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On another newsgroup, I pointed out the evidence that PGE2, which probably came to be rich in semen at the same time the "AIDS epidemic" began (due to the widespread dietary use of linoleic acid-rich oils), is highly "immunosuppressive." Some of the relevant studies are cited below. What is perhaps more interesting is that these very intriguing findings were not "followed up," for instance, were mostly the "receptive" people engaging in anal sex with partners who had PGE2-rich semen the ones getting "AIDS?" We won't know for sure until the scientific method is followed. At this point in history, obviously, the notion that a "retrovirus" can cause "AIDS" predominates, despite the lack of molecular-level evidence for it, and also the molecular-level that exists for non-viral explanations.
Clin Exp Immunol. 1989 Mar;75(3):387-91.
In this paper we report studies undertaken to determine the contribution of seminal prostaglandins to some of the known immunosuppressive properties of human seminal plasma. Initial studies revealed that fractions of seminal plasma enriched in E series prostaglandins, obtained by reverse phase chromatography, had a pronounced inhibitory effect on the PHA-induced proliferation of peripheral blood lymphocytes and on the NK-cell-mediated lysis of K562 target cells. Additional investigations revealed that similar inhibitory effects could be achieved with purified PGE2 (10(-6) to 10(-9) M) and 19-OH PGE1 (10(-6) to 10(-7) M), both of which are present in uniquely high concentrations in human seminal plasma. In contrast, 19-OH PGF1 which is found in lower concentrations in semen was slightly stimulatory in proliferative assays and had no effect on NK-cell-mediated cytotoxicity. Removal of the seminal prostaglandins by absorption chromatography resulted in a dramatic decrease in immune suppressive activity. Further studies with fractions obtained by ion-exchange HPLC of desalted seminal plasma indicated that prostaglandins complexed with seminal proteins, and these too were immunosuppressive. The possible relevance of these results to sexually transmitted disease is discussed.
J Reprod Immunol. 1992 Aug;22(2):185-95.
Human seminal plasma contains uniquely high concentrations of prostaglandins of the E series which are believed to contribute to its immunosuppressive effects in vivo. In order to obtain further insight into their activity we have compared the immunosuppressive properties in vitro of PGE1, PGE2 and 19-OH PGE using three immunological systems known to be modulated by prostaglandins, namely, mitogen induced lymphocyte proliferation, IL-2 and transferrin receptor expression and NK-cell mediated cytotoxicity. These studies revealed that PGE1 and PGE2 exerted a greater immunosuppressive effect than 19-OH PGE, but considerably higher levels of 19-OH PGE in semen might contribute the majority of immunosuppressive activity in vivo. Our studies also show that the lower stability of 19-OH PGE in culture media may be responsible for its lower immunosuppressive effect observed in vitro.
J Immunol. 1985 Aug;135(2):1172-9.
The mechanism by which prostaglandin E2 (PGE2) inhibits human T lymphocyte activation and proliferation was studied. We analyzed the effect of physiologic concentrations of PGE2 on interleukin 2 (IL 2) production, expression of IL 2 receptor (Tac antigen), and expression of the transferrin receptor after in vitro activation with phytohemagglutinin. PGE2 inhibited T lymphocyte proliferation by 80 to 90% of control values. This was associated with a similar degree of inhibition of IL 2 production while the expression of IL 2 receptor was not affected. This was in marked contrast to the expression of the transferrin receptor, which was inhibited 65% after 72 hr of in vitro activation. The addition of exogenous, purified IL 2 reconstituted lymphocyte proliferation to 50% of control values, but had no effect on transferrin receptor expression. Because PGE2 is known to increase the intracellular concentration of 3',5' cyclic adenosine monophosphate (cAMP), we investigated the effect of another adenylate cyclase activator, i.e., isoproterenol, as well as the effect of extracellular administration of the cAMP derivative dibutyryl cAMP (dBcAMP) on IL 2 production, Tac antigen expression, and transferrin receptor expression. It was demonstrated that isoproterenol, as well as dBcAMP, inhibited transferrin receptor expression on PHA-activated T lymphocytes to the same extent as PGE2, and exogenous IL 2 could not counteract the down-regulation of the receptor expression. In contrast, neither isoproterenol nor dBcAMP had any significant effect on IL 2 receptor expression. Prostaglandin F2 alpha (PGF2 alpha), which has been reported to elevate intracellular cyclic GMP levels, had no effect on lymphocyte activation and proliferation, and did not counteract the PGE2-induced depression in IL 2 production. In contrast to its effect on peripheral blood lymphocytes, PGE2 had no effect on transferrin receptor expression or cell proliferation by IL 2-dependent T cell clones and IL 2-independent T cell lines. These studies demonstrate that PGE2 exerts its inhibitory effects on T cell activation and proliferation via two distinct pathways: inhibition of IL 2 production and inhibition of transferrin receptor expression. The transferrin receptor inhibition is mediated via the cAMP pathway and is IL 2-independent.
Cell Immunol. 1987 Jan;104(1):24-36.
...Our results demonstrate that PGE2 has a direct inhibitory effect on an early step of T-cell activation, resulting in decreased IL-2 production, decreased IL-2-receptor expression, decreased responsiveness to exogenous IL-2, and decreased proliferation. However, PGE2 does not affect IL-2-driven proliferation of activated T cells. The inhibitory effect on T-cell activation is not mediated through suppressor T cells, nor through inhibition of accessory cell function.
Proc Natl Acad Sci U S A. 1986 May; 83(10): 3487�?490.
Acquired immune deficiency syndrome (AIDS)-associated virus is thought to be transmitted effectively through semen during sexual activities from male to male or from male to female. Prostaglandin (PG) E2 is one of the immunosuppressive compounds present in high concentrations in human semen. We, therefore, investigated direct effects of PGE2 and other PGs on AIDS-associated virus infection and replication in vitro. First, type III human T-lymphotropic virus (HTLV-III) was used to infect a T-cell line (MT-4) in culture. PGE2 (10 nM to 10 microM) added to the culture medium enhanced the production of infectious virus in a dose-dependent fashion. In the presence of 5 microM PGE2, 2.5-fold more virus were released from the infected MT-4 cells as compared to untreated control cells on day 3 after infection. Second, when we used an HTLV-III continuous-producer cell line (Molt-4/HTLV-III), PGE2 and PGD2 added to the culture medium increased the number of viruses released from Molt-4/HTLV-III cells. Other PGs such as PGF2 alpha and 13,14-dihydro-15-keto PGE2 did not affect the replication of HTLV-III in this system. These results indicate that some PGs including seminal PGs enhance the AIDS-associated virus replication in vitro. We propose that PGE2 in human semen might directly facilitate the infection of AIDS-associated virus and cause the efficient transmission of the virus during sexual activities.
Proceedings of the National Academy of Sciences of the United States of America, Vol. 83, No. 8 (Apr. 15, 1986), pp. 2682-2683.
To explain a possible pathogenesis of acquired immune deficiency syndrome (AIDS) in homosexual males, we propose the following hypothesis. Prostaglandin E2 in human semen given via anus during anal intercourse may cause an immune dysregulation in the male semen recipients; this immunosuppressive effect of prostaglandin E2 may be one of the underlying factors that stimulate AIDS-associated virus infection or that trigger the latent AIDS-associated virus. This hypothesis is supported by the following experimental results. Anal infusion of prostaglandin E2 or D2 into male rats reduced in vitro responses of T lymphocytes to phytohemagglutinin. However, the T-cell response of female rats was not reduced significantly by the anal infusion of seminal prostaglandins. |
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Is it possible to think that the PGE2 in the semen will be much LESS immunosuppressive if the receptive people engaging in anal sex have a strong "deficiency" in arachidonic acid ? Without arachidonic acid in the body of the receptive people, the PGE2 in the semen will be perhaps much less capable of reacting upon the body of the receptive people and, therefore, much less bad and immunosuppressive ? Or PGE2 (coming from outside) is immunosuppressive in the receptive body with ou without arachidonic acid in the receptive body ?
It's just a question.
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| PGE2 is made from arachidonic acid in the donor's body so its presence in the recipient plays no role. |
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| Actually, with no AA in the person's cells there will either be no or almost no PGE2 produced. This is why I'm not surprised that the "AIDS epidemic" began when it did, because before this generation of young people, the one before it likely had mostly Mead acid rather than AA in their cells. |
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| They claim PGE2 is in the semen, so how could they be wrong about that? It's either there or it's not. I've read that it is used to "immunosuppress" in the context of helping sperm fertilize the egg. I have not read exactly when the AA is metabolized into PGE2 - that is an interesting question. |
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Here another metabolite of AA termed 11,12- epoxyeicosatrienoic acid (EET) seems to prevent impotence:
FASEB J. 2006 Mar;20(3):539-41. Epub 2006 Jan 13.
Cytochrome P450 epoxygenases provide a novel mechanism for penile erection.
Jin L, Foss CE, Zhao X, Mills TM, Wang MH, McCluskey LP, Yaddanapud GS, Falck JR, Imig JD, Webb RC.
Department of Physiology,Medical College of Georgia, Augusta, Georgia, USA. [email protected]
Erectile dysfunction (ED) is estimated to affect more than 30 million American men and 152 million men worldwide. Therapeutic agents targeting the nitric oxide/cyclic GMP signaling pathway have successfully treated patients with ED; however, the efficacies of these treatments are significantly lower in specific populations such as patients with diabetes. The goal of this study was to discover and identify new endothelium-derived relaxing factors involved in the regulation of erectile function, providing alternative therapeutic targets for treatment of ED. Immunoblotting results showed that protein expressions of epoxygenases from cytochrome P450 (CYP)2B, 2C and 2J subfamilies, as well as NADPH CYP reductase were present in rat corpora cavernosa, which was confirmed by immunohistochemical analysis. Furthermore, CYP2C was localized in cavernosal endothelial cells using double immunolabeling. CYP epoxygenase activity was analyzed by reverse-phase high-pressure liquid chromatography; and the results showed that 11,12- epoxyeicosatrienoic acid (EET) was the major product metabolized by CYP epoxygenases in rat corpora cavernosa. Inhibition of EETs function by injection of an EETs antagonist into rat penis significantly decreased intracavernosal pressure-induced by electrical stimulation of the major pelvic ganglion in vivo. In conclusion, our results suggest that EETs, produced by CYP epoxygenases, in penile endothelial cells serve as vasodilators. Inhibition of this pathway attenuated erectile function, suggesting that EETs are required for normal erection.
PMID: 16415108 |
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