Inflammation

Inflammation is the body's main natural defense mechanism in response to injury and infection. When something injures or infects the body, the immune system kicks into gear, and this activation is called inflammation. Immune activation can include intracellular, cellular, and extracellular components. Immune activation can be limited to a specific tissue or expand to the blood or beyond.

In some cases, chronic inflammation can develop due to pathogens that the body cannot break down, foreign bodies that remain in the system, or abnormal immune system responses. Some types of chronic inflammation produce symptoms such as fatigue, mouth ulcers, chest pain, abdominal pain, fever, rash, and joint pain.

Classical inflammation vs. Neuroinflammation

The original ancient Greco-Roman definition of inflammation relied on four cardinal signs: swelling, redness, heat, and pain. Over time, the signs of swelling, redness, and heat were understood to be due to blood infiltrating the inflamed tissue. Later research clarified that the blood infiltrating the inflamed tissue brought with it immune cells that worked to fight the infection or repair the injury. This understanding forms the basis of classical inflammation.

More recently, scientific research has elucidated the early stages of immune activation, before blood infiltrates the inflamed tissue. In the early stage of immune activation, immune cells such as tissue-resident macrophages patrol each body tissue looking for infection or injury. When an infection or injury is found, these immune cells activate and try to fix the problem. If they are unable to fix the problem on their own, they secrete cytokines to attract immune cells from the blood to help out. Some tissues, such as the brain, eyes, and testes, have barriers that resist infiltrating immune cells from the blood. These “immune-privileged” tissues instead rely primarily on activation of the tissue-resident macrophages to address any infection or injury. This understanding forms the basis of neuroinflammation. Unlike classical inflammation, neuroinflammation does not imply infiltration of tissues by blood-borne immune cells.

Notable studies

• 2017, The Neuroinflammatory Etiopathology of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) - (Full text)

See also

• Immune system
• Neuroinflammation
• Brain
• List of abnormal findings in chronic fatigue syndrome and myalgic encephalomyelitis

myalgic encephalomyelitis (M.E.) - A disease often marked by neurological symptoms, but fatigue is sometimes a symptom as well. Some diagnostic criteria distinguish it from chronic fatigue syndrome, while other diagnostic criteria consider it to be a synonym for chronic fatigue syndrome. A defining characteristic of ME is post-exertional malaise (PEM), or post-exertional neuroimmune exhaustion (PENE), which is a notable exacerbation of symptoms brought on by small exertions. PEM can last for days or weeks. Symptoms can include cognitive impairments, muscle pain (myalgia), trouble remaining upright (orthostatic intolerance), sleep abnormalities, and gastro-intestinal impairments, among others. An estimated 25% of those suffering from ME are housebound or bedbound. The World Health Organization (WHO) classifies ME as a neurological disease.

See myalgic encephalomyelitis.

See chronic fatigue syndrome.