Microglial cells (red) in rat brain



Neuroinflammation is inflammation of nervous tissue in the peripheral or central nervous system. It may occur in response to a variety of triggers including trauma, infection, toxins, or auto-immune processes.

Neuroinflammation plays a central role in chronic pain but also in disorders such as fibromyalgia, depression, PTSD, multiple sclerosis, Parkinson’s Disease, Alzheimer Disease, brain and spinal cord injuries including chronic traumatic encephalopathy (CTE), stroke and schizophrenia.



See also:


Neurobiology of Pain

Neuropathic (Nerve) Pain

Neurobiology of Opioids


Opioid Tolerances

Central Sensitization

Medications for Pain

Gabapentin (Neurontin) & Pregabalin (Lyrica)

Palmitoylethanolamide (PEA)

Toll-Like Receptor Antagonists (TLR-4)

Traumatic Brain Injury


 Definitions and Terms Related to Pain

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Inflammation is a complex biological response that is basic to how the body addresses injury and infection to eliminate the initial cause of cell injury and repair tissues. While acute inflammation is normally a beneficial response, chronic inflammation often results from an inappropriate immune response that can lead to tissue damage and ultimately tissue destruction. Inflammation in the nervous system or “neuroinflammation,” especially when prolonged, can be particularly harmful. While inflammation per se may not cause disease, it contributes importantly to the process of disease in both the peripheral and central nervous systems. Treatment of neuroinflammation may significantly impact the progression and symptomatic manifestation of those conditions associated with neuroinflammation.


 Neuroinflammation is implicated in:

  1. Pain
  2. Opioid tolerance
  3. Fibromyalgia
  4. Reward Deficiency Syndrome (RDS)
  5. Traumatic brain injury (TBI)
  6. Arachnoiditis
  7. Depression
  8. Multiple Sclerosis
  9. Alzheimer disease
  10. Parkinson disease
  11. Autism Spectrum Disorder


(1). Pain and Neuroinflammation

Until recently, opioids and medications such as gabapentin (Neurontin), pregabalin (Lyrica) and duloxetine (Cymbalta) have been the conventional approach to reduce pain by their action on transduction and transmission in neurons, which likely accounts for the limited success in controlling chronic pain and its  progression. This “nerve-based” view fails to address the fact that initiation and maintenance of neuropathic pain depends to a great extent on non-nerve cells such as spinal microglia and astrocytes, together with elements of the peripheral immune system.

Chronic pain is maintained in part by central sensitization, a process involving adaptations at the nerve synapses and increased responsiveness to painful stimul in the pain pathways. Central sensitization is  driven by neuroinflammation in the peripheral and central nervous system. Neuroinflammation, characterized by the activation of glial cells such as microglia and astrocytes in the spinal cord and brain, leads to the release of proinflammatory cytokines and chemokines. These cytokines and chemokines impact  nerves, inducing hyperalgesia and allodynia, and their sustained release in the central nervous system promotes chronic widespread pain affecting multiple body sites. Thus, understanding how neuroinflammation in the peripheral and central nervous system drives widespread chronic pain via central sensitization has gained recent attention for its importance in understanding and treating chronic pain and other conditions. See Treatment of Neuroinflammation (below).

See Central Sensitization

(2). Opioid Tolerance and Neuroinflammation

Classical neuron-centered concepts about tolerance, such as internalization of opioid receptors, upregulation of N-methyl-D-aspartate (NMDA) receptor function, or downregulation of glutamate transporter activity only partially explain the phenomenon of tolerance. Recent evidence confirms that glial activation and upregulation of inflammatory mediators in the central nervous system play pivotal roles in neuropathic pain and opioid tolerance.

(3). Fibromyalgia and Neuroinflammation

Coming soon…

(4). Reward Deficiency Syndrome and Neuroinflammation

See: Reward Deficiency Syndrome and Chronic Pain

(5). Traumatic Brain Injury and Neuroinflammation

See: Traumatic Brain Injury

(6). Arachnoiditis

See: Arachnoiditis

(7). Depression and Neuroinflammation

Coming soon… 

Treatment of Neuroinflammation

Early studies suggest that medications or supplements that reduce neuroinflammation by inhibiting glial activation and/or stabilizing mast cells may reduce the development of chronic nerve pain or reduce the severity of existing nerve pain. They may also be useful in suppressing the development of opioid tolerance. Various inhibitors of glial activation that are being evaluated for clinical use in the managment of chronic pain include minocycline, a tetracycline-class antibiotic, low dose naltrexone, palmitoylethanolamide (PEA) and Acetyl-L-carnitine. There is some evidence as well that gabapentin may inhibit glial cell activation as another mechanism of action responsible for its effectiveness in treating nerve pain. Furthermore, there may be a role for antioxidants and NRF2 activators as well in the management of chronic nerve pain related to glial cell activation.


At this time, the following agents are considered good candidates for treating neuroinflammation through stabilization and/or suppression of glial cells and mast cells:


  1. Palmitoylethanolamide (PEA)
  2. Cannabidiol (CBD)
  3. Minocycline – Recognized as a microglia inhibitor
  4. Low-dose naltrexone
  5. DHEA – Early/weak evidence for benefit in depression and regulation of the blood-brain barrier


Understanding Neuroinflammation

Understanding communication between the nervous system and the immune system is fundamental to understand neuroinflammation. Immune cell-derived inflammatory molecules regulate of host responses to inflammation. Although these molecules can originate from various non-neuronal (non-nerve) cells, their most important sources are immune cells: microglia and mast cells, together with astrocytes and possibly also oligodendrocytes. Understanding neuroinflammation also requires an appreciation that non-neuronal cell—cell interactions, between both glia and mast cells and glia themselves, are an integral part of the inflammation process. Within this context the mast cell occupies a key niche in orchestrating the inflammatory process, from initiation to prolongation.


Normal, optimal inflammatory responses and physiological levels of inflammatory mediators are beneficial and protect the body as they remove unwanted waste materials and repair damaged tissues. As such, the initial, acute inflammatory response is protective, and lipid mediators such as eicosanoids (prostaglandins and leukotrienes produced from the essential fatty acid arachidonic acid) play critical roles in the initial response, with interactions between prostaglandins, leukotrienes and pro-inflammatory cytokines amplifying inflammation.

Normally, these altered and reactive immune cells diminish their activity within 10–14 days after injury and the inflammatory response ceases. However, in some cases, this neuroinflammation continues and becomes chronic, leading to many of the manifestations of nerve pain, or “neuropathic” pain, such as hyperalgesia, allodynia and peripheral and central sensitization, all of which are characterized by a magnification of pain experience.


The Players in Neuroinflammation

The process of neuroinflammation can be understood on a (1) structural level, including the blood-brain barrier (BBB), on a (2) cellular level including immune cells such as mast cells, microglia, astrocytes and oligodendrocytes or on a (3) chemical level including cytokines, chemokines and others.


Neuroinflammation and the Blood-Brain Barrier (BBB)

In normal physiological conditions, the blood-brain barrier (BBB) prevents entry of most drugs, chemicals, toxins and peripheral blood cells into the brain and central nervous system. The BBB is an extensive network of endothelial cells (ECs) in brain capillaries together with neurons and glial cells, including microglia, that form a neurovascular unit (NVU). The communication between these cells maintains a proper environment for brain function.


The integrity of the BBB which prevents”inappropriate” molecules from entering the central nervous system and brain is dependent on the maintenance of “tight junctions,” where the cells of the blood vessel interface with adjoining cells. Changes in the interactions between blood vessel endothelium and microglia are associated with a variety of inflammation-related diseases where BBB permeability is compromised. Evidence indicates that activated microglia modulate expression of tight junctions, which are essential for BBB integrity and function. On the other hand, the endothelium can in turn regulate the state of microglial activation.


Trauma and its associated stress induces a local inflammatory response causing disruption and dysfunction of the BBB increasing its permeability. This results in the infiltration of peripheral immune and inflammatory cells such as neutrophils, monocytes, mast cells (see below), and T cells into the brain. These cells become “activated,” immediately releasing inflammatory proteins called cytokines and chemokines within hours post-injury. These mast cell-derived inflammatory mediators further increase blood brain barrier (BBB) permeability and activate localized brain-based immune glial cells such as microglia and astrocytes (see below). When activated, microglia and astrocytes increase production of similar inflammatory cytokines. Furthermore, all of these inflammatory mediators increase vascular permeability and increase escape and recruitment of immune and inflammatory cells at the site of injury. When the integrity of the BBB is compromised through inflammation or injury, there is increased permeability of the BBB, allowing for increased introduction of inflammatory chemicals, drugs and toxins to enter the central nervous system (CNS)  – spinal cord and brain.


Although loss of BBB integrity is associated with several neuropathological disorders, treatments that improve or stabilise the BBB are scarce. A 2017 study suggests that dehydroepiandrosterone sulfate (DHEAS) supports the integrity
of the BBB and DHEA has shown evidence for benefit in the treatmemt of depression. At this time, one focus of treatment of impaired BBB integrity lies in the stabilization of glial cells and mast cells.


The Blood Brain Barrier and the Intestinal Epithelial Barrier (IEB)

A growing body of evidence demonstrates that the integrity of the BBB is linked to the integrity of the intestinal epithelial barrier (IEB), the analogous structure to the BBB in the gut. In turn, the integrity of the IEB is linked to the gut microbiome, the populati0n of microbes in the intestinal tract, Disruption of the IEB leads to a condition called “leaky gut syndrome,” in which a disruption of the tight junctions of the cells lining the gut wall allows for the pathologic migration of agents within the gut into the blood and systemic circulation. These agents include bacterial products and dietary antigens which trigger an immune response causing the release of pro-inflammatory chemicals. This in turn contributes to the condition of systemic inflammation which is tied into neuroinflammation, and the potential development of a number of disease states. The gut microbiome appears to be a significant factor contributing to the maintenance or the breakdown of the IEB and the gut microbiome is influenced and modified by a number of factors including stress and drugs, in particular NSAIDs and opioids. Leaky gut syndrome is believed to be associated with many pathological states, especially stress-related disorders including IBS, inflammatory bowel disease (Crohn’s and ulcerative colitis), fibromyalgia, depression, headaches and other chronic pain-related conditions.

See: Leaky Gut (Coming soon… )



Neuroinflammation and Glial Cells

Glial cells are cells found in the central and peripheral nervous system.  They function to maintain balance in nerve and neurotransmitter activity, they form myelin (the coating of some nerve cells), and provide support and protection for neurons (nerve cells). Glial cells are derived from the immune system, the most common of which are microglia cells and astrocytes. Glia cells provide a supportive matrix for nerve cells, supplying nutrients and oxygen and aid in the repair of damaged cells. However, when activated, glial cells also are important in the evolution and maintenance of chronic nerve pain through the release of peptides known as cytokines that are pro-inflammatory, triggering chronic pain. They may play a role in opioid function including opioid-induced hyperalgesia and opioid tolerance. It is believed that pathologic glial cell activation plays a significant role in the evolution of fibromyalgia pain, central sensitization and other chronic pain syndromes.


Following activation, glia cells release pro-inflammatory cytokines/chemokines including:

(1) Tumor necrosis factor (TNF)

(2) Interleukin-1beta (IL-1β)

(3) Interleukin-6 (IL-6)

(4) Interleukin-8 (IL-8)

(5) Chemokine (C–C motif) ligand 2 (CCL-2), also known as monocyte chemoattractant protein 1 (MCP-1)

(6) Brain-derived neurotrophic factor (BDNF)

(7) Nerve growth factor (NGF)

(8) Glutamate

(9) Substance P (SP)

Neuroinflammation and Mast Cells

Glial cells participate in inflammation not only directly, but also in to response to molecular mediators produced by other immune system-derived cells, both blood-borne (dendritic cells, lymphocytes, neutrophils), and tissue-resident (mast cells). Mast cell are an important signaling link between the peripheral immune system and the brain in an inflammatory setting. Due to their widespread tissue presence near blood vessels and surfaces exposed to the environment, mast cells function as environmental “sensors” to communicate physiological and/or immune responses. Mast cells detect and respond to changes in environmental temperature and barometric pressure and are believed to play a role in the increased perception of pain associated with changes in weather.


Mast cells are manufactured in the bone marrow and enter the circulation and then into peripheral tissues including connective tissue cells and mucosal cells. They maintain broad tissue distribution, often close to blood vessels and near boundaries between the body’s external environment and the internal milieu, such as skin, mucosa of lungs and digestive tract, and in mouth, eye conjunctiva, and nose. Mast cells also found in the nervous system, including meningeal tissures that surround the brain, brain tissue, and nerve sleeves. They are integral in allergic reactions and anaphylactic shock, stress,  mood disorders, inflammatory pain, chronic and neuropathic pain and acute and chronic neurodegenerative disorders.

Mast cells are found in tissues innervated by small caliber sensory nerve fibers (A-delta and C-fibers responsible for pain transmission that extend from the periphery to the spinal cord and brain), in meninges, and apposing cerebral blood vessels. Mast cell’s key role in the inflammatory process, when activated, is to rapidly release granules (degranulation) of bioactive chemicals, pro-inflammatory mediators such as cytokines and others into the surrounding tissues. Degranulation is triggered by direct injury (physical or chemical), stimulation of immune receptors (such as IgE in allergies) or by activated complement proteins. More than 50 mediators are known and their expression by mast cells is complex
and determined to a large extent by tissue location. Additionally, mast cell-derived chemoattractants recruit other immune cells including eosinophils, monocytes, and neutrophils, and can induce T cell activation, proliferation, and cytokine secretion.

As such, it is clear that glial cells and mast cells play major roles in neuroinflammatiom through their release of chemically active protein mediators that impact tissues and stimulate pain, acutely and chronically. Current research is focusing on medications and other agents that can stabilize glial cells and mast cells, suppress their release of mediators and thereby reduce the development and/or maintenance of chronic pain.

Neuroinflammation and Oligodendrocytes

Oligodendrocytes, the myelin-producing cells of the central nervous system (CNS), may also participate in the pain process. In addition to their production of myelin, oligodendrocytes support nerve function and long-term integrity. Oligodendrocyte damage/dysfunction leads to spinal nerve axon pathology and the induction/maintenance of increased pain sensitivity. Also, like glial cells and mast cells, they produce and respond to chemokines/cytokines that modulate CNS immune responses and interact with microglia.   In the case of multiple sclerosis (MS), for example, autoimmune inflammation driven by invading peripheral immune cells leads to injury/degeneration of oligodendrocytes and neurons, and contributes to the neuropathic pain often experienced by MS patients.

New Frontiers – Resolving Inflammation

The resolution of neuroinflammation has previously been considered a passive process. Recent research, however, has identified mediators with the capacity to actively resolve inflammation, endogenous agents called resolvins, protectins & maresins, that are involved with the process of shutting down neuroinflammation. It is hoped that in the future the means of harnessing these agents for therapeutic purposes will become available. What is believed at this time, however, is that production of these agents may be promoted by low dose aspirin and omega-3 essential fatty acids while NSAIDs may inhibit their production.

Coming Soon…



  1. Introduction to Pain Pathways and Mechanisms
  2. Pain and the Neuromatrix in the Brain 2001
  3. Neuropathic pain – mechanisms and their clinical implications – 2014
  4. Hypothesizing that brain reward circuitry genes are genetic antecedents of pain sensitivity and critical diagnostic and pharmacogenomic treatment targets for chronic pain conditions – 2009

Neuroinflammation – Blood Brain Barrier (BBB)

  1. Opioids and the Blood-Brain Barrier – A Dynamic Interaction with Consequences on Drug Disposition in Brain – 2017
  2. Targeting Transporters – Promoting Blood-Brain Barrier Repair in Response to Oxidative Stress Injury – 2015
  3. The opioid epidemic – a central role for the blood brain barrier in opioid analgesia and abuse – 2017
  4. The role of the blood–brain barrier in the development and treatment of migraine and other pain disorders – 2014
  5. Dehydroepiandrosterone sulfate augments blood-brain barrier and tight junction protein expression in brain endothelial cells – 2017
  6. The impact of microglial activation on blood-brain barrier in brain diseases – 2014

Neuroinflammation – Mast Cells

  1. Activated mast cells infiltrate in close proximity to enteric nerves in diarrhea-predominant irritable bowel syndrome. – 2003
  2. Mast cells, glia and neuroinflammation – partners in crime? – 2013

Neuroinflammation – Glial Cells

  1. evidence-for-brain-glial-activation-in-chronic-pain-patients-2015
  2. importance-of-glial-activation-in-neuropathic-pain-pubmed-ncbi
  3. glial-contributions-to-visceral-pain-implications-for-disease-etiology-and-the-female-predominance-of-persistent-pain-2016
  4. evidence-of-different-mediators-of-central-inflammation-in-dysfunctional-and-inflammatory-pain-interleukin-8-in-fibromyalgia-and-interleukin-1-B-in-rheumatoid-arthritis-2015
  5. Mast cells, glia and neuroinflammation – partners in crime? – 2013
  6. Opioid-induced Central Immune Signaling – Implications for Opioid Analgesia – 2015
  7. Microglia in the spinal cord and neuropathic pain – 2016
  8. Modulation of microglia can attenuate neuropathic pain symptoms and enhance morphine effectiveness – 2008
  9. Neuropeptides and Microglial Activation in Inflammation, Pain, and Neurodegenerative Diseases – 2017


Neuroinflammation – Epigenetics

  1. the-emerging-field-of-neuroepigenetics-2013
  2. epigenetic-mechanisms-of-chronic-pain-2015
  3. epigenetic-regulation-of-chronic-pain-2015
  4. epigenetic-regulation-of-persistent-pain-2015
  5. targeting-epigenetic-mechanisms-for-chronic-pain-a-valid-approach-for-the-development-of-novel-therapeutics-pubmed-ncbi
  6. targeting-epigenetic-mechanisms-for-pain-relief-pubmed-ncbi
  7. telomeres-and-epigenetics-potential-relevance-to-chronic-pain-2012
  8. could-targeting-epigenetic-processes-relieve-chronic-pain-states-pubmed-ncbi


Neuroinflammation – Intestinal Epithelial Barrier, Leaky Gut and the Microbiome

  1. Breaking down the barriers – the gut microbiome, intestinal permeability and stress-related psychiatric disorders – 2015
  2. Intestinal mucosal barrier function in health and disease – 2009
  3. Altered intestinal permeability in patients with primary fibromyalgia and in patients with complex regional pain syndrome – 2008
  4. The Brain-Gut-Microbiome Axis – 2018
  5. Gut-Brain Psychology – Rethinking Psychology From the Microbiota–Gut–Brain Axis – 2018
  6. Microbiome—The Missing Link in the Gut-Brain Axis – Focus on Its Role in Gastrointestinal and Mental Health – 2018
  7. Gut-microbiota-brain axis and effect on neuropsychiatric disorders with suspected immune dysregulation. – 2015
  8. Microbiome, probiotics and neurodegenerative diseases: deciphering the gut brain axis. – PubMed – NCBI – 2017
  9. Gut microbiome in health and disease – linking the microbiome- gut-brain axis and environmental factors in the pathogenesis of systemic and neurodegenerative diseases – 2016
  10. A Review of Traumatic Brain Injury and the Gut Microbiome – Insights into Novel Mechanisms of Secondary Brain Injury and Promising Targets for Neuroprotection – 2018
  11. The bidirectional gut-brain-microbiota axis as a potential nexus between traumatic brain injury, inflammation, and disease. – PubMed – NCBI
  12. Microbiome-microglia connections via the gut-brain axis. – PubMed – NCBI


Neuroinflammation – Epigenetics, Acute Pain Transition to Chronic Pain

  1. epigenetics-and-the-transition-from-acute-to-chronic-pain-2012
  2. epigenetics-in-
  3. < a href=”https://accurateclinic.com/wp-content/uploads/2016/03/Epigenetics-of-chronic-pain-after-thoracic-surgery.-PubMed-NCBI-2.pdf”>epigenetics-of-chronic-pain-after-thoracic-surgery-pubmed-ncbi


Neuroinflammation – Epigenetics, Opioids

  1. chronic-opioid-use-is-associated-with-increased-dna-methylation-correlating-with-increased-clinical-pain-pubmed-ncbi
  2. epigenetic-regulation-of-opioid-induced-hyperalgesia-dependence-and-tolerance-in-mice-2013
  3. epigenetic-regulation-of-spinal-cord-gene-expression-controls-opioid-induced-hyperalgesia-2014-no-highlights

Neuroinflammation – Opioid Tolerance

  1. Opioid-induced Central Immune Signaling – Implications for Opioid Analgesia – 2015
  2. Microglia in the spinal cord and neuropathic pain – 2016
  3. Modulation of microglia can attenuate neuropathic pain symptoms and enhance morphine effectiveness – 2008
  4. Neuroimmune activation and neuroinflammation in chronic pain and opioid tolerance:hyperalgesia. – PubMed – NCBI – 2004
  5. Role of Neuroinflammation in Opioid Tolerance: Translational Evidence from Human-to-Rodent Studies. – PubMed – NCBI – 2018

Neuroinflammation – Addiction & Reward Deficiency Syndrome (RDS)

Glial and neuroinflammatory targets for treating substance use disorders – 2017

Neuroinflammation – Pain

  1. Activated mast cells infiltrate in close proximity to enteric nerves in diarrhea-predominant irritable bowel syndrome. – 2003
  2. An Integrative Approach to Neuroinflammation in Psychiatric disorders and Neuropathic Pain – 2018 Neuroinflammation and Central Sensitization in Chronic and Widespread Pain. – PubMed – NCBI
  3. A-Pharmacological-Rationale-to-Reduce-the-Incidence-of-Opioid-Induced-Tolerance-and-Hyperalgesia-A-Review-2018
  4. The Uses of Low-Dose Naltrexone in Clinical Practice
  5. A Pharmacological Rationale to Reduce the Incidence of Opioid Induced Tolerance and Hyperalgesia – A Review – 2018
  6. Alternatives to Opioids in the Pharmacologic Management of Chronic Pain Syndromes – A Narrative Review of Randomized, Controlled, and Blinded Clinical Trials – 2017


Neuroinflammation – Treatment Overviews

  1. An Integrative Approach to Neuroinflammation in Psychiatric disorders and Neuropathic Pain – 2018 Neuroinflammation and Central Sensitization in Chronic and Widespread Pain. – PubMed – NCBI
  2. A-Pharmacological-Rationale-to-Reduce-the-Incidence-of-Opioid-Induced-Tolerance-and-Hyperalgesia-A-Review-2018
  3. The Uses of Low-Dose Naltrexone in Clinical Practice
  4. A Pharmacological Rationale to Reduce the Incidence of Opioid Induced Tolerance and Hyperalgesia – A Review – 2018
  5. Alternatives to Opioids in the Pharmacologic Management of Chronic Pain Syndromes – A Narrative Review of Randomized, Controlled, and Blinded Cli
    nical Trials – 2017

Neuroinflammation Treatment – Minocycline

Resolving Inflammation

  1. Vagus nerve controls resolution and pro-resolving mediators of inflammation – 2014
  2. The Resolution Code of Acute Inflammation – Novel Pro-Resolving Lipid Mediators in Resolution – 2015
  3. Resolvins in inflammation: emergence of the pro-resolving superfamily of mediators. – PubMed – NCBI – 2018
  4. Resolvins and protectins – mediating solutions to inflammation – 2009
  5. Resolvins and inflammatory pain – 2011
  6. Resolution of inflammation – an integrated view – 2013
  7. Protectins and maresins – New pro-resolving families of mediators in acute inflammation and resolution bioactive metabolome – 2014
  8. Proresolving lipid mediators and mechanisms in the resolution of acute inflammation – 2014
  9. Novel Pro-Resolving Lipid Mediators in Inflammation Are Leads for Resolution Physiology – 2014
  10. Novel Anti-Inflammatory — Pro-Resolving Mediators and Their Receptors – 2011
  11. Lipid Mediators in the Resolution of Inflammation – 2015
  12. PPARγ activation ameliorates postoperative cognitive decline probably through suppressing hippocampal neuroinflammation in aged mice. – PubMed – NCBI – 2017
  13. Postoperative cognitive dysfunction in the aged: the collision of neuroinflammaging with perioperative neuroinflammation. – PubMed – NCBI – 2018
  14. The Role of Neuroinflammation in Postoperative Cognitive Dysfunction – Moving From Hypothesis to Treatment – 2018
  15. Treating inflammation and infection in the 21st century: new hints from decoding resolution mediators and mechanisms – 2017
  16. Structural Elucidation and Physiologic Functions of Specialized Pro-Resolving Mediators and Their Receptors – 2017
  17. LPS is a Switch for Inflammation in the Gut and Beyond
  18. Identification of specialized pro-resolving mediator clusters from healthy adults after intravenous low-dose endotoxin and omega-3 supplementation – a methodological validation – 2018
  19. The Protectin Family of Specialized Pro-resolving Mediators – Potent Immunoresolvents Enabling Innovative Approaches to Target Obesity and Diabetes – 2018
  20. Protectins and Maresins – New Pro-Resolving Families of Mediators in Acute Inflammation and Resolution Bioactive Metabolome – 2014
  21. Functional Metabolomics Reveals Novel Active Products in the DHA Metabolome – 2012

Emphasis on Education


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