Support
In addition to Dr. Kita, the Mayo Clinic research team includes
Seung-Heon Shin, M.D.; Jens Ponikau, M.D.; David Sherris, M.D. (now at
the University of Buffalo); David Congdon, M.D.; Evangelo Frigas, M.D.;
Henry Homburger, M.D.; and Mark Swanson. The University of Utah
collaborator was Gerald Gleich, M.D. Their work was supported by a
grant from The National Institute for Allergy and Infectious Diseases
and by the Mayo Foundation.
In accordance with the Bayh-Dole Act of 1980, Mayo Clinic has licensed
technology for the treatment of chronic rhinosinusitis with antifungals
to a commercial entity and will receive royalties from that license.
---------------------------------------------------------------------------------------------------------------------------------------------------

http://mayoresearch.mayo.edu/mayo/research/staff/kita_h.cfm

SUMMARY OF CURRENT WORK
Research is focused on eosinophil biology and immunological mechanisms
of chronic airway inflammation. Ongoing studies include: 1.)
elucidating the roles of adhesion molecules, Fc receptors, G
protein-coupled receptors in activation and mediator release by
eosinophils; 2.) characterizing the innate immune functions of
eosinophils and airway epithelial cells; 3.) dissecting the mechanisms
of chronic airway inflammation and its outcomes by using murine models
and by analyzing the specimens obtained from patients with diseases;
and, 4.) elucidation of the immunological mechanisms of diseases, such
as bronchial asthma and chronic sinusitis, and development of novel
therapeutic approaches for the patients.
A number of recent studies indicate that immunological processes play
important roles in the pathophysiology of chronic airway diseases, such
as bronchial asthma and chronic sinusitis, and that eosinophils (a type
of white blood cells) are one of the major effector cells in these
disease processes. Furthermore, eosinophils are likely involved in the
mechanisms of other chronic diseases, such as inflammatory bowel
disease, as well as in host defense on the mucosal surface.
Our laboratory's goals are to better understand the immunobiology of
eosinophilic leukocytes and to elucidate the immunological mechanisms
of allergic and chronic airway disorders with the ultimate goals being
identification of novel ways to treat patients with these diseases. To
this end, a variety of studies are currently ongoing in our laboratory.
The first project focuses on the dissection of the cellular biological
mechanisms of eosinophil activation. We found that a number of
biological molecules, such as immunoglobulins, cytokines, and lipid
mediators, induce eosinophil activation and production of inflammatory
mediators by this cell type. Importantly, adhesion molecules,
particularly the beta2 integrins, are critically involved in eosinophil
activation induced by various classes of secretagogues. Furthermore,
these molecules play important roles in recruitment of eosinophils into
the sites of inflammation. Therefore, we are characterizing the
regulatory mechanisms and functions of eosinophil integrins in
comparison to those on neutrophils and are elucidating the roles of
these molecules in eosinophilic inflammation using several in vitro
systems and in vivo models of allergic inflammation.
The second project is the analysis of the innate immune functions of
eosinophils and airway epithelial cells. We are currently focusing on
the interaction of these cell types with enzymatic microbial products,
such as protease and glycosidase, because these molecules are likely
produced at the sites of bacterial infection and fungus colonization.
We are evaluating which receptors on eosinophils and airway epithelial
cells are used to recognize these enzymes, what are the downstream
signaling pathways after receptor activation, and what are the
functional outcomes.
The third project examines the pathophysiologic mechanisms of allergic
and chronic airway disorders, such as bronchial asthma, chronic
sinusitis, and COPD, in humans. We phenotype the inflammatory
mediators, such as cytokines, chemokines and immunoglobulins, involved
in patients with diseases, characterize the nature of inflammatory
cells (e.g. lymphocytes, eosinophils, natural killer cells, dendritic
cells), and seek to elucidate how exposure to the etiologic agents
(e.g. antigen and microbial products) results in pathologic and
physiologic changes of the patients. Several animal models, such as
allergen-challenged animals and transgenic and gene knockout mice, are
also used to investigate how pharmacologic or immunologic intervention
would affect the disease process.
Finally, the fourth project focuses on the hypersensitivity responses
of patients with asthma and chronic sinusitis to non-pathologic
microorganisms such as environmental fungi. Strong collaboration is
established with the Department of Medicine, the Department of
Immunology, the Department of Pediatrics and Adolescent Medicine, and
the Department of Otorhinolaryngology to address the disease mechanisms
and patient treatment.

found  the following two fairly recent articles from Mayo Cine.
Please read both before judging the first.  Perhaps this may set up the
initial response but when it persists for a long time or the immune
system goes awry, then the anitifungals don't work?  I hope everyone
had a great Thanksgiving!!

http://www.mayoclinic.org/news2004-rst/2459.html

Mayo Clinic in Rochester
Friday, October 08, 2004
Mayo Clinic Research Shows Common Airborne Fungi Cause Chronic Stuffy
Nose, Suggests New Treatment Strategy
ROCHESTER, Minn. -- A team led by Mayo Clinic researchers has
determined that over-reactive immune responses to airborne fungi could
cause the stuffy noses and airway inflammation among sufferers of
chronic rhinosinusitis. These findings could one day lead to a new,
longer-lasting treatment.
"It's time to recognize there is a greater sensitivity to airborne
fungi in some patients, and therefore we need to remove or reduce the
fungal exposure," says lead investigator Hirohito Kita, M.D.
In today's electronic edition of the Journal of Allergy and Clinical
Immunology
<http://www2.us.elsevierhealth.com/scripts/om.dll/serve?action=searchDB&searchDBf
or=home&id=ai>,
the Mayo Clinic researchers and a colleague from the University of Utah
conclude that certain species of airborne fungus produce spores and
by-products, that when inhaled, prompt irregular and damaging immune
responses. The responses, in turn, produce the congestion and
inflammation. Chronic rhinosinusitis costs society about $5.6 billion a
year. And that doesn't include an estimated $70 million in annual
lost work days, as well as a diminished quality of life.
Implications of Research
"The fungi we're talking about are very common," Dr. Kita.
"They are airborne fungi found anywhere in the United States. Now
that we know the role of the fungi, we can work toward reducing the
potential role of the fungi through such treatments as nasal
irrigations (flushing with water) that clear the fungi, or prescription
of antifungal medicines taken by mouth."
Preliminary results show that the irrigation treatment relieves
symptoms. Larger, multicenter studies are needed before this treatment
can move into general use. But the results are encouraging because they
support the idea that reducing fungal exposure in sensitive individuals
could offer a new treatment option to sufferers worldwide.
Background
Chronic rhinosinusitis is one of the most common chronic illnesses in
the United States. Its symptoms include persistent stuffy nose, thick
mucus production and loss of smell. Though chronic rhinosinusitis
causes significant discomfort and health problems, it is not well
understood. Viruses, bacteria and allergic reactions all have been
researched and debated as potential mechanisms driving the responses.
The immune system mounts different kinds of responses for different
invaders -- a bacterium gets attacked by a different cell or system
than an allergy-prompting particle, for example. That's why it's
critical to identify the key mechanisms in the immune response to
chronic rhinosinusitis, allowing researchers to design treatments to
relieve the distressing symptoms.
The Mayo Clinic work is the first to provide data for the role of
airborne fungi in chronic rhinosinusitis and to show that several
immune system branches appear to collaborate in response to the fungi
-- resulting in an abnormally enhanced response that causes troublesome
inflammation and congestion. The research team's data show that
specific cells in 90 percent of chronic rhinosinusitis patients produce
an enhanced immune-system response to one fungus in particular,
Alternaria. Another kind of common fungus, Cladosporium, also provoked
an abnormally enhanced immune response.
Mayo Clinic scientists previously used antifungal therapies to treat
patients with chronic sinusitis, which marked a new clinical approach.
These new findings serve to further support this perspective and will
prompt additional research.
The Investigation
Researchers tested blood from 18 patients with chronic rhinosinusitis
and 15 healthy persons to evaluate how specific immune system cells
responded to common airborne fungi. The immune systems of those with
chronic rhinosinusitis reacted more robustly than those of healthy
individuals. In fact, when exposed to Alternaria, one branch of the
immune system's response was five times greater in the chronic
rhinosinusitis patients than in the healthy volunteers.
The research team investigated the body's responses to this fungal
exposure by measuring components within the two branches of the
adaptive immune system. The adaptive immune system takes several days
to mount a response to foreign invaders. The two branches of the
adaptive immune system are: 1) a cell-directed branch that involves
special cells known as T lymphocytes and 2) the humoral branch, which
works primarily through cells known as B lymphocytes.
Research Team Members and Support
In addition to Dr. Kita, the Mayo Clinic research team includes
Seung-Heon Shin, M.D.; Jens Ponikau, M.D.; David Sherris, M.D. (now at
the University of Buffalo); David Congdon, M.D.; Evangelo Frigas, M.D.;
Henry Homburger, M.D.; and Mark Swanson. The University of Utah
collaborator was Gerald Gleich, M.D. Their work was supported by a
grant from The National Institute for Allergy and Infectious Diseases
and by the Mayo Foundation.
In accordance with the Bayh-Dole Act of 1980, Mayo Clinic has licensed
technology for the treatment of chronic rhinosinusitis with antifungals
to a commercial entity and will receive royalties from that license.
---------------------------------------------------------------------------------------------------------------------------------------------------

http://mayoresearch.mayo.edu/mayo/research/staff/kita_h.cfm

SUMMARY OF CURRENT WORK
Research is focused on eosinophil biology and immunological mechanisms
of chronic airway inflammation. Ongoing studies include: 1.)
elucidating the roles of adhesion molecules, Fc receptors, G
protein-coupled receptors in activation and mediator release by
eosinophils; 2.) characterizing the innate immune functions of
eosinophils and airway epithelial cells; 3.) dissecting the mechanisms
of chronic airway inflammation and its outcomes by using murine models
and by analyzing the specimens obtained from patients with diseases;
and, 4.) elucidation of the immunological mechanisms of diseases, such
as bronchial asthma and chronic sinusitis, and development of novel
therapeutic approaches for the patients.
A number of recent studies indicate that immunological processes play
important roles in the pathophysiology of chronic airway diseases, such
as bronchial asthma and chronic sinusitis, and that eosinophils (a type
of white blood cells) are one of the major effector cells in these
disease processes. Furthermore, eosinophils are likely involved in the
mechanisms of other chronic diseases, such as inflammatory bowel
disease, as well as in host defense on the mucosal surface.
Our laboratory's goals are to better understand the immunobiology of
eosinophilic leukocytes and to elucidate the immunological mechanisms
of allergic and chronic airway disorders with the ultimate goals being
identification of novel ways to treat patients with these diseases. To
this end, a variety of studies are currently ongoing in our laboratory.
The first project focuses on the dissection of the cellular biological
mechanisms of eosinophil activation. We found that a number of
biological molecules, such as immunoglobulins, cytokines, and lipid
mediators, induce eosinophil activation and production of inflammatory
mediators by this cell type. Importantly, adhesion molecules,
particularly the beta2 integrins, are critically involved in eosinophil
activation induced by various classes of secretagogues. Furthermore,
these molecules play important roles in recruitment of eosinophils into
the sites of inflammation. Therefore, we are characterizing the
regulatory mechanisms and functions of eosinophil integrins in
comparison to those on neutrophils and are elucidating the roles of
these molecules in eosinophilic inflammation using several in vitro
systems and in vivo models of allergic inflammation.
The second project is the analysis of the innate immune functions of
eosinophils and airway epithelial cells. We are currently focusing on
the interaction of these cell types with enzymatic microbial products,
such as protease and glycosidase, because these molecules are likely
produced at the sites of bacterial infection and fungus colonization.
We are evaluating which receptors on eosinophils and airway epithelial
cells are used to recognize these enzymes, what are the downstream
signaling pathways after receptor activation, and what are the
functional outcomes.
The third project examines the pathophysiologic mechanisms of allergic
and chronic airway disorders, such as bronchial asthma, chronic
sinusitis, and COPD, in humans. We phenotype the inflammatory
mediators, such as cytokines, chemokines and immunoglobulins, involved
in patients with diseases, characterize the nature of inflammatory
cells (e.g. lymphocytes, eosinophils, natural killer cells, dendritic
cells), and seek to elucidate how exposure to the etiologic agents
(e.g. antigen and microbial products) results in pathologic and
physiologic changes of the patients. Several animal models, such as
allergen-challenged animals and transgenic and gene knockout mice, are
also used to investigate how pharmacologic or immunologic intervention
would affect the disease process.
Finally, the fourth project focuses on the hypersensitivity responses
of patients with asthma and chronic sinusitis to non-pathologic
microorganisms such as environmental fungi. Strong collaboration is
established with the Department of Medicine, the Department of
Immunology, the Department of Pediatrics and Adolescent Medicine, and
the Department of Otorhinolaryngology to address the disease mechanisms
and patient treatment.