Endotoxin-Induced Uveitis suppressed by VIP

[Guest guest]

Wouldn't it also make sense that environmental toxins like mold that

suppress VIP might thereby induce diseases like Autoimmune

Uveoretinitis because they disturb the body's natural ability to

protect itself from endotoxins present in the gut or elsewhere?

http://archopht.ama-assn.org/cgi/content/abstract/122/8/1179

Prevention of Experimental Autoimmune Uveoretinitis by Vasoactive

Intestinal Peptide

Hiroshi Keino, MD, PhD; Takeshi Kezuka, MD, PhD; Masaru Takeuchi, MD,

PhD; Naoyuki Yamakawa, PhD; Takaaki Hattori, MD; Masahiko Usui, MD,

PhD

Arch Ophthalmol. 2004;122:1179-1184.

Background: Vasoactive intestinal peptide (VIP), a neuropeptide that

is known to be present in lymphoid tissue microenvironments, shows

prominent anti-inflammatory actions.

Objective To examine the potential effect of VIP on the development

of experimental autoimmune uveoretinitis (EAU).

Design We immunized C57BL/6 mice with human interphotoreceptor

retinoid-binding protein peptide 1-20 (h-IRBP peptide). Vasoactive

intestinal peptide was administered intraperitoneally on alternate

days until day 21 after immunization (entire group). In some cases,

VIP was injected at different time points after the induction of

immunity with h-IRBP peptide (efferent group). In each experiment, a

control group of mice was injected with phosphate-buffered saline

instead of VIP. Development of EAU was evaluated by means of

histological examination on day 21 after immunization. Furthermore, we

determined whether intravenous injection of peritoneal exudate cells

cultured with VIP overnight in vitro abrogated EAU. We analyzed

delayed hypersensitivity for h-IRBP peptide and the occurrence and

severity of EAU using evaluation of histopathological sections for

inflammatory ocular disease.

Results Treatment with VIP suppressed the expression of delayed

hypersensitivity responses to h-IRBP peptide significantly (positive

control vs entire group, P = .02; positive control vs efferent group,

P<.001). Mice treated with VIP (n = 10) showed a lower occurrence

(40%) and decreased severity of EAU (entire group mean score, 0.3;

median score, 0) compared with untreated mice (occurrence, 80%; mean

score, 0.85; median score, 0.75), as assessed by histopathological

analyses (P = .049). Suppressive effects of VIP on EAU were also

observed, even when VIP was administered on days 8 through 20 after

immunization (efferent group [n = 9] occurrence, 11%; mean score, 0.1;

median score, 0) (P = .003). Moreover, expression of EAU was

significantly suppressed when the animals were pretreated with

peritoneal exudate cells pulsed with h-IRBP in the presence of VIP

(control mean score, 1.2; median score, 1.0; occurrence, 80% [n = 10])

compared with the VIP-treatment group (mean score, 0.3; median score,

0; occurrence, 30% [n = 10]) (P = .004). In addition, VIP-treated

peritoneal exudate cells generated regulator T cells in the spleens of

recipient mice that were able to interfere with the development of EAU

(control group mean score, 0.5; median score, 0.5; occurrence, 63% [n

= 8]) compared with the VIP-treatment group (mean score, 0.08; median

score, 0; occurrence, 17% [n = 6]) (P = .08).

Conclusion Treatment with VIP is a highly effective therapy to suppress EAU.

Clinical Relevance As a result of its efficacy in preventing EAU, VIP

might be considered as a novel therapeutic modality for human uveitis.

From the Department of Ophthalmology, Tokyo Medical University, Tokyo,

Japan. The authors have no relevant financial interest in this

article.

Endotoxin-Induced Uveitis

[Guest guest]

Live, I think that many acute exposures to many foreign

invaders/toxins/chemicals/patogens/allergens could cause autoimmune

diseases, and maybe some chronic exposures too.

[Guest guest]

Jeanine, you are right.

It's not a matter of conjecture.

That is how they start.

It's been repeatedly proven.

On Tue, Sep 30, 2008 at 8:28 PM, who <jeaninem660@...> wrote:

> Live, I think that many acute exposures to many foreign

> invaders/toxins/chemicals/patogens/allergens could cause autoimmune

> diseases, and maybe some chronic exposures too.

>

[Guest guest]

are you seeing the difference in even a moderate dose with chronic

exposure and although with seepage and symptoms it's still very much

different than a acute exposure that attacks you mucosae to the point

of severe damage and liver malfunction and loss of immunity

protection and that allergies obtained at this point are possably the

defineing point of weither you can heal or not with any protocal

available to us.this is why the defence no longer denies that those

with resulting allergies to molds from their exposure may indeed have

a hard time recovering if at all. this is why everyone should be

tested for allergies to molds. allergic autoimmunity/anaphalaxis

reactions to mold. allergies are caused by high exposure and they are

a autoimmune disease. loss of immunity means you had systemic

invasion. as in my first home with years of exposure from lower up to

a fairly high exposure I had lot's of symptoms and was in major pain

and it was miserable but I still had a resistent system and still

could get relief when I was out of that house for a period of time.

this changed with the second exposure which was acute and very

damageing.

> > Live, I think that many acute exposures to many foreign

> > invaders/toxins/chemicals/patogens/allergens could cause

autoimmune

> > diseases, and maybe some chronic exposures too.

> >

>