Tempo Bioscience’s Post

Do you know that your mood, your depression, has effect on your immune system? Recently, I went through a review article. I have found a new type of peptide, no these are not like the peptides that our skin secrets like the anti-microbial peptides. These are called Neuropeptides (NPYs). NPYs are secreted by enteric neurons, post ganglionic sympathetic neurons. One will think these might be anti-microbial, no these are not. The NPYs are secreted by the neurons present in the descending inhibitory motoneurons of the myenteric plexus and non-cholinergic secretomotor complex of submucosal plexus into the vascular system. Also, brain is the most abundant producer of NPYs. These NPYs play diverse functions. Alongside functioning in maintaining ionic balance in colon it has immune-modulatory roles. The innate and adaptive systems have NPY receptors. Also, they can autoregulate their expression as macrophages, B and T lymphocytes can also secrete NPYs. NPYs secreted by the nerve fibres residing close to gut influences IgA secretion in the lamina propria region of ileum. The Y1 receptor is anti-inflammatory in nature. Once triggered it reduces the secretion of other NPYs thus reducing the inflammation in an area. NPYs plays crucial role in immune cell extravasation, Th-subset differentiation, cytokine secretion, natural killer cells activity ROS and RNS production. Title: Neuropeptide Y, peptide YY and pancreatic polypeptide in the gut-brain axis. The information was extracted from this article.

From bone remodeling to immune regulation, sRANKL plays a vital role that extends beyond what meets the eye. Discover how this key player in osteoclastogenesis could reshape therapies for conditions like osteoporosis, arthritis, and even immune disorders. Read more at scioverleaf and stay informed!!! #BoneHealth #Immunology #Osteoimmunology #BoneRemodeling https://lnkd.in/gsEhjWRd

The relationship between exposure to #electromagneticfields (#EMFs) and human health is more and more in focus. This is mainly because of the rapid increasing use of such EMFs within our modern society. Exposure to EMFs has been linked to different #cancer forms, e.g. #leukemia, brain #tumors, #neurologicaldisorder, such as #alzheimers disease, #asthma and #allergy, and recently to the phenomena of 'electrosupersensitivity' and 'screen #dermatitis'. There is an increasing number of reports about cutaneous problems as well as #symptomss from internal #organs, such as the #heart, in people exposed to video display terminals (VDTs). #cancerresearch #hearthealth https://lnkd.in/d8Cq3zJu

Covid-19 and brain fog. 1. IL-1β is necessary for learning and memory processes, but, when expressed at aberrant levels, it is involved in cognitive dysfunction induced by infections and sterile inflammation. Reference: The role of IL-1 family cytokines and receptors in neuroinflammatory and neurodegenerative diseases. https://lnkd.in/dMiuyigP 2. #SARSCoV2 infection increased interleukin-1 beta (IL-1β) levels in the brain, so is a potential mechanism driving cognitive decline in long-Covid. 3. Previous #COVID19 vaccination reduced brain inflammation and reduced IL-1β levels.  Reference: Vaccination reduces central nervous system IL-1β and memory deficits after COVID-19 in mice https://lnkd.in/dzN6uMru

Who will win in the hidden war between endothelium and the immune system in Sepsis Endothelium characterised by its diversity in morphology and function either in vascular system or organs Pathophysiology of Septic endothelial dysfunction Endothelial integrity is essential for Vascular homeostasis Inflammatory modulation And maintenance of barrier integrity Glycocalyx is a gel like layer of endothelial cells compressing many substances that are responsible for vascular barrier integrity like proteoglycan ,glycoprotein and syndecan-1 Endotoxin and the pathogenesis of Sepsis trigger endothelial inflammation, oxidative damage and coagulation In Sepsis Glycocalyx shedding is primarily induced by inflammation and oxidative injury causing barrier disruption and exacerbate MODS Circulating level of Glycocalyx components such as proteoglycan ,glycoprotein and hyaluronan serve as diagnostic biomarkers in early Sepsis Sepsis induced tissue hyperpermiability lead to tissue edema via Glycocalyx shedding  inflammatory invasion and Dysregulation of tight junction protein Acute Septic Myocardial injury characterised by temporary and reversible stage where decline of EF ,Ventricular diltation and diminished response to fluid and inotrope ECs are crucial for the structural and functional integrity of CVS ,regulating vascular tone and cellular proliferation ECs facilitate the oxygen supply and nutrients to cardiomyocytes ,development, promotion of contraction and mitigation of ischaemic injuries Overproduction of ROS leading to oxidative damage and Impaired Myocardial contractility Upregulation of EC adhesion molecules recruit Neutrophils and macrophages to the Myocardium leading to insufficiency and endocarditis Some specific endogenous protein can reduce the adhesion molecules and ameliorate SAMI Glycocalyx shedding lead to Myocardial edema and ANP

Discover how bome the key player in osteoclastogenesis could reshape therapies for conditions like osteoporosis, arthritis, and even immune disorders. Read more and stay informed !!! #BoneHealth #Immunology #Osteoimmunology #BoneRemodeling https://lnkd.in/g5q5jzfU

Dear network, Recently I posted a comparison between movies and immune responses revealing an intriguing parallel: action movies mirror acute inflammation. Just as action films are quick, dramatic, and high-energy, acute inflammation swiftly responds to immediate threats like infections or injuries. This rapid immune reaction involves activating cells and inflammatory mediators to eliminate the problem efficiently. Acute inflammation, a vital process of the innate immune system, initiates in response to infections or tissue damage. Triggered by molecular patterns, sentinel cells secrete cytokines and mediators rapidly after injury. Pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs) activate sentinel cells, such as macrophages, dendritic cells (DCs), and mast cells, to secrete cytokines and other mediators and usually start within minutes or hours after the initial injury. Some of these mediators increase the permeability of capillaries, leading to the entry of plasma proteins into the tissues, and others increase the expression of endothelial adhesion molecules and chemokines that promote the movement of leukocytes from the post-capillary venules into the tissues. The accumulation of leukocytes, proteins, and fluids leads to the hallmark characteristics of acute inflammation: pain, redness, swelling, and heat, facilitating tissue repair. After migrating to tissue, leukocytes can destroy microbes, clear damaged cells, and promote more inflammation and/or tissue repair. Is there any other comparison involving immune response or acute inflammation you know? Figure: https://lnkd.in/d64B-d93

Scientists think Alzheimer’s might be an autoimmune disease, where the brain’s defense system attacks its own cells by mistake. It suggests that beta-amyloid, rather than being an abnormal protein, is actually a component of the brain's immune system. Scientists say Alzheimer’s might not be a brain disease after all: The common theory that Alzheimer's disease is caused by the buildup of beta-amyloid plaques in the brain is now being challenged by a new theory. Scientists say Alzheimer's may be an autoimmune disease. This theory is based on 30 years of research. It suggests that beta-amyloid, rather than being an abnormal protein, is actually a component of the brain's immune system. Its role is to protect the brain from injury and infection, but due to the similarity between the fat molecules in bacterial membranes and brain cell membranes, beta-amyloid mistakenly attacks the brain cells it's meant to defend. This leads to a chronic, progressive loss of brain function, ultimately resulting in dementia. This autoimmune misfire redefines Alzheimer’s as a disorder of the immune system. The autoimmune theory opens up new avenues for treatment by focusing on immune-regulating pathways in the brain, rather than solely targeting beta-amyloid. It offers a promising new direction for research and treatment, potentially leading to more effective therapies for Alzheimer's disease. Autoimmune diseases occur when your immune system mistakenly attacks your body's own tissues, leading to inflammation and damage. There are over 80 recognized types, including rheumatoid arthritis, lupus, and multiple sclerosis. Common symptoms include fatigue, joint pain, skin rashes, and fever. While the exact causes are unclear, factors like genetics, infections, and environmental exposures may contribute.

The researchers determined that a subset of patients with long COVID had traces of the SARS-CoV-2 virus in their stool samples even months after acute COVID-19 infection, which suggests that components of the virus remain in the gut of some patients long after infection. They found that this remaining virus, called a viral reservoir, triggers the immune system to release proteins that fight the virus, called interferons. These interferons cause inflammation that reduces the absorption of the amino acid tryptophan in the gastrointestinal (GI) tract. Tryptophan is a building block for several neurotransmitters, including serotonin, which is primarily produced in the GI tract and carries messages between nerve cells in the brain and throughout the body. It plays a key role in regulating memory, sleep, digestion, wound healing, and other functions that maintain homeostasis within the body. Serotonin is also an important regulator of the vagus nerve, a system of neurons that mediate the communication between the body and the brain. The researchers found that when tryptophan absorption is reduced by persistent viral inflammation, serotonin is depleted, leading to disrupted vagus nerve signaling, which in turn can cause several of the symptoms associated with long COVID, such as memory loss.

Recent work in the field of #neuroimmunology has identified that peripheral neurons (nociceptors) play a large role in the immune system by detecting harmful stimuli but also modulate the reaction to the immune system through the amplification or dampening of inflammation in a tissue- and context-dependent manner. Not a neuroscientist but still interested to know more? Read more about it below: 👇 https://lnkd.in/eTfFGxsx