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  Discussion on Research Summary: Sweet Itch potential mechanisms of cause and control
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Moderator:
DrO

Posted on Tuesday, Jan 29, 2008 - 11:13 am:

Because of the highly technical nature of this piece of research I almost passed over it for posing. However on close reading there is an amazing fact that comes out that is of concern to all who own horses where there are no culicoides: If you move an adult horse which has never been exposed to culicoides to an area that does, he has a significant chance (appx. 50%) of developing Sweet Itch (culicoides hypersensitivity).

Though this idea is somewhat speculative the conclusion controls for genetic factors by looking at the incidence of adult horses moved into areas with culicoides and comparing it to their progeny which were exposed from birth. If they are born in an area with culicoides they have less than a 10% incidence of Sweet Itch.

This observation strongly suggests that early exposure to the biting midges has a protective effect on developing the allergy. We are not without precedent on this idea. The rising incidence of asthma in humans for instance has been hypothesized to have a similar mechanism based on the observation than asthma is less common in households where children have been exposed to indoor pets.

The report is also interesting as it gives some ideas on control. The hypothesis that is shaping up around this work is that exposure to culicoides at an early age stimulates a antigen-specific mechanism that helps to control (down-regulate) the development of an allergic response to the culicoides. Large surveys in other works suggest that about 30% of the adults who develop Sweet Itch get over it while 70% stay the same or worsen over time. If all of this pans out, the question is will it be possible to stimulate this antigen specific down regulation? Using the proper antigens and immunotherapy might be such a therapeutic regimen. Unfortunately the current antigens available are not well characterized for containing the appropriate antigens. For instance some scientific work in the past has suggested that different species of culicoides may have different allergy producing allergens.

Or what if we could non-specifically down-regulate this inflammatory response? Would there be downsides to this type of non-specific down regulation? Stay tuned while I bone up on some of these newer immunological systems that have been elucidated since I left school.
DrO

Vet Immunol Immunopathol. 2007 Nov 9;
Reduced incidence of insect-bite hypersensitivity in Icelandic horses is associated with a down-regulation of interleukin-4 by interleukin-10 and transforming growth factor-beta1.

Hamza E, Wagner B, Jungi TW, Mirkovich J, Marti E.

Institute of Veterinary Virology, Vetsuisse Faculty, University of Bern, Laenggassstrasse 122, CH-3001 Bern, Switzerland.

Insect bite hypersensitivity (IBH) is an allergic dermatitis of horses caused by IgE-mediated reactions to bites of insects of the genus Culicoides. IBH does not occur in Iceland due to the absence of Culicoides. However, Icelandic horses exported to mainland Europe as adults (1st generation) have a >/=50% incidence of developing IBH. In contrast, their progeny (2nd generation) has a <10% incidence of IBH. Here we show that peripheral blood mononuclear cells (PBMC) from Icelandic horses born in mainland Europe and belonging either to the IBH or healthy subgroup produce less interleukin (IL)-4 after polyclonal or allergen-specific stimulation when compared with counterparts from horses born in Iceland. We examined a role of IL-10 and transforming growth factor (TGF)-beta1 in down-regulation of IL-4 in healthy 2nd generation Icelandic horses. Supernatants of PBMC from 2nd generation healthy horses down-regulated the proportion of IL-4-producing cells and IL-4 production in stimulated cultures of PBMC from 1st generation IBH. This inhibition was mimicked by a combination of IL-10 and TGF-beta1 but not by the single cytokines. Cultures of stimulated PBMC of healthy 2nd generation horses produced a low level of IL-4, but IL-4 production was increased by anti-equine IL-10 and anti-human TGF-beta1. This shows for the first time that in horses, IL-10 and TGF-beta1 combined regulate IL-4 production in vitro. It is suggested that in this naturally occurring IgE-mediated allergy, IL-10 and TGF-beta1 have a role in the down-regulation of IL-4-induced allergen-specific Th2 cells, thereby reducing the incidence of IBH.
Member:
isabe

Posted on Wednesday, Sep 24, 2008 - 6:57 am:

Dear Dr. Oglesby,
I read with interest our article concerning sweet itch and the result of the research.
I have a 18 months warmblood who this summer developed sweet itch. Mother and father do not suffer from it. She started in August (so late in summer) to damage her mane and tail by violently scratching herself against trees. Since situation worsen quite a lot we are treating her with cortisone (dexamethasone) - 5CC for 2 days, 10 cc for 2 days. Pruritus did not decrease till now but inflammation under the mane skin decreased. Is this normal that she is still hitching notwithstanding cortisone? Do I have, according to the research, any possibility that she get over this problem when adult?
Thank you very much in advance for your reply.
Regards

Isabella
Moderator:
DrO

Posted on Wednesday, Sep 24, 2008 - 9:08 am:

Isabella, back up one page and start a new discussion. This will help others find your post and keep Horseadvice organized. The Start a New Discussion button is at the bottom of the list of preexisting discussions.
DrO
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