Inflammation Linked to Chemo Brain

Inflammation Linked to Chemo Brain

Summary: A new study reports inflammation in the blood may play a role in cognitive problems following chemotherapy. Researchers report identifying the inflammatory biomarkers and reducing inflammation may prevent some of the symptoms of chemo brain.

Source: University of Rochester.

Inflammation in the blood plays a key role in “chemo-brain,” according to a published pilot study that provides evidence for what scientists have long believed.

The research is important because it could lead to a new practice of identifying inflammatory biomarkers in cancer patients and then treating the inflammation with medications or exercise to improve cognition and other symptoms, said senior author Michelle C. Janelsins, Ph.D., associate professor of Surgery in the Cancer Control and Survivorship program at the Wilmot Cancer Institute.

Published in the Journal of Neuroimmunology, the preliminary research is believed to be among the first studies to look at cancer patients in active treatment and whether inflammation is involved in their chemo-brain symptoms.

Results showed that among 22 breast cancer patients taking chemotherapy, those with higher levels of inflammatory biomarkers in their blood did worse on neuropsychological tests for visual memory and concentration.

Chemo-brain, or cancer-related cognitive impairment, is estimated to impact 80 percent of people in treatment. Patients report fogginess, forgetfulness, and difficulty with multitasking and other problem-solving skills.

Researchers discovered that one particular biomarker for acute inflammation—tumor necrosis factor-alpha—was the strongest indicator of cognitive problems. Generally, higher levels of inflammation can be caused by cancer, its treatment, or other health problems; but until lately little had been known about the interplay of inflammation, cancer, and quality of life.

a brain is shown

Last year another study led by Janelsins —one of the largest to date for this problem—showed that women with breast cancer continued to report cognitive deficits for as long as six months after finishing treatment. That study not only validated that chemo-brain was pervasive, but Janelsins and her team also began parsing the data to understand the biological mechanisms, such as inflammation, that may put some patients at greater risk for chemo-brain.

“I’m happy that my team’s research is starting to shed light on what might be causing cognitive problems in patients with cancer,” Janelsins said, “and I’m hopeful that we’ll be able to come up with treatments in the future.”

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

Funding: The current study’s first author was AnnaLynn Williams, M.S., a doctoral student in UR’s Division of Epidemiology and a researcher in Janelsins’ lab. Williams recently received a $372,000 National Cancer Institute F99/K00 Award supporting six years of pre-doctoral and postdoctoral research and career development. She is studying cognitive impairment in people with chronic lymphocytic leukemia under the guidance of Janelsins and Edwin van Wijngaarden, Ph.D., chief of the Division of Epidemiology in the Department of Public Health Sciences.

Source: Leslie Orr – University of Rochester
Publisher: Organized by NeuroscienceNews.com.
Image Source: NeuroscienceNews.com image is in the public domain.
Original Research: Abstract for “Associations between inflammatory markers and cognitive function in breast cancer patients receiving chemotherapy” by AnnaLynn M. Williams, Raven Shah, Michelle Shayne, Alissa J. Huston, Marcia Krebs, Nicole Murray, Bryan D. Thompson, Kassandra Doyle, Jenna Korotkin, Edwinvan Wijngaarden, Sharon Hyland, Jan A. Moynihan, Deborah A. Cory-Slechta, and Michelle C. Janelsins in Journal of Neuroimmunology. Published online October 18 2017 doi:10.1016/j.jneuroim.2017.10.005

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Gut Bacteria Linked to Age Related Conditions

Gut Bacteria Linked to Age Related Conditions

Source: Frontiers.

A new study shows for the first time that gut bacteria from old mice induce age-related chronic inflammation when transplanted into young mice. Called “inflammaging,” this low-grade chronic inflammation is linked to life-limiting conditions such as stroke, dementia and cardiovasuclar disease. The research, published today in open-access journal Frontiers in Immunology, brings the hope of a potentially simple strategy to contribute to healthy ageing, as the composition of bacteria in the gut is, at least in part, controlled by diet.

“Since inflammaging is thought to contribute to many diseases associated with ageing, and we now find that the gut microbiota plays a role in this process, strategies that alter the gut microbiota composition in the elderly could reduce inflammaging and promote healthy ageing,” explains Dr Floris Fransen, who performed the research at the University Medical Center Groningen, The Netherlands. “Strategies that are known to alter gut microbiota composition include changes in diet, probiotics, and prebiotics.”

Previous research shows that the elderly tend to have a different composition of gut bacteria than younger people.

Immune responses also tend to be compromised in the elderly, resulting in inflammaging.

Knowing this, Fransen and his team set out to investigate a potential link.

The scientists transferred gut microbiota from old and young conventional mice to young germ-free mice, and analysed immune responses in their spleen, lymph nodes and tissues in the small intestine. They also analysed whole-genome gene expression in the small intestine.

All results showed an immune response to bacteria transferred from the old mice but not from the young mice.

The results suggest that an imbalance of the bacterial composition in the gut may be the cause of inflammaging in the elderly. Imbalances, or “dysbiosis” of gut bacteria results in “bad” bacteria being more dominant than “good” bacteria. An overgrowth of bad bacteria can make the lining of the gut become more permeable, allowing toxins to enter the bloodstream where they can travel around the body with various negative effects.

Dysbiosis can have serious health implications: several disorders, such as inflammatory bowel disease, obesity, diabetes, cancer, anxiety and autism are already linked to the condition.

“Our gut is inhabited by a huge number of bacteria” explains Fransen. “Moreover, there are many different kinds of bacterial species, and the bacterial species that are present can vary a lot from person to person.”

gut

Maintaining a healthy gut microbiota is clearly important to a healthy body and healthy ageing, but why the gut microbiota is different in the elderly is not fully understood. Many people are aware of the effect a course of antibiotics can have on the digestive system for example, but as Fransen explains, it may not be down to just one thing: “It is likely a combination of factors such as reduced physical activity, changes in diet, but also as part of a natural process.”

Most, if not all, age-related diseases can be linked back to inflammaging. Despite the fact that this particular study was conducted on mice, it is clear that maintaining a healthy gut microbiota is key to a healthy lifestyle. However, more research is needed to confirm that the human body mirrors the mice in this study.

“Both in humans and mice there is a correlation between altered gut microbiota composition and inflammaging, but the link between the two remains to be proven in humans” concludes Fransen.

The article is part of the Frontiers Research Topic Immunomodulatory Functions of Nutritional Ingredients in Health and Disease.

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

Source: Frontiers
Publisher: Organized by NeuroscienceNews.com.
Image Source: NeuroscienceNews.com image is in the public domain.
Original Research: Full open access research for “Aged Gut Microbiota Contributes to Systemical Inflammaging after Transfer to Germ-Free Mice” by Floris Fransen, Adriaan A. van Beek, Theo Borghuis, Sahar El Aidy, Floor Hugenholtz, Christa van der Gaast – de Jongh, Huub F. J. Savelkoul, Marien I. De Jonge, Mark V. Boekschoten, Hauke Smidt, Marijke M. Faas, and Paul de Vos in Frontiers in Immunology. Published online November 2 2017 doi:10.3389/fimmu.2017.01385

CITE THIS NEUROSCIENCENEWS.COM ARTICLE
Frontiers “Gut Bacteria Linked to Age Related Conditions.” NeuroscienceNews. NeuroscienceNews, 5 November 2017.
<http://neurosciencenews.com/microbiome-aging-inflammation-7878/&gt;.

Abstract

Aged Gut Microbiota Contributes to Systemical Inflammaging after Transfer to Germ-Free Mice

Advanced age is associated with chronic low-grade inflammation, which is usually referred to as inflammaging. Elderly are also known to have an altered gut microbiota composition. However, whether inflammaging is a cause or consequence of an altered gut microbiota composition is not clear. In this study, gut microbiota from young or old conventional mice was transferred to young germ-free (GF) mice. Four weeks after gut microbiota transfer immune cell populations in spleen, Peyer’s patches, and mesenteric lymph nodes from conventionalized GF mice were analyzed by flow cytometry. In addition, whole-genome gene expression in the ileum was analyzed by microarray. Gut microbiota composition of donor and recipient mice was analyzed with 16S rDNA sequencing. Here, we show by transferring aged microbiota to young GF mice that certain bacterial species within the aged microbiota promote inflammaging. This effect was associated with lower levels of Akkermansia and higher levels of TM7 bacteria and Proteobacteria in the aged microbiota after transfer. The aged microbiota promoted inflammation in the small intestine in the GF mice and enhanced leakage of inflammatory bacterial components into the circulation was observed. Moreover, the aged microbiota promoted increased T cell activation in the systemic compartment. In conclusion, these data indicate that the gut microbiota from old mice contributes to inflammaging after transfer to young GF mice.

“Aged Gut Microbiota Contributes to Systemical Inflammaging after Transfer to Germ-Free Mice” by Floris Fransen, Adriaan A. van Beek, Theo Borghuis, Sahar El Aidy, Floor Hugenholtz, Christa van der Gaast – de Jongh, Huub F. J. Savelkoul, Marien I. De Jonge, Mark V. Boekschoten, Hauke Smidt, Marijke M. Faas, and Paul de Vos in Frontiers in Immunology. Published online November 2 2017 doi:10.3389/fimmu.2017.01385

Zinc jams shut a protein transporter in bacteria preventing infection this winter

After delivering babies, mothers would feed a young mother with soup from clams, spinach, garlic, mushrooms, onions. This soup is rich in zinc and other flavones that can kill bacteria, virus and infection. This coming winter season, more seniors get hospitalized from pneumonia. So fill your kitchen storage with onions, garlic, mushrooms, seeds, nuts, citrus fruits , herbs (turmeric, curcumin, tyme,sage) and other zinc-rich foods.

If you have no time to prepare most of the above foods and wanted to supplement, I suggest anti-inflammatory supplements (Lifepak and AGELOC family) at :

http://www.clubalthea.pxproducts.com

Zinc jams shut a protein transporter in bacteria

Published today in the journal Nature Chemical Biology, the researchers describe how zinc “jams shut” a protein transporter in the bacteria so that it cannot take up manganese, an essential metal that Streptococcus pneumoniae needs to be able to invade and cause disease in humans.

zinc

 

Flavones block the actions of leukotrienes

Inhibition of the 5-lipoxygenase pathway

Some chemicals found in trace amounts in food, and some dietary supplements, also have been shown in inhibit 5-LOX, such as baicalein, caffeic acid, curcumin, hyperforin and St John’s wort (contra-indicated when you are taking antibiotics, other meds).

  1. https://en.wikipedia.org/wiki/BaicaleinBaicalein (5,6,7-trihydroxyflavone) is a flavone, a type of flavonoid, originally isolated from the roots of Scutellaria baicalensis and Scutellaria lateriflora. It is also …

  2. http://www.jbc.org/content/279/26/26846.fullJun 25, 2004  Baicalein is a flavonoid with antioxidant properties; upon oxidation, it forms several products including quinones. We show here that low …

  3. https://www.ncbi.nlm.nih.gov/pubmed/17976269J Pharm Pharmacol. 2007 Nov;59(11):1567-72. Scutellaria baicalensis and a constituent flavonoidbaicalein, attenuate ritonavir-induced gastrointestinal …

  4. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2573395/Aug 23, 2008  The flavonoid baicalein inhibits fibrillation of α-synuclein, which is a major component of the Lewy bodies in Parkinson’s disease. It has been …

  5. https://selfhacked.com/blog/baicalein-baicalin-top-7-health-benefits-flavanoid/3 days ago  Baicalein is a flavone, a type of polyphenolic flavonoid, that is extracted from the roots of Scutellaria baicalensis and Scutellaria lateriflora that …

  6. http://journal.frontiersin.org/article/212440Aug 29, 2016  A commentary on. The Flavonoid Baicalein Rescues Synaptic Plasticity and Memory Deficits in a Mouse Model of Alzheimer’s Disease

  7. https://www.hindawi.com/journals/ecam/2013/635694/Jun 10, 2013  The estrogenic activity of two flavonoidsbaicalein and daidzein, were demonstrated by their strong abilities in stimulating estrogen receptor …

  8. http://pubs.acs.org/doi/abs/10.1021/acs.biochem.6b00578Jul 19, 2016  Amyloid formation of the 37-residue amylin is involved in the pathogenesis of type 2 diabetes and potentially, diabetes-induced neurological …

  9. http://www.sciencedirect.com/science/article/pii/S0304383510002375Nov 1, 2010  Baicalein is a flavonoid derived from the root of Scutellaria baicalensis, widely used in Chinese herbal medicine. Historically, S. baicalensis has …

  10. http://www.sciencedirect.com/science/article/pii/S0166432816303369May 24, 2016  Baicalein prevents memory deficits in AD model. … Our results strengthen the potential of the flavonoid baicaleinas a novel and promising oral …

Leukotrienes are a family of eicosanoid inflammatory mediators produced in leukocytes by the oxidation of arachidonic acid(AA) and the essential fatty acid eicosapentaenoic acid (EPA) by the enzyme arachidonate 5-lipoxygenase.[1][2][3]

Leukotrienes use lipid signaling to convey information to either the cell producing them (autocrine signaling) or neighboring cells (paracrine signaling) in order to regulate immune responses. The production of leukotrienes is usually accompanied by the production of histamine and prostaglandins, which also act as inflammatory mediators.[citation needed]

One of their roles (specifically, leukotriene D4) is to trigger contractions in the smooth muscles lining the bronchioles; their overproduction is a major cause of inflammation in asthma and allergic rhinitis.[4] Leukotriene antagonists are used to treat these disorders by inhibiting the production or activity of leukotrienes.

How to attain healthy blood and muscles to prevent Alzheimer’s ?

How to attain healthy blood and muscles to prevent Alzheimer’s ?

Adequate sleep

During sleep, our body is detoxing. Many of my cancer and Alzheimer’s clients do not sleep well at night.

Adequate sunshine or Vitamin D

Many of those with Alzheimer’s do not exercise often and are not taking Vitamin D.

Normal blood sugar

Their blood tests shows high levels of blood sugar.

Stronger immune system

Search this site for immune system, lymphatic, massage , Vitamin D, blood, ketogenic diet, restricted calorie diet, inflammation, toxins and sleep

Quality supplementation for stronger blood vessels

Nutrients that are important to have strong blood vessels include Vitamin D, C, E, A, B complex, sufur rich foods (e.g., onions, garlic) and probiotics. Visit this site to try these supplements (Lifepak and AGELOC family of products ) at:

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Connie Dello Buono


 

Alzheimer’s Disease Might Be a ‘Whole Body’ Problem

Summary: Using a technique called parabiosis on pairs of mice, researchers discover what they call ‘cancer like mobility’ of amyloid beta, reporting it can travel to the brain from other parts of the body.

Source: University of British Columbia.

Alzheimer’s disease, the leading cause of dementia, has long been assumed to originate in the brain. But research from the University of British Columbia and Chinese scientists indicates that it could be triggered by breakdowns elsewhere in the body.

The findings, published today in Molecular Psychiatry, offer hope that future drug therapies might be able to stop or slow the disease without acting directly on the brain, which is a complex, sensitive and often hard-to-reach target. Instead, such drugs could target the kidney or liver, ridding the blood of a toxic protein before it ever reaches the brain.

The scientists demonstrated this cancer-like mobility through a technique called parabiosis: surgically attaching two specimens together so they share the same blood supply for several months.

UBC Psychiatry Professor Dr. Weihong Song and Neurology Professor Yan-Jiang Wang at Third Military Medical University in Chongqing attached normal mice, which don’t naturally develop Alzheimer’s disease, to mice modified to carry a mutant human gene that produces high levels of a protein called amyloid-beta. In people with Alzheimer’s disease, that protein ultimately forms clumps, or “plaques,” that smother brain cells.

Normal mice that had been joined to genetically modified partners for a year “contracted” Alzheimer’s disease. Song says the amyloid-beta traveled from the genetically-modified mice to the brains of their normal partners, where it accumulated and began to inflict damage.

Not only did the normal mice develop plaques, but also a pathology similar to “tangles” – twisted protein strands that form inside brain cells, disrupting their function and eventually killing them from the inside-out.

Other signs of Alzheimer’s-like damage included brain cell degeneration, inflammation and microbleeds.

In addition, the ability to transmit electrical signals involved in learning and memory – a sign of a healthy brain – was impaired, even in mice that had been joined for just four months.

mice

Besides the brain, amyloid-beta is produced in blood platelets, blood vessels and muscles, and its precursor protein is found in several other organs.

But until these experiments, it was unclear if amyloid-beta from outside the brain could contribute to Alzheimer’s disease. This study, Song says, shows it can.

“The blood-brain barrier weakens as we age,” says Song, a Canada Research Chair in Alzheimer’s Disease and the Jack Brown and Family Professor. “That might allow more amyloid beta to infiltrate the brain, supplementing what is produced by the brain itself and accelerating the deterioration.”

Song, head of UBC’s Townsend Family Laboratories, envisions a drug that would bind to amyloid-beta throughout the body, tagging it biochemically in such a way that the liver or kidneys could clear it.

“Alzheimer’s disease is clearly a disease of the brain, but we need to pay attention to the whole body to understand where it comes from, and how to stop it,” he says.

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

Source: Brian Kladko – University of British Columbia
Publisher: Organized by NeuroscienceNews.com.
Image Source: NeuroscienceNews.com image is credited to University of British Columbia.
Original Research:Abstract for “Blood-derived amyloid-β protein induces Alzheimer’s disease pathologies” by X-L Bu, Y Xiang, W-S Jin, J Wang, L-L Shen, Z-L Huang, K Zhang, Y-H Liu, F Zeng, J-H Liu, H-L Sun, Z-Q Zhuang, S-H Chen, X-Q Yao, B Giunta, Y-C Shan, J Tan, X-W Chen, Z-F Dong, H-D Zhou, X-F Zhou, W Song and Y-J Wang in Molecular Psychiatry. Published online October 31 2017 doi:10.1038/mp.2017.204

CITE THIS NEUROSCIENCENEWS.COM ARTICLE
University of British Columbia “Alzheimer’s Disease Might Be a ‘Whole Body’ Problem.” NeuroscienceNews. NeuroscienceNews, 31 October 2017.
<http://neurosciencenews.com/alzheimers-whole-body-7840/&gt;.

Abstract

Blood-derived amyloid-β protein induces Alzheimer’s disease pathologies

The amyloid-β protein (Aβ) protein plays a pivotal role in the pathogenesis of Alzheimer’s disease (AD). It is believed that Aβ deposited in the brain originates from the brain tissue itself. However, Aβ is generated in both brain and peripheral tissues. Whether circulating Aβ contributes to brain AD-type pathologies remains largely unknown. In this study, using a model of parabiosis between APPswe/PS1dE9 transgenic AD mice and their wild-type littermates, we observed that the human Aβ originated from transgenic AD model mice entered the circulation and accumulated in the brains of wild-type mice, and formed cerebral amyloid angiopathy and Aβ plaques after a 12-month period of parabiosis.

AD-type pathologies related to the Aβ accumulation including tau hyperphosphorylation, neurodegeneration, neuroinflammation and microhemorrhage were found in the brains of the parabiotic wild-type mice. More importantly, hippocampal CA1 long-term potentiation was markedly impaired in parabiotic wild-type mice.

To the best of our knowledge, our study is the first to reveal that blood-derived Aβ can enter the brain, form the Aβ-related pathologies and induce functional deficits of neurons.

Our study provides novel insight into AD pathogenesis and provides evidence that supports the development of therapies for AD by targeting Aβ metabolism in both the brain and the periphery.

“Blood-derived amyloid-β protein induces Alzheimer’s disease pathologies” by X-L Bu, Y Xiang, W-S Jin, J Wang, L-L Shen, Z-L Huang, K Zhang, Y-H Liu, F Zeng, J-H Liu, H-L Sun, Z-Q Zhuang, S-H Chen, X-Q Yao, B Giunta, Y-C Shan, J Tan, X-W Chen, Z-F Dong, H-D Zhou, X-F Zhou, W Song and Y-J Wang in Molecular Psychiatry. Published online October 31 2017 doi:10.1038/mp.2017.204


From Wiki:

Normal function

 

The normal function of Aβ is not well understood.[7] Though some animal studies have shown that the absence of Aβ does not lead to any obvious loss of physiological function,[8][9] several potential activities have been discovered for Aβ, including activation of kinase enzymes,[10][11] protection against oxidative stress,[12][13]regulation of cholesterol transport,[14][15] functioning as a transcription factor,[16][17] and anti-microbial activity (potentially associated with Aβ’s pro-inflammatory activity).[18]

The glymphatic system clears metabolic waste from the mammalian brain, and in particular beta amyloids.[19] The rate of removal is significantly increased during sleep.[20] However, the significance of the glymphatic system in Aβ clearance in Alzheimer’s disease is unknown.[21]

Disease associations

Aβ is the main component of amyloid plaques (extracellular deposits found in the brains of patients with Alzheimer’s disease).[22] Similar plaques appear in some variants of Lewy body dementia and in inclusion body myositis (a muscle disease), while Aβ can also form the aggregates that coat cerebral blood vessels in cerebral amyloid angiopathy. The plaques are composed of a tangle of regularly ordered fibrillar aggregates called amyloid fibers,[23] a protein fold shared by other peptides such as the prions associated with protein misfolding diseases.

Brain Aβ is elevated in patients with sporadic Alzheimer’s disease. Aβ is the main constituent of brain parenchymal and vascular amyloid; it contributes to cerebrovascular lesions and is neurotoxic.[32][33][34][35] It is unresolved how Aβ accumulates in the central nervous system and subsequently initiates the disease of cells. Some researchers have found that the Aβ oligomers induce some of the symptoms of Alzheimer’s Disease by competing with insulin for binding sites on the insulin receptor, thus impairing glucose metabolism in the brain.[36] Significant efforts have been focused on the mechanisms responsible for Aβ production, including the proteolytic enzymes gamma- and β-secretases which generate Aβ from its precursor protein, APP (amyloid precursor protein).[37][38][39][40] Aβ circulates in plasma, cerebrospinal fluid (CSF) and brain interstitial fluid (ISF) mainly as soluble Aβ40[32][41] Senile plaques contain both Aβ40 and Aβ42,[42] while vascular amyloid is predominantly the shorter Aβ40. Several sequences of Aβ were found in both lesions.[43][44][45] Generation of Aβ in the CNS may take place in the neuronal axonal membranes after APP-mediated axonal transport of β-secretase and presenilin-1.[46]

Increases in either total Aβ levels or the relative concentration of both Aβ40 and Aβ42 (where the former is more concentrated in cerebrovascular plaques and the latter in neuritic plaques)[47] have been implicated in the pathogenesis of both familial and sporadic Alzheimer’s disease. Due to its more hydrophobic nature, the Aβ42 is the most amyloidogenic form of the peptide. However the central sequence KLVFFAE is known to form amyloid on its own, and probably forms the core of the fibril.[citation needed] One study further correlated Aβ42 levels in the brain not only with onset of Alzheimer’s, but also reduced cerebrospinal fluid pressure, suggesting that a build-up or inability to clear Aβ42 fragments may play a role into the pathology.[

Low-temperature and low-salt conditions allowed to isolate pentameric disc-shaped oligomers devoid of beta structure.[65] In contrast, soluble oligomers prepared in the presence of detergents seem to feature substantial beta sheet content with mixed parallel and antiparallel character, different from fibrils;[66] computational studies suggest an antiparallel beta-turn-beta motif instead for membrane-embedded oligomers.[67]

The suggested mechanisms by which amyloid beta may damage and cause neuronal death include the generation of reactive oxygen species during the process of its self-aggregation. When this occurs on the membrane of neurons in vitro, it causes lipid peroxidation and the generation of a toxic aldehyde called 4-hydroxynonenalwhich, in turn, impairs the function of ion-motive ATPases, glucose transporters and glutamate transporters. As a result, amyloid beta promotes depolarization of the synaptic membrane, excessive calcium influx and mitochondrial impairment.[68] Aggregations of the amyloid-beta peptide disrupt membranes in vitro.


Connie’s comments:

 

 

 

 

 

 

Understanding How Omega 3 Dampens Inflammatory Reactions

Understanding How Omega 3 Dampens Inflammatory Reactions

Summary: Researchers from NTNU find new evidence of how omega 3 fatty acids can dampen inflammatory reactions in the body.

Source: Norwegian University of Science and Technology.

Omega-3 supplements may help slow the development of diseases like cancer, Alzheimer’s and multiple sclerosis.

Omega-3 fatty acids, which we primarily get through eating fatty fish, have long been thought to be good for our health. Many dietary studies have suggested that high intake is associated with a reduced risk of various disorders. Clinical trials have also shown beneficial anti-inflammatory effects in patients taking omega-3 supplements.

Recent research from NTNU supports previous discoveries, and has also found new, useful effects of omega-3 supplements and how these lipids dampen harmful inflammatory reactions in the body.

Effects little known

Despite numerous published dietary and clinical studies, we still don’t fully understand how omega-3 fatty acids affect our cells and if this varies from person to person, between healthy and ill individuals, or whether the mechanism of action varies in different tissues and cells. What we are most sure of is that omega-3 fatty acids can dampen inflammatory reactions. Inflammatory reactions are very important in combating infections, but they can be harmful if activated too strongly or in the absence of bacteria and viruses, like in autoimmune diseases and organ transplants.

Macrophages, which are immune cells that live in all tissues and organs, play a key role in coordinating inflammatory reactions in the body and monitor everything that happens in our tissues. The macrophages convert the information they obtain through various sensors or receptor on their surface to secretion of various hormone-like signal substances that control all parts of inflammatory reactions.

Inflammation can be harmful

We have increasingly become aware that macrophages can be more or less potent in activating inflammatory reactions. So-called sterile inflammatory reactions, such as autoimmune diseases, are often directly harmful.

The ability of macrophages to stimulate inflammatory reactions depends on processes within the macrophage.

Autophagy is one of the processes within macrophages that is important for whether a macrophage is calm or hyperactive. Autophagy (meaning “self-eating”) is a key process for degradation of dysfunctional or unnecessary proteins and other components within our cells.

In the last few years, we’ve learned a lot about how important this process is, say the researchers. The Nobel Prize in Physiology or Medicine 2016 was given to Yoshinori Ohsumi for his discovery of the key genes that control autophagy.

Autophagy is constantly going on in all cells and increases if the cells are starving or injured. We hypothesized that omega-3 fatty acids could dampen inflammatory reactions by elevating autophagy in macrophages. If so, we surmised that this effect might change the signal transformation in the macrophage and as a result, suppress activation of inflammatory reactions.

Activates self-cleaning process

By studying macrophages isolated from mice and humans, we found that the omega-3 fatty acids activated the autophagy and specifically affected some proteins that transform the signals from the environment. Furthermore, we found that omega-3 fatty acids dampened many inflammatory mechanisms within the macrophages, but especially reduced what is known as the type 1 interferon response.

Image shows omega 3 pills.

The factor CXCL-10, which macrophages secrete as part of this interferon response following many types of stimuli, was the most clearly reduced factor after adding omega-3 to the cells.

We then examined blood samples from a clinical study in cardiac transplant patients where we knew that omega-3 supplements improved their clinical status. In these cases, we found that omega-3 fatty acids reduced the level of CXCL-10.

Supplements beneficial

Autophagy thus changes in macrophages in response to omega-3 fatty acids and specifically inhibits the secretion of inflammatory factors that belong to the interferon response, with CXCL-10 showing the clearest reduction. The results of this study are being published in the journal Autophagy.

These findings indicate that omega-3 fatty acid supplements may be particularly beneficial in patients who have conditions that are driven or aggravated by a strong interferon response and CXCL-10.

Our research group hopes that this one day will benefit patients with different forms of cancer, meningitis, multiple sclerosis, Alzheimer’s disease or jaundice. But we must emphasize that a lot of work remains.

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

The work being published by PhD candidate Jennifer Mildenberger and colleagues was conducted at CEMIR and at NTNU’s Department of Biomedical Laboratory Science in the Faculty of Natural Science. In addition, researchers in St. Louis, USA carried out important sub studies. The blood tests were from a clinical trial conducted at Oslo University Hospital.

Article author Geir Bjørkøy is a professor in the Department of Biomedical Laboratory Science at NTNU.

Article author Jennifer Mildenberger works for NTNU-Cemir.

Source: Jennifer Mildenberger – Norwegian University of Science and Technology
Image Source: NeuroscienceNews.com image is in the public domain.
Original Research: Abstract for “N-3 PUFAs induce inflammatory tolerance by formation of KEAP1-containing SQSTM1/p62-bodies and activation of NFE2L2” by Jennifer Mildenberger, Ida Johansson, Ismail Sergin, Eli Kjøbli, Jan Kristian Damås, Babak Razani, Trude Helen Flo & Geir Bjørkøy in Autophagy. Published online August 18 2017 doi:10.1080/15548627.2017.1345411

CITE THIS NEUROSCIENCENEWS.COM ARTICLE
Norwegian University of Science and Technology “Understanding How Omega 3 Dampens Inflammatory Reactions.” NeuroscienceNews. NeuroscienceNews, 24 August 2017.
<http://neurosciencenews.com/inflammation-response-omega-3-7369/&gt;.

Abstract

N-3 PUFAs induce inflammatory tolerance by formation of KEAP1-containing SQSTM1/p62-bodies and activation of NFE2L2

Inflammation is crucial in the defense against infections but must be tightly controlled to limit detrimental hyperactivation. Our diet influences inflammatory processes and omega-3 polyunsaturated fatty acids (n-3 PUFAs) have known anti-inflammatory effects. The balance of pro- and anti-inflammatory processes is coordinated by macrophages and macroautophagy/autophagy has recently emerged as a cellular process that dampens inflammation. Here we report that the n-3 PUFA docosahexaenoic acid (DHA) transiently induces cytosolic speckles of the autophagic receptor SQSTM1/p62 (sequestosome 1) (described as SQSTM1/p62-bodies) in macrophages.

We suggest that the formation of SQSTM1/p62-bodies represents a fast mechanism of NFE2L2/Nrf2 (nuclear factor, erythroid 2 like 2) activation by recruitment of KEAP1 (kelch like ECH associated protein 1). Further, the autophagy receptor TAX1BP1 (Tax1 binding protein 1) and ubiquitin-editing enzyme TNFAIP3/A20 (TNF alpha induced protein 3) could be identified in DHA-induced SQSTM1/p62-bodies. Simultaneously, DHA strongly dampened the induction of pro-inflammatory genes including CXCL10 (C-X-C motif chemokine ligand 10) and we suggest that formation of SQSTM1/p62-bodies and activation of NFE2L2 leads to tolerance towards selective inflammatory stimuli. Finally, reduced CXCL10 levels were related to the improved clinical outcome in n-3 PUFA-supplemented heart-transplant patients and we propose CXCL10 as a robust marker for the clinical benefits mobilized by n-3 PUFA supplementation.

“N-3 PUFAs induce inflammatory tolerance by formation of KEAP1-containing SQSTM1/p62-bodies and activation of NFE2L2” by Jennifer Mildenberger, Ida Johansson, Ismail Sergin, Eli Kjøbli, Jan Kristian Damås, Babak Razani, Trude Helen Flo & Geir Bjørkøy in Autophagy. Published online August 18 2017 doi:10.1080/15548627.2017.1345411


Connie’s comments: You can order anti-oxidants to fight inflammation here:

http://clubalthea.pxproducts.com/products-2

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