Blood testis barrier

[demode33]

Hello guys , what do you think of the idea that sperms enter into blood and causes an  immune reaction ?

https://www.reddit.com/r/POIS/comments/12extv9/maybethis_could_be_the_fundamenta

"Blood testis barrier is a barrier present in our testis which prevents sperms to enter into blood and lymphatic circulation. Suppose, our ?blood testis barrier? has been damaged,so now there is no barrier to prevent sperms enter into the circulation. When sperms enter into the bloodstream, immune system will be activated, immune system will destroy those antigens(sperms).And immune system will make antibody against our own sperms (antigens) . If once antibody would be made then those antibody will enter into testis and will destroy all sperms and germ cell (from which sperms form).
So,like that,same process will be processed when you inject sperm in your bloodstream.But here antibody may not enter into testis from circulation because of ?blood testis barrier?,but it is sure that antibody will form against our sperm." 
 
also i have a weird symtom when i ejaculate :  Gray spots appears in my lower belly ( 2cm-- 3cm ) that produces a Dandruff .
can that be related to a leak of sperms ? or leaky gut ?

[Sisyphus]

Yes, I have also come across this idea of blood testis barrier disruption, its association with autoimmunity and wondered about it as a possible link with pois. There are a small handful of posts on this forum about it. There are plenty of online articles about the blood testis barrier. I think it's worth considering. It would be interesting to hear from anyone on the forum who has looked into this and is perhaps able to understand a bit more.

"The blood-testis barrier (BTB) is one of the tightest blood-tissue barriers in the mammalian body".
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3250082/

COVID can disrupt it:-
"SARS-CoV-2 could induce the up-regulation of the pro-inflammatory cytokine and down-regulation of junctional proteins of the BTB, which can disrupt BTB and ultimately impair spermatogenesis."
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8387554/

Trauma can disrupt it ex/ in the case of a vasectomy
https://en.wikipedia.org/wiki/Blood%E2%80%93testis_barrier

Could it cause pois?
That would be quite a revelation if it was found to be disrupted in someone with pois. How can we find this out? Can a physical exam/scan establish that it is intact and functioning as it should?

[sartre02]

I believe it's possible through testing the immunoglobulins which would prove that semen cam into the bloodstream which explains the high antisperm antibodies...
the treatment might be a strong immunosuppressant like ciclosporin , but the question is , can the barrier be fixed ??
I read somewhere that riluzole can fix it but not sure, can someone help with info ?

[Progecitor]

I believe it's possible through testing the immunoglobulins which would prove that semen cam into the bloodstream which explains the high antisperm antibodies...
the treatment might be a strong immunosuppressant like ciclosporin , but the question is , can the barrier be fixed ??
I read somewhere that riluzole can fix it but not sure, can someone help with info ?

I believe you meant this study. I quoted the information that looked more important. Testing riluzole could be an interesting experiment, though I doubt it would be easy to get a prescription for it.

Sertoli cells (SCs) are important somatic cells that nourish and develop spermatogonial stem cells (SSCs) by providing nutrients, cytokines, and paracrine factors. Additionally, SCs form tight junctions (TJs) as part of the blood-testis barrier (BTB), which is necessary for normal spermatogenesis.
Proteins such as Zonula occludens-1 (ZO-1), claudins, occludins and connexin 43 (Cx43) contribute to the formation, stability, and function of tight junctions. They play essential roles in controlling paracellular transport, maintaining barriers of BTB, and regulating spermatogenesis. The deficiency of these proteins can lead to spermatogenesis failure.
In our previous study, we accidentally found that riluzole, the first drug approved by the FDA for the clinical treatment of amyotrophic lateral sclerosis (ALS), had the ability to induce reprogramming of mouse embryonic fibroblastic cells (MEFs) into Sertoli-like cells (CiSCs). Interestingly, our study also revealed that treatment with riluzole resulted in a significant upregulation of gene expression levels of various secreted factors in SCs. These factors, including Gdnf, Bmp4, Scf, Cxcl12, Inhibin B, and Fgf2, are known to be critical for the proliferation and differentiation of SSCs.
Our study revealed that riluzole enhanced the integrity of the BTB by improving the functioning of SCs. Transcriptomic analysis showed that calcium signaling pathways play a significant role in this process. Previous research has shown that riluzole binds near a calcium ion and can activate TRPC5. Our research validates that riluzole specifically binds to TRPC5, leading to the activation of calcium signaling pathways. This, in turn, enhances the expression of tight junction proteins, particularly ZO-1 and Cx43. These proteins play a key role in interacting with the actin cytoskeleton and forming linkages with various junction types within the BTB.
https://www.biorxiv.org/content/10.1101/2024.04.26.591381v1.full