In article
<130e46ed-f1de-488d-a1ab-db9a629a4f03@[EMAIL PROTECTED]
>,
Taka <taka0038@[EMAIL PROTECTED]
> wrote:
> Good post, thanks Kofi. Finally some research which taps directly
> into the molecular mechanism of allergies and not just another
> antihistamine drug. PGE2 stimulates the tolerance via TREGs and
> helminths do induce PGE2 (e.g. PMID: 17544219, 18305957,16009364). Is
> there something suppressing prostaglandins while increasing
> leukotrienes like NSAIDs common to people with allergies? E.g. I was
> taking frequently paracetamol (PMID: 17884974) for colds when my
> pollen allergies started ...
>
It signals through EP4. Thanks. I missed the prostaglandin/helminth
link.
COX-2 inhibitors do directly depress Treg function, thus - according to
this lastest paper - elevating allergies. COX-2 inhibition will also
worsen pretty much any form of autoimmunity you've got (and block stem
cells from their repair work, hence shrinking joints and impairing the
healing process all over the body). The direct mechanism on Tregs has
been understood since 2005 but people were noticing how the
prostaglandin network regulated antigen tolerance a long time before
that. The FDA has failed to warn anybody about this.
FYI, helminths also deplete iron (see my earlier posts on the
gut-protective HIF-1a pathway and iron chelators/prolyl hydroxylase
inhibitors) and, the last time I went hunting for it, there was even
tantalizing evidence the critters produce butyrate in the gut.
Do you know anything about beta-glucuronidase and any of these topics?
It's a very effective therapy for inducing tolerance to allergens. You
need about four shots a year to maintain your protection. I know it's
related to heparanse and that sticks it somewhere in the HIF network but
that's about all I got.
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in lung cancer, COX-2 and PGE2 underlie an immunosuppressive network
that is im****tant in the formation of non-small cell lung cancer; CD4+
CD25+ regulatory T-cells (Tregs) block antitumor immune responses when
tumors secrete PGE2 and activate Foxp3 in the Tregs which increases Treg
activity; this effect was significantly reduced without an EP4
(E-prostanoid) receptor and totally absent without an EP2 receptor;
COX-2 inhibitors (Vioxx, Celebrex) reduced Treg activity, blocked FoxP3
and decreased tumor growth (this provides a pathway whereby COX-2
inhibitors can exaggerate allergies) [PMID 15958566]
broad-spectrum COX inhibitors can be arthritigenic interfering with the
acquisition of tolerance to some arthritigens [PMID 16259716]
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