Attacking Ourselves

Human proteins added to vaccines

Synthetic proteins mimic the real thing

Neuron cell death caused by overactive immune system

Epigenetic regulation of inducible gene expression in the immune system

Effects of Cannabinoids on T-cell Function and Resistance to Infection

Cannabinoids to Treat Acute Respiratory Distress Syndrome

"The common feature of Acute Respiratory Distress Syndrome (ARDS) includes systemic hyperactivation of immune response leading to inflammation in the lungs followed by the development of pulmonary edema, alveolar damage, and respiratory failure.

There are over 200,000 people affected by ARDS annually in the US and three million people globally, and ARDS causes over 75,000 deaths in the US alone.

ARDS can result from a wide range of insults, and the precise nature of antigens or factors that trigger hyperactivation of the immune response, is unclear.

The most challenging question which remains unanswered is whether hyperactivation of immune response seen in patients with the severe form of COVID-19 results from hyperimmune response against the virus or against secondary infections seen in these patients or a combination of both.

It is less likely that the hyperactivation of the immune response is against the virus itself because these are the same patients who are immunocompromized that fail to exhibit an optimum response to the virus.

The prevalence of coinfection varies but it can account for up to 50% among patients who die from COVID-19 (Lai et al., 2020).

The copathogens include, Streptococcus pneumoniae, Staphylococcus aureus, Klebsiella pneumoniae, and the like (Lai et al., 2020).

Some of these bacteria produce toxins such as Staphylococcus enterotoxin B (SEB) which can activate a large proportion of T cells, thereby causing cytokine storm, ARDS, and multiorgan failure."

Δ9-Tetrahydrocannabinol Prevents Mortality from Acute Respiratory Distress Syndrome

A transcriptomic analysis of immune cells from the lungs revealed an increase in mitochondrial respiratory chain enzymes following THC treatment.

Metabolomic analysis revealed elevated serum concentrations of amino acids, lysine, n-acetyl methionine, carnitine, and propionyl L-carnitine in THC-treated mice.

THC caused the downregulation of miR-185, which correlated with an increase in the pro-apoptotic gene targets.

Interestingly, the gene expression datasets from the bronchoalveolar lavage fluid (BALF) of human COVID-19 patients showed some similarities between cytokine and apoptotic genes with SEB-induced ARDS.

Collectively, this study suggests that the activation of cannabinoid receptors may serve as a therapeutic modality to treat ARDS associated with COVID-19.

Natural Autoimmunity as the Master Conductor of Homeostasis

Cannabinoids Decrease the Th17 Inflammatory Autoimmune Phenotype

Modulation of cellular redox homeostasis by the endocannabinoid system

"If you wanted to wipe out a group of people, the best way would be to disable their immune systems, making them ready victims of illness."

JD Trout

Nagalase in Blood

Cannabinoid system immune modulation

Ensuring Uptake of Vaccines against SARS-CoV-2

Researchers discover novel link between immune system, social behavior

UMMS researchers discover novel link between immune system, social behavior

Immune System Affects Social Behaviour and Personality

Tolerance is a fundamental property of the immune system.

Tolerance involves non-self discrimination which is the ability of the normal immune system to recognize and respond to foreign antigens, but not self.

Autoimmunity is evoked when this tolerance to self antigen is broken.

Immunological tolerance within an individual normally begins as a fetus.

In maternal fetal tolerance T cells express receptors specific for a specific antigen enters the circulation of the developing fetus via the placenta.

Fetal T cells orginate in the bone marrow where they begin growth but must travel to thymus where maturation of T cells occurs.

Within the thymus fetal T cells encounter various self and foreign antigens.

In this manner T cells, attenuated to pathogens, become pathogen hunters.

Approximately 99 percent of fetal T cells die through induction of apoptosis in the thymus in the attempt to convert T cells into pathogen hunters.

Gut plethora of microbes

Exercise stalls cancer growth

Fasting triggers stem cell regeneration

Modulation of Adult Hippocampal Neurogenesis:
Environmental Challenges Trigger Immune Activation

An autoimmune response can be incited through molecular mimicry.

Molecular mimicry involves the ability of similar molecular structures from dissimilar genes or proteins to mimic similar organic self structures.

Dissimilar sequence partial structures may elicite an autoimmune response.

Virulent proteins, through molecular surfaces, can mimic host protein surfaces.

Through molecular mimicry a pathogen can generate autoimmunity.

The pathogen may mimic either the linear amino acid sequence or the conformational fit of the immunodominant epitope.

An autoimmune response is then generated by any similar pathogen.

Pathogens alter macrophage function, act as mutagens and cause the release of cytokines.

Due to similar sequence homology in the immunodominant epitope between the pathogen and the host, cells and tissues of the host associated with the protein are hunted down as a result of the autoimmune response.

Findings from biological research suggest that sustained involvement in gratifying activities such as the creation of works of art or walking through Ponderosa pine forests result in positive immune system responses.

Cannabidiol Protects Dopaminergic Neuronal Cells from Cadmium

The protective effect of cannabidiol (CBD), the non-psychoactive element of Cannabis sativa, against neuronal toxicity induced by cadmium chloride (CdCl2 10 µM) was investigated in a retinoic acid (RA)-differentiated SH-SY5Y neuroblastoma cell line. These data showed that Cd-induced neuronal injury was ameliorated by CBD treatment and it was concluded that CBD may represent a potential option to protect neuronal cells from the detrimental effects of Cd toxicity.

Molecular Mechanisms of Cannabinoid Protection from Neuronal Excitotoxicity

Cannabinoids protect neurons from excitotoxic injury. We investigated the mechanisms involved by studying N-methyl-d-aspartate (NMDA) toxicity in cultured murine cerebrocortical neurons in vitro and mouse cerebral cortex in vivo. Cannabinoids seem to protect neurons against NMDA toxicity at least in part by activation of CB1R and downstream inhibition of PKA signaling and NO generation.

Δ9-tetrahydrocannabinol protects hippocampal neurons from excitotoxicity

Cannabinoid receptor agonists act presynaptically to inhibit glutamate release. The effect of prolonged drug exposure on the neuroprotection afforded by cannabinoid receptor agonists was also studied. Desensitization of CB(1) receptors diminishes the neuroprotective effects of cannabinoids. This study demonstrates the importance of agonist efficacy and the duration of treatment on the neuroprotective effects of cannabinoids.

Neuroprotection by Δ9-Tetrahydrocannabinol, the Main Active Compound in Marijuana, against Ouabain-Induced In Vivo Excitotoxicity

In summary, we have shown that in an in vivo model of neurodegeneration Δ9-THC reduces neuronal damage via a CB1-receptor-mediated mechanism. This holds in both the acute and late phase after induction of excitotoxicity. Δ9-THC inhibits astrogliosis via a non-CB1-receptor-controlled mechanism. The results strengthen the concept that the endogenous cannabinoid system may serve to establish a defense system for the brain. This system may be functional in several neurodegenerative diseases in which excitotoxicity is thought to play a role, such as amyotrophic lateral sclerosis, Huntington's and Parkinson's diseases, and also in acute neuronal damage as found in stroke and traumatic brain injury. It is conceivable that the endogenous cannabinoid system can be exploited for therapeutic interventions in these types of primarily incurable diseases.

36 natural substances help to support immune system

unique library index

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