|"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
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
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
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
The prevalence of coinfection varies but it can account for up to
50% among patients who die from COVID-19 (Lai et al., 2020).
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."
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 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.
study suggests that the activation of cannabinoid receptors may serve as a
therapeutic modality to treat ARDS associated with COVID-19.
Tolerance is a fundamental property of the immune
Tolerance involves non-self discrimination which is the
ability of the normal immune
system to recognize and respond to foreign
antigens, but not
Autoimmunity is evoked when this tolerance to self antigen is
tolerance within an individual normally begins as a fetus.
maternal fetal tolerance T cells express receptors specific for a specific
antigen enters the circulation of the developing fetus via the
Fetal T cells orginate in the bone marrow where they begin
growth but must travel to thymus where maturation of T cells
Within the thymus fetal T cells encounter various self and
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.
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
Through molecular mimicry a pathogen can generate
The pathogen may mimic
either the linear amino acid sequence or the conformational fit of the
autoimmune response is then generated by any similar pathogen.
Pathogens alter macrophage function, act as
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
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
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
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.
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.
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
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