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"Vitamin D" - Marshall Protocol perspective
Some are claiming that 5G causes Covid, this is wrong however the above would indicate it could exacerbate it if RF turns off VDRs.
looked into that for a bit and it's like everything else, you have to figure out how to sort the forest and the trees, and try to avoid the wood-chippers. I don't know much about power-levels re: 5G causing anything. I looks like a lot of the funding of millimeter-wave papers is from the likes of General Dynamics, and thus is related to developing crowd-control and lethal tech, presumably at higher power levels than 5G tech. I recall from some distant first-hand source saying you never wanted to hang-glide in front of a microwave tower, but there's some inverse-square-distance thing in play, or we'd all be cooked. Here's some quickees on papers.
Millimeter Wave Exposure Induces Apoptosis in Human Melanoma A375 Cells in vitro (2019)
Conclusions: 35.2 GHz millimeter wave irradiation induces apoptosis in A375 cells by activating the caspase-3 protein.
Millimeter Wave Treatment Induces Apoptosis via Activation of the Mitochondrial-Dependent Pathway in Human Osteosarcoma Cells (2012)
In addition, MW treatment caused loss of plasma membrane asymmetry, release of cytochrome c, collapse of mitochondrial membrane potential, activation of caspase-9 and -3, and increase of the ratio of pro-apoptotic Bax to anti-apoptotic Bcl-2. Taken together, the results indicate that the U-2OS cell growth inhibitory activity of MW was due to mitochondrial-mediated apoptosis, which may partly explain the anticancer activity of millimeter wave treatment.
In Vitro Study of Inhibitory Millimeter Wave Treatment Effects on the TNF-α-induced NF-κB Signal Transduction Pathway (2011)
Therefore, we can conclude that millimeter wave treatment can inhibit the activation of the TNF-α-mediated NF-κB signal transduction pathway through the down-regulation of RIP, TAK1, IKK-ß and NF-κB, and the up-regulation of IkB-α, in chondrocytes.
Millimeter Wave Radiations Affect Membrane Hydration in Phosphatidylcholine Vesicles (2013)
Millimeter waves significantly affect the polar interface of the membrane causing a decrease of the heavy water quadrupole splitting. This effect is as important as inducing the transition from the fluid to the gel phase when the membrane exposure occurs in the neighborhood of the transition point. On the molecular level, the above effect can be well explained by membrane dehydration induced by the radiation.
Gene Expression Changes in the Skin of Rats Induced by Prolonged 35 GHz Millimeter-Wave Exposure (2008)
Microscopic findings observed in the dermis of rats exposed to 35 GHz millimeter waves included aggregation of neutrophils in vessels, degeneration of stromal cells, and breakdown of collagen…. prolonged exposure to 35 GHz millimeter waves causes thermally related stress and injury in skin while triggering repair processes involving inflammation and tissue matrix recovery.
Protein Changes in Macrophages Induced by Plasma From Rats Exposed to 35 GHz Millimeter Waves (2010)
These altered proteins are associated with inflammation, oxidative stress, and energy metabolism. Findings of this study indicate both environmental heat and 35 GHz millimeter wave exposure elicit the release of macrophage-activating mediators into the plasma of rats.
Comparison of Blood Pressure and Thermal Responses in Rats Exposed to Millimeter Wave Energy or Environmental Heat (2006)
Electromagnetic fields at millimeter wave lengths are being developed for commercial and military use at power levels that can cause temperature increases in the skin. Previous work suggests that sustained exposure to millimeter waves causes greater heating of skin, leading to faster induction of circulatory failure than exposure to environmental heat (EH)……. These data indicate that body core heating is the major determinant of induction of hemodynamic collapse, and the influence of heating of the skin and subcutis becomes significant only when a certain threshold rate of heating of these tissues is exceeded.
Quote from hillcountry on May 26, 2020, 11:32 amhey puddleduck - yes, indeed. The 25-D and 1,25-D relationship is where that gets so interesting. Amy Proal and Trevor Marshall wrote a chapter in Metagenomics of the Human Body years ago that goes into great depth on the question(s).
https://www.researchgate.net/publication/226416035_Autoimmune_Disease_and_the_Human_Metagenome
she's hanging out these days with the microbiome researchers and has a bit of a Twitter following and a blog somewhere.
I'm open to the L-form, cell-wall deficient bacteria thing, much more than the corrupted virus science. Lida Mattman's textbook is a very interesting read. Cell Wall Deficient Forms: Stealth Pathogens.
Have you run across Virus Mania? It's available @ https://archive.org/details/VirusMania
Now we just have to tie retinoic acid into the equation.
For those interested, here is Amy Proal’s blog: http://microbeminded.com/author/amyproal/ I have enjoyed her posts as well as her lectures on YouTube! 👍
Thank you for letting me know about the chapter in the Metagenomics book, and Mattman’s book, too, John. There is so much to learn, and seeing observations fit together into new ways of understanding how the body works is exciting.
Okay, I have downloaded Virus Mania, started reading, and am hooked. 🤯 Looking forward to reading more this afternoon. Thanks for sharing all these interesting ideas and resources, John! 🙂
I work at an RF company, the engineers there poo poo all the ideas about it being harmful. Of course they would, right? but most are all old like me and indistinguishable from the rest of society health-wise... even though they've been right on top of it their whole working lives.
Quote from hillcountry on May 24, 2020, 7:06 pmHi y'all - I survived the Gominak D3-B-complex protocol with some early sleep-benefits but not much else. Reading a post by Josh on another site led me to reconsider, which then led me to review the Marshall Protocol perspective again. I excerpted a few portions of the linked page to give a quick overview of their understanding. I think it will provide some insight regarding "Vit A" as well. I'll poke around and see where they're at on the question. Hope y'all find it useful in some way.
https://mpkb.org/home/pathogenesis/vitamind#supplemental_vitamin_d_tends_to_be_immunosuppressive
In some ways low-A protocol is even more restricted than the above one - in "Marshall Protocol" only "vitamin" D should be restricted(via withdrawing from supplements/specific food), while on low-A its actually A+D+C - feels like a big step forward towards innate immunity restore.
Electrosmog Radiation - Effects on the VDR (and beyond):
Vitamin effects on the immune system: vitamins A and D take centre stage
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2906676/
[..]In addition, vitamins have a role in the immune system, which extends to both innate and adaptive immune responses. Although some vitamins, such as vitamins C and E and members of the B complex, can act in a relatively nonspecific manner in the immune system (for example, as antioxidants)2–4, other vitamins, such as vitamins A and D, can influence the immune response in highly specific ways (see Supplementary information S1 (table)). Here we review the most important effects of vitamins on the immune system, with special emphasis on vitamins A and D, which have received particular attention owing to recent discoveries of their multi-faceted interactions with the immune system.
Vitamins A and D are notably distinct from other vitamins in that their respective bioactive metabolites, retinoic acid and 1,25-dihydroxyvitamin D3 (1,25(OH)2VD3), have hormone-like properties.
Both of these metabolites are synthesized from their vitamin precursors by different tissues and cells in the body and exert their effects on target cells remotely by binding to nuclear-hormone receptors.
Effects on adaptive immune-cell subsets:
Vitamin A metabolites can also affect some aspects of the adaptive immune response (FIG. 3). Retinoic acid enhances cytotoxicity and T-cell proliferation, the latter probably mediated, at least in part, by enhancing IL-2 secretion and signalling in T cells. Consistent with an in vivo role for vitamin A in T-cell function, vitamin A-deficient mice have defects in TH-cell activity.
A possible mechanism for this observation is that in the setting of vitamin A deficiency, retinoic acid does not compete with 1,25(OH)2VD3 for their common nuclear binding partner RXR and, therefore, the inhibitory effects of 1,25(OH)2VD3 on T-cell function (including TH-cell activity) are not offset by retinoic acid.
Retinoic acid can also modulate antigen presentation by exerting direct effects on DC function. For example, retinoic acid increases the expression of matrix metalloproteinases, thereby increasing the migration of tumour-infiltrating DCs to the draining lymph nodes, which have the potential to boost tumour-specific T-cell responses. In addition, in the presence of inflammatory stimuli, such as tumour-necrosis factor (TNF), retinoic acid enhances DC maturation and antigen-presenting capacity, both of which are effects mediated by RXR receptors. However, it should be noted that DCs pre-treated with retinoic acid can apparently store this metabolite50, which when released could ultimately act directly on T cells and/or other cells and contribute to the final outcome of an immune response.
All-trans Retinoic Acid Antagonizes the Action of Calciferol and Its Active Metabolite, 1,25-Dihydroxycholecalciferol, in Rats
https://academic.oup.com/jn/article/135/7/1647/4663843
An antagonistic interaction between retinol and calciferol has been established. However, the mechanism by which this antagonism occurs is unclear. One possibility is that retinol affects the metabolism of calciferol. To investigate this hypothesis, retinol- and calciferol-depleted rats were given various amounts of ergocalciferol, cholecalciferol, 1α,25-dihydroxycholecalciferol [1,25(OH)2D3], or 24,24-difluoro-1α,25-dihydroxycholecalciferol [24-F2-1,25(OH)2D3] in combination with various amounts of retinyl acetate or all-trans retinoic acid (ATRA) in a series of studies. Rats administered 1720 or 3440 μg retinyl acetate once every 3 d for 33 d in combination with 25.8 ng ergocalciferol or 25 ng cholecalciferol every 3 d had lower serum calcium and greater serum phosphorus concentrations than rats fed 0 or 11.4 μg retinyl acetate every 3 d. In addition, rats fed 400 μg ATRA/d in combination with 25.8 ng ergocalciferol every 3 d, 25 ng cholecalciferol every 3 d, 2–5 ng 1,25(OH)2D3/d, or 0.5–1 ng 24-F2-1,25(OH)2D3/d had significantly lower serum calcium and higher serum phosphorus concentrations than rats not given ATRA in the diet. Therefore, both retinyl acetate and ATRA are able to antagonize the action of ergocalciferol and cholecalciferol in vivo. Additionally, ATRA antagonizes the in vivo action of 1,25(OH)2D3 and an analog, 24-F2-1,25(OH)2D3, that cannot be 24-hydroxylated. Together, these results suggest that retinol does not antagonize the action of calciferol by altering the metabolism of calciferol or 1,25(OH)2D3, but does so by another mechanism.
...
Although an antagonistic relation between retinol and calciferol has been firmly established, the exact nature of this interaction has yet to be determined. Several studies indicated that retinol may affect the metabolism of calciferol (13,14). Retinol may either decrease the production of the active form of calciferol, 1,25(OH)2D3, or it may increase the destruction of this compound. Another possible mechanism of interaction is that retinol may affect the production of the vitamin D receptor (VDR) (15,16). However, this effect is not clearly established and may depend on species and cell type. A third possible mechanism is suggested by the fact that both all-trans retinoic acid (ATRA) and 1,25(OH)2D3, the active forms of retinol and calciferol, require the retinoid X receptor (RXR) to carry out their effects on gene transcription (17–19). Both ATRA and 1,25(OH)2D3 accomplish their biological functions by binding to specific receptors, retinoic acid receptor (RAR) and VDR, respectively (20,21). These proteins form heterodimers with RXR before binding to specific response elements in the promoter region of ATRA- and 1,25(OH)2D3-regulated genes (22,23). Hence, ATRA or 9-cis retinoic acid (9CRA), the ligand for RXR, may have some effect on 1,25(OH)2D3-induced gene expression. In fact, an RXR-specific ligand, LG100268, was shown to stimulate a calciferol-regulated gene, cytochrome P450 (CYP)24 (24).
Therefore, although an antagonistic interaction between retinol and calciferol has been established in vivo, there is no clear explanation of how this antagonism occurs. The purpose of this study was to investigate the interaction between the 2 vitamins and to gain a better understanding of the mechanism behind it.
Vitamin A antagonizes calcium response to vitamin D in man
https://pubmed.ncbi.nlm.nih.gov/11585356/
For unknown reasons, the highest incidence of osteoporosis is found in northern Europe. In these populations, the sunlight exposure is limited and the vitamin A intake is high. The interaction between vitamin A and D has been the subject of several in vitro and animal studies. We have studied the acute effects of vitamin A and D on calcium homeostasis in 9 healthy human subjects. We compared the effect of (i) 15 mg of retinyl palmitate, (ii) 2 microg of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3], (iii) 15 mg of retinyl palmitate plus 2 microg of 1,25(OH)2D3, and (iv) placebo in a double-blind crossover study. The subjects took vitamin preparations at 10:00 p.m. and the following day blood samples were collected five times from 8:00 a.m. to 4:00 p.m. Serum levels of 1,25(OH)2D3 and retinyl esters increased (1.7-fold and 8.3-fold, respectively; p < 0.01). As expected, serum calcium (S-calcium) increased (2.3%; p < 0.01) and S-parathyroid hormone (PTH) decreased (-32%; p < 0.05) after 1,25(OH)2D3 intake. In contrast, retinyl palmitate intake resulted in a significant decrease in S-calcium when taken alone (-1.0%; p < 0.05) and diminished the calcium response to 1,25(OH)2D3 after the combined intake (1.4%; p < 0.01). S-PTH was unaffected by retinyl palmitate. No significant changes in serum levels of the degradation product of C-telopeptide of type I collagen (CrossLaps), or U-calcium/creatinine levels were found.
In conclusion, an intake of vitamin A corresponding to about one serving of liver antagonizes the rapid intestinal calcium response to physiological levels of vitamin D in man.
I wonder, what if high D1.25 and low D25 is (mainly, or in part) the result of Vit A occupying(or influencing) VDR receptors, i.e. the body upregulates D1.25 production to push through antagonistic properties of Vit A.
Loose thoughts for you
Sunshine denatures the pigments, right? Hay isn't as green as grass. Dried herbs are not as bright as fresh.
So, here you are a person with plant pigments clogging up your system, in your cappilaries, fats, skin (because you are taking in more than you can get rid of). You may even appear orange. And then the sun shines on you, breaking those pigments down.
Sunning is a thing I see many animals do--my chickens and cats are great sunbathers. There sure seems to be an instinct for it. It feels great. I think probably sunning is meant to help denature pigments, and at the same time manufacture some D. Two goals that help survival on the planet.
I can see, though, that if the animal has an over-abundance of pigments gumming up the works there might be issues. I'm sure that having too much denaturing poison gets in the way of proper skin processes like VD absorption. You might start coming out in rashes, especially in the spring after a long time without denaturing.
One of my pet theories is that head hair is about VD manufacture. That the oils on each strand are exposed to the sun on your head (isn't that ergonomic) (just think of the surface area) and that in the hours afterward your scalp absorbs that VD from the hair. (cats lick it off their fur, chickens preen it off their feathers) Well, I'm betting that the scalp is a place where pigments clog, at the top of our vascular tree there. (the dandruff, graying and thinning hair of the VA-toxic speaks to that). The scalp isn't a happy place in the VA-toxic. It's sort of interesting to think that the scalp would have been shaded as well.
It's a shame so many men buzz their heads! Is the comb-over instinctual, LOL? It is interesting that some cultures believe that hair should be allowed to grow out and attributed certain benefits to it.
[2020] Higher 25-hydroxyvitamin D level is associated with increased risk for Behçet's disease
https://pubmed.ncbi.nlm.nih.gov/32593521/
Background & aim: Previous studies showed a vitamin D deficiency in patients with Behçet's disease, suggesting potential benefits of vitamin D supplementation in the prevention and treatment of Behçet's disease. Interpretation of these studies may be limited by reverse causality or confounding bias. We aim to determine the causal association between serum 25-hydroxyvitamin D [25(OH)D] and the risk of Behçet's disease by Mendelian randomization.
On the basis of evidence in 7909 human beings, this study provides the newest indication that a lifelong higher 25(OH)D level is associated with an increased risk of Behçet's disease. Special attention should be paid to the potential harm of long-term or high-dose use of vitamin D supplements in clinical practice.
follow-up to:
[2014] Vitamin D deficiency in patients with Behcet’s disease
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3996194/
[2017] High Vitamin D Levels May Downregulate Inflammation in Patients with Behçet's Disease
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5474237/
[2011] Vitamin D status in patients with Behcet's Disease
https://www.scielo.br/scielo.php?script=sci_arttext&pid=S1807-59322011000500002
In patients with Behcet's Disease, 25-hydroxyvitamin D values were significantly lower than those of the healthy controls (p<0.001). Serum Ca, P, and ALP levels were similar in both groups. Serum ESR and CRP levels were significantly higher in patients than controls (p<0.05). There was no correlation between 25-hydroxyvitamin D levels and age, body mass index (BMI), disease duration, ESR, or CRP levels.
[2008] Effects of vitamin D on expression of Toll-like receptors of monocytes from patients with Behcet's disease
https://pubmed.ncbi.nlm.nih.gov/18411217/
Objectives: Recent studies have shown the immunomodulatory effect of vitamin D(3) through down-regulation of Toll-like receptor (TLR) expression in human monocytes. To understand the implication of innate immunity with the role of vitamin D affecting TLR expression in Behçet's disease (BD), we focused on the association between the TLR expression and the serum vitamin D concentration in BD.
Methods: The expression of TLR2, TLR4 and CD16 on monocytes was detected by flow cytometric analysis and RT-PCR. Serum 25-hydroxyvitamin D [25(OH)D] levels were measured in the patients with BD, psoriasis and healthy controls, and then the expression of TLRs was correlated with the value of serum 25(OH)D levels. To assess the influence of vitamin D(3) on expression and function of TLRs in vitro, human monocytes were treated with increasing concentrations of 1,25(OH)(2)D(3).
Results: We found that the monocytes of active BD patients showed higher expressions of TLR2 and TLR4 than those of controls, and serum 25(OH)D levels tended to be lower in active BD. Furthermore, 25(OH)D levels were inversely correlated with the expressions of TLR2, TLR4 and clinical indicators. In vitro analysis showed that vitamin D(3) was found to dose-dependently suppress the protein and mRNA expressions of TLR2 and TLR4. TNF-alpha synthesis was also decreased upon TLR ligand stimulation in vitamin D(3)-treated monocytes.
Conclusion: These results suggest that the inflammation triggered through TLR2 and TLR4 is important in the pathogenesis of BD. And it seems possible that vitamin D may be used as a therapeutic option by modulating TLR2 and TLR4 expression of monocytes in BD.
https://pubmed.ncbi.nlm.nih.gov/10549626/
Toll-like receptor (TLR) 2 and TLR4 are implicated in the recognition of various bacterial cell wall components, such as lipopolysaccharide (LPS). To investigate in vivo roles of TLR2, we generated TLR2-deficient mice. In contrast to LPS unresponsiveness in TLR4-deficient mice, TLR2-deficient mice responded to LPS to the same extent as wild-type mice. TLR2-deficient macrophages were hyporesponsive to several Gram-positive bacterial cell walls as well as Staphylococcus aureus peptidoglycan. TLR4-deficient macrophages lacked the response to Gram-positive lipoteichoic acids. These results demonstrate that TLR2 and TLR4 recognize different bacterial cell wall components in vivo and TLR2 plays a major role in Gram-positive bacterial recognition.
https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1007390
What is TLR4 and what are its ligands?
The innate immune system recognizes pathogen-associated molecular patterns (PAMPs) of viral or bacterial intruders via pattern recognition receptors (PRRs). This includes the family of TLRs that consists of related, transmembrane proteins that play a central role in the initiation of inflammatory responses, including the secretion of cytokines and chemokines.
TLR4, which is mainly expressed on cells of the immune system—including monocytes, macrophages and dendritic cells—has long been recognized as a PRR that senses lipopolysaccharide (LPS), a component of the outer membrane of gram-negative bacteria. Activation of TLR4 by LPS, its best studied ligand, is a multistep process. The initial step involves the LPS binding protein (LBP) which extracts LPS from bacterial membranes and LPS-containing vesicles to transfer it to the TLR4 coreceptor cluster of differentiation 14 (CD14). CD14 exists in two forms, soluble and membrane-bound. Both forms are able to interact with LPS-loaded LBP. CD14 breaks down LPS aggregates and transfers monomeric LPS into a hydrophobic pocket on myeloid differentiation factor 2 (MD-2) that is part of the MD-2/TLR4 complex. The high-affinity binding of LPS leads to dimerization and activation of the MD-2/TLR4 complex [6, 7]. Activation of TLR4 results in the recruitment of the intracellular adaptor protein, myeloid differentiation primary response 88 (MyD88), and/or toll/interleukin-1 receptor (TIR)-domain-containing adapter-inducing interferon-β (TRIF), ultimately resulting in the expression and secretion of pro-inflammatory mediators [6, 7].
TLR4 has also been shown to be a sensor for damage-associated molecular patterns (DAMPs). These include a wide variety of molecules released from injured or dying tissues as well as molecules actively released in response to cellular stress from intact cells [6, 8]. In addition to bacterial PAMPs and cellular DAMPs, TLR4 also recognizes PAMPs from other pathogens including fungi, parasites, and viruses [9]. How the TLR4 complex is activated by DAMPs and non-LPS PAMPs, which vary widely in their structure—some with no structural similarities to LPS [8, 10]—remains to be determined. Resolving the structure of these complexes is a critical part toward dissecting their mechanisms of activation.
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So called "Behcet’s disease" is another good example of basket-case diagnosis of a chronic, body-wide inflammation:
https://www.mayoclinic.org/diseases-conditions/behcets-disease/diagnosis-treatment/drc-20351331
If you have moderate to severe Behcet's disease, your doctor might prescribe: Corticosteroids to control inflammation. Corticosteroids, such as prednisone, are used reduce the inflammation caused by Behcet's disease. Doctors often prescribe them with another medication to suppress the activity of your immune system.
Scientists discover how neuroactive steroids dampen inflammatory signaling in cells
https://www.sciencedaily.com/releases/2019/02/190213142713.htm
For the first time, scientists discovered how neuroactive steroids naturally found in the brain and bloodstream inhibit the activity of a specific kind of protein called Toll-like receptors (TLR4), which have been known to play a role in inflammation in many organs, including the brain.
The effect of systemic corticosteroid therapy on the expression of toll-like receptor 2 and toll-like receptor 4 in the cutaneous lesions of leprosy Type 1 reactions
https://pubmed.ncbi.nlm.nih.gov/22348338/
We have demonstrated that the gene hARP-P0 is a suitable control gene for TLR gene expression studies in this population. The gene and protein expression of TLR2 and TLR4 were both reduced significantly during corticosteroid treatment.
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Potential Infectious Etiology of Behçet's Disease
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3255303/
Behçet's disease is a multisystem inflammatory disorder characterized by recurrent oral aphthous ulcers, genital ulcers, uveitis, and skin lesions. The cause of Behçet's disease remains unknown, but epidemiologic findings suggest that an autoimmune process is triggered by an environmental agent in a genetically predisposed individual. An infectious agent could operate through molecular mimicry, and subsequently the disease could be perpetuated by an abnormal immune response to an autoantigen in the absence of ongoing infection. Potential bacteria are Saccharomyces cerevisiae, mycobacteria, Borrelia burgdorferi, Helicobacter pylori, Escherichia coli, Staphylococcus aureus, and Mycoplasma fermentans, but the most commonly investigated microorganism is Streptococcus sanguinis. The relationship between streptococcal infections and Behçet's disease is suggested by clinical observations that an unhygienic oral condition is frequently noted in the oral cavity of Behçet's disease patients. Several viral agents, including herpes simplex virus-1, hepatitis C virus, parvovirus B19, cytomegalovirus, Epstein-Barr virus and varicella zoster virus, may also have some role.
TLR2 and TLR4 mediated host immune responses in major infectious diseases: a review
https://www.bjid.org.br/en-tlr2-tlr4-mediated-host-immune-articulo-S141386701500224X
During the course of evolution, multicellular organisms have been orchestrated with an efficient and versatile immune system to counteract diverse group of pathogenic organisms. Pathogen recognition is considered as the most critical step behind eliciting adequate immune response during an infection. Hitherto Toll-like receptors (TLRs), especially the surface ones viz. TLR2 and TLR4 have gained immense importance due to their extreme ability of identifying distinct molecular patterns from invading pathogens. These pattern recognition receptors (PRRs) not only act as innate sensor but also shape and bridge innate and adaptive immune responses. In addition, they also play a pivotal role in regulating the balance between Th1 and Th2 type of response essential for the survivability of the host. In this work, major achievements rather findings made on the typical signalling and immunopathological attributes of TLR2 and TLR4 mediated host response against the major infectious diseases have been reviewed. Infectious diseases like tuberculosis, trypanosomiasis, malaria, and filariasis are still posing myriad threat to mankind. Furthermore, increasing resistance of the causative organisms against available therapeutics is also an emerging problem. Thus, stimulation of host immune response with TLR2 and TLR4 agonist can be the option of choice to treat such diseases in future.