Author Topic: POIS Theory Master List  (Read 4105 times)

Muon

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POIS Theory Master List
« on: March 13, 2021, 04:07:11 PM »
Post theories/ideas regarding the Pathophysiology of POIS. This thread can function as a central hub. You may dump links to threads from other members in the comment section.

Rudimentary version
Or a combination of the above.

What else?
« Last Edit: July 23, 2021, 05:42:34 AM by Muon »

Muon

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Re: POIS Theory Master List
« Reply #1 on: March 13, 2021, 04:07:56 PM »
Reminder: Some ideas might be left inside other threads like POIS paper treatment summary etc.
« Last Edit: April 22, 2021, 06:35:23 AM by Muon »

Muon

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Re: POIS Theory Master List
« Reply #2 on: March 13, 2021, 04:09:02 PM »
Reserved 2

Muon

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Re: POIS Theory Master List
« Reply #3 on: March 13, 2021, 04:10:24 PM »
Reserved final

Muon

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Re: POIS Theory Master List
« Reply #4 on: March 19, 2021, 07:42:34 AM »

Muon

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Re: POIS Theory Master List
« Reply #5 on: April 20, 2021, 07:23:55 AM »
Running nose and nasal congestion can be related to vasomotor dysfunction (ANS, endothelial dysfunction?) which is unrelated to allergy, people might not be aware of this:

Vasomotor rhinitis

https://en.wikipedia.org/wiki/Nonallergic_rhinitis

Muon

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Re: POIS Theory Master List
« Reply #6 on: April 22, 2021, 06:51:26 AM »
Fox:
Gluten sensitivity
Improves on Niacin rich food
Slight blood pooling upon standing (Sympathetic activation? Vasomotor function?)

I do remember that a certain subset of Tregs plays a role in gluten sensitivity, it was the CD39 subset if I'm not mistaken (paper needed for confirmation). Now throw Niacin into the mix and combine it with the following post, see pic: https://poiscenter.com/forums/index.php?topic=3765.msg40413#msg40413

Could Niacin intake affect Tryp/5HT pathway and improves vasomotor function, thus blood pooling?

What does Testosterone therapy have to do with this?---> T is able to increase Treg population directly. POISers who improved on antibiotics could have altered Treg populations. Treg increase can also be seen in some individuals who have done allergic desensitization therapy with succesful outcome (generally speaking that is, but could play a role in desensitized POISers). These points can be used to support MCAS theory as well. Tramadol--->Tregs?
« Last Edit: April 22, 2021, 09:43:32 AM by Muon »

Muon

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Re: POIS Theory Master List
« Reply #7 on: June 03, 2021, 02:20:20 PM »
An Overview of Seminal Plasma Hypersensitivity and Approach to Treatment

Can’t copy stuff from tablet. Read part about: PAR2 and dust mite. Possible protease-activated receptor-mediated epithelial barrier dysfunction.

Systemic and localized seminal plasma hypersensitivity patients exhibit divergent immunologic characteristics

Proteases constitute more than 8% of all SPPs in WSP8 and can augment IgE-independent inflammatory responses by disrupting the epithelial permeability barrier and activating protease-activated receptors (PARs) on epithelial cells.9 PAR-2 activation, which has been demonstrated in response to proteases from dust mite and cockroach and in seafood workers exposed to high aerosolized levels of proteases, can augment epithelial barrier dysfunction and localized mucosal inflammation independent of specific IgE responses.9,  10 Moreover, it has been demonstrated that semen proteases such as PSA can activate PAR-2 on spermatozoa cell membranes.11 We have recently confirmed the presence of PAR-2 receptors on vaginal keratinocytes by using western blotting and flow cytometry as well as calcium influx in SPP-stimulated vaginal keratinocytes using confocal microscopy, which was blocked by a protease inhibitor (unpublished data; Ghosh D and Bernstein JA, 2014, manuscript in preparation).

Thus, PAR-2 activation in vaginal epithelium might contribute to localized SPH, although other possible mechanisms such as IgE-independent mast cell activation and neurogenic responses involving bradykinin-mediated inflammatory/pain pathways should be investigated. In addition, prostaglandins (present in a considerable amount in WSP), which can cause antigen presenting cells to release proinflammatory cytokines, may also contribute to localized vaginal inflammation, as we have observed in some cases of women with localized SPH who experience attenuation of their symptoms if they take a nonsteroidal anti-inflammatory agent before unprotected intercourse (unpublished data). Thus, these mechanisms, summarized in Fig E2 in this article's Online Repository at www.jacionline.org, could potentially explain reactions observed in women with localized SPH in which specific IgE does not play a critical role. To conclude, our data demonstrate that although women with systemic and localized SPH have similar clinical outcomes, the mechanism(s) of action for these responses is distinctly different. Further investigation of the mechanism(s) related to localized SPH is warranted.



Fig E2Postulated mechanisms for localized SPH: Although women with systemic SPH sensitized to PSA can induce a specific serum IgE response through the classical TH2 pathway, women with localized SPH may exhibit symptoms as a result of seminal plasma proteases causing degradation of mucosal tight junctions, leading to the activation of PAR-2 receptors on epithelial cells that results in the release of proinflammatory cytokines and localized inflammation. Seminal plasma also contains high levels of prostaglandin E2 (PGE2), which can activate antigen-presenting cells (APCs) lining the inner face of the vaginal epithelium, leading to the release of proinflammatory cytokines, causing localized mucosal inflammation.

Table 2:
https://sci-hub.se/10.1111/jsm.12813#

HDM, cockroach allergens or seminal protease—>PAR2–>leakage of PGE2 and other stuff. MCA is another possibility.
« Last Edit: June 03, 2021, 02:51:32 PM by Muon »

Muon

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