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"Luteolin exposure resulted in 90 percent drop in IL-6 production"

(NaturalNews)
Researchers at the University of Illinois report that a plant compound
found in abundance in celery and green peppers can disrupt a key
component of the inflammatory response in the brain. The findings have
implications for research on aging and diseases such as Alzheimer's
and multiple sclerosis.

Inflammation can be a blessing or a blight. It is a critical part of
the body's immune response that in normal circumstances reduces injury
and promotes healing. When it goes awry, however, the inflammatory
response can lead to serious physical and mental problems.

Inflammation plays a key role in many neurodegenerative diseases and
also is implicated in the cognitive and behavioral impairments seen in
aging.

The new study looked at luteolin (LOO-tee-OH-lin), a plant flavonoid
known to impede the inflammatory response in several types of cells
outside the central nervous system. The purpose of the study was to
determine if luteolin could also reduce inflammation in the brain,
said animal sciences professor and principal investigator Rodney
Johnson.

"One of the questions we were interested in is whether something like
luteolin, or other bioactive food components, can be used to mitigate
age-associated inflammation and therefore improve cognitive function
and avoid some of the cognitive deficits that occur in aging," Johnson
said.

The researchers first studied the effect of luteolin on microglia.
These brain cells are a key component of the immune defense. When
infection occurs anywhere in the body, microglia respond by producing
inflammatory cytokines, chemical messengers that act in the brain to
orchestrate a whole-body response that helps fight the invading
microorganism.

This response is associated with many of the most obvious symptoms of
illness: sleepiness, loss of appetite, fever and lethargy, and
sometimes a temporary diminishment of learning and memory. Neuro-
inflammation can also lead some neurons to self-destruct, with
potentially disastrous consequences if it goes too far.

Graduate research assistant Saebyeol Jang studied the inflammatory
response in microglial cells. She spurred inflammation by exposing the
cells to lipopolysaccharide (LPS), a component of the cell wall of
many common bacteria.

Those cells that were also exposed to luteolin showed a significantly
diminished inflammatory response. Jang showed that luteolin was
shutting down production of a key cytokine in the inflammatory
pathway, interleukin-6 (IL-6). The effects of luteolin exposure were
dramatic, resulting in as much as a 90 percent drop in IL-6 production
in the LPS-treated cells.

"This was just about as potent an inhibition as anything we had seen
previously," Johnson said.

But how was luteolin inhibiting production of IL-6?

Jang began by looking at a class of proteins involved in intracellular
signaling, called transcription factors, which bind to specific
"promoter" regions on DNA and increase their transcription into RNA
and translation into proteins.

Using electro-mobility shift assays, which measure the binding of
transcription factors to DNA promoters, Jang eventually determined
that luteolin inhibited IL-6 production by preventing activator
protein-1 (AP-1) from binding the IL-6 promoter.

AP-1 is in turn activated by JNK, an upstream protein kinase. Jang
found that luteolin inhibited JNK phosphorylation in microglial cell
cultures. The failure of the JNK to activate the AP-1 transcription
factor prevented it from binding to the promoter region on the IL-6
gene and transcription came to a halt.

To see if luteolin might have a similar effect in vivo, the
researchers gave mice luteolin-laced drinking water for 21 days before
injecting the mice with LPS.

Those mice that were fed luteolin had significantly lower levels of
IL-6 in their blood plasma four hours after injection with the LPS.
Luteolin also decreased LPS-induced transcription of IL-6 in the
hippocampus, a brain region that is critical to spatial learning and
memory.

The findings indicate a possible role for luteolin or other bioactive
compounds in treating neuro-inflammation, Johnson said.

"It might be possible to use flavonoids to inhibit JNK and mitigate
inflammatory reactions in the brain," he said. "Inflammatory cytokines
such as interleukin-6 are very well known to inhibit certain types of
learning and memory that are under the control of the hippocampus, and
the hippocampus is also very vulnerable to the insults of aging," he
said. "If you had the potential to decrease the production of
inflammatory cytokines in the brain you could potentially limit the
cognitive deficits that result."

The study appeared recently in Proceedings of the National Academy of
Sciences.

Herbalists have known about the cooling properties of celery for
decades and prescribe it for arthritis, hot flashes, and for cooling
down the body on hot summer days.

News Source:

University of Illinois at Urbana-Champaign (2008, May 23). Plant
Flavonoid In Celery And Green Peppers Found To Reduce Inflammatory
Response in the Brain
(http://www.uiuc.edu/)

About the author
Leslee Dru Browning is a 6th generation Medical Herbalist &
Nutritionist from the ancestral line of Patty Bartlett Sessions;
Pioneer Mid-Wife & Herbalist. Leslee practiced Medical Herbalism and
Nutritional Healing for over 25 years and specialized in Cancer
Wellness along with Chronic Illness. She now devotes her career to
teaching people, through her writing, about Natural Healing from An
Herbal Perspective.

-----------------------------

Source: Johns Hopkins Medical Institutions Released: Fri
23-Sep-2005, 08:45 ET
Key Protein Linked to Transverse Myelitis and Multiple Sclerosis
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Medical News Keywords
JOHNS HOPKINS IL-6 TRANSVERSE MYELITIS MULTIPLE SCLEROSIS

Hopkins researchers have discovered a single molecule that is a cause
of an autoimmune disease in the central nervous system, called
transverse myelitis (TM), that is related to multiple sclerosis.


Newswise - Hopkins researchers have discovered a single molecule that
is a cause of an autoimmune disease in the central nervous system,
called transverse myelitis (TM), that is related to multiple
sclerosis.


In a study published in the October issue of The Journal of Clinical
Investigation, psychiatrist Adam Kaplin, M.D., Ph.D., an assistant
professor at The Johns Hopkins University School of Medicine, and
neurologist Douglas Kerr, M.D., Ph.D., also an assistant professor at
Hopkins, showed that the levels of the protein, IL-6, are dramatically
elevated in the spinal fluid of transverse myelitis (TM) patients.


Although the majority of TM patients suffer a single attack, 15
percent to 30 percent of patients go on to develop full-blown MS. TM
evolves rapidly and without warning and usually results in permanent
impairment, including weakness of the legs and arms, bowel and bladder
dysfunction, pain and paralysis.


IL-6 is a chemical messenger that cells of the immune system use to
communicate with one another. One of the cell types injured by high
levels of IL-6 includes oligodendrocytes, which help produce the
protective myelin sheath coating around nerve cells. The findings
offer one possible mechanism responsible for demyelinating disorders,
such as TM and MS, and may aid in the development of effective
therapies against these disorders, the researchers say.


"This is the first time a single culprit has been identified as
causing a CNS autoimmune disease," said Kaplin.


The researchers began investigating the protein IL-6 when they became
aware that TM patients suffered from memory impairment and depression.
IL-6 has been implicated in mood and concentration disorders.


"This discovery is a success story that begins with listening
carefully to what patients are telling us about their suffering and
then collaborating across disciplines to open up new avenues of
investigation," said Kaplin.


"TM is related to other autoimmune disorders of the nervous system,
including Guillain-Barré syndrome, MS and acute disseminated
encephalomyelitis.
This study may give us a foothold in understanding all of these
disorders and how they are linked together.
The benefit is, therefore, not only to those who are paralyzed by TM,
but to those who have disabilities due to a variety of autoimmune
disorders. We are actively using these findings to aid in developing
future diagnostic, prognostic and therapeutic advancements," said
Kerr, director of the Johns Hopkins Transverse Myelitis Center, the
only center devoted to TM in the world.


Researchers analyzed 42 inflammatory proteins in the cerebrospinal
fluid of both TM and healthy patients. They found that IL-6 was
consistently elevated in TM patients' spinal fluid. Further, the level
of IL-6 directly correlated with the severity of paralysis.


Using cell culture and animal studies, the researchers confirmed that
elevated IL-6 levels were directly injurious to the spinal cord. They
showed that spinal fluid from TM patients induced death of spinal cord
cells when cultured in a dish and that IL-6, when infused in adult
rats, induced paralysis. Under the microscope, tissue from IL-6-
infused rats showed demyelination and injury of axons, pathology that
was nearly identical to that seen in human patients with TM.


Kerr and Kaplin also deduced that the reason IL-6 elevations injure
only the spinal cord and not other regions of the nervous system was
because distinct regions of the nervous system have different
responses to IL-6. They concluded that these different types of
responses might be a part of why different autoimmune disorders of the
nervous system affect distinct regions and cause distinct symptoms.


"When we started, we knew nothing about the bad players in this drama
in the spinal cord of CNS autoimmune diseases - it was a classic
murder mystery and we set out together to find out 'who done it',"
said Kaplin. "We've answered who could have done it, and how, and
where."


Funding for this study was provided by the National Institutes of
Health. Other investigators involved in this study, conducted solely
at Hopkins, were Deepa M. Deshpande, M.S.; Erick Scott, B.S.; Chitra
Krishnan, M.S.; Jessica S. Carmen, B.S.; Irina Shats, M.S.; Tara
Martinez, B.S.; Jennifer Drummond, B.S.; Sonny Dike, M.D.; Mickail
Pletnikov, M.D., Ph.D.; Sanjay C. Keswani, M.B.; Timothy H. Moran,
Ph.D.; Carlos A. Pardo, M.D., and Peter A. Calabresi, M.D.


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© 2005 Newswise. All Rights Reserved.



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