Mast cell

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A mast cell is a type of white blood cell that protects the body from immune threats by promoting inflammation[1]. Mast cells are present in all tissues. They are most commonly known for their role in the immune system of mucosal membranes; however, they are necessary in maintaining basic human health and defending against pathogens.

When a mast cell encounters a perceived immune threat, pro-inflammatory mediators are released through a process known as degranulation. Some anti-inflammatory mediators may include histamine, cytokines, proteases, or heparin[1].

Mast cell activation[edit | edit source]

Degranulation[edit | edit source]

Mast cells can become activated when they encounter a foreign substance. A cascade response allows for degranulation to begin and a subsequent release of inflammatory granules into the bloodstream.[1]

Mechanisms of inhibition[edit | edit source]

There are several proposed supplements or treatments that might grant temporary mast cell degranulation inhibition:

Antioxidants: these are substances that are considered to remove potentially harmful reactive oxygen species from the body. Vitamin C, vitamin A, vitamin E, and beta-carotene are examples of antioxidants. The properties of such antioxidants have been noted to be capable of reducing blood histamine levels[2]. The exact mechanisms that cause blood histamine levels to decrease are still unknown. However, antioxidants have been noted to be capable of inhibiting mast cell production and altering the enzymes that form (diamine oxidase) or breakdown (histidine decarboxylase) histidine.

Phototherapy: UVA and UVA1 phototherapy has been observed to significantly inhibit histamine release from mast cells and other white blood cells.[3]

Infection[edit | edit source]

Past findings have suggested that mast cell activation due to a viral infection may play part in initiating autoimmune disease. The Coxsackievirus infection has been observed to up-regulate toll-like receptor 4 (TLR4) on mast cells in mice, immediately following the period of infection.[4]TLR4 up-regulation can have negative consequences on the immune system because TLR4 activation indirectly activates the innate immune system and the inflammatory response system.

Gastrointestinal Tract and the Nervous system[edit | edit source]

Mast cells are found within the nervous system and are capable of crossing the blood-brain barrier (this separates blood from the central nervous system). The gastrointestinal tract and the brain are capable of communicating through the blood brain barrier, also known as the gut-brain axis (GBA). Exchange of information between the central (brain) and peripheral (gut) nervous systems ensures that the stomach and intestines are communicating with the brain. "Immune activation, intestinal permeability, enteric reflex, and entero-endocrine signaling" are all influenced by the GBA. Therefore mast cells are likely a type of cell that indirectly affect neurological functioning when the gut is inflammed[5].

Role in human disease[edit | edit source]

Mast cell activation disorder[edit | edit source]

See full article: Mast cell activation disorder

Mast cell activation disorder (MCAD) is a condition in which mast cells are over-responsive to various environmental triggers. When mast cells are over-responsive the result can be an increase in the release histamine and other inflammatory molecules. Excessive inflammation can result from such a condition.

MCAD is often found in patients with Ehlers-Danlos syndrome (EDS) and postural orthostatic tachycardia syndrome (POTS), a form of orthostatic intolerance,[6] two conditions commonly co-morbid with ME. The overlap between EDS, POTS, and MCAD is thought to be due to increased tryptase production owing to an extra copy of a gene called TPSAB [7].

MCAD should be distinguished from mastocytosis, a genetic disorder causing excessive production of mast cells.

Myalgic encephalomyelitis[edit | edit source]

Individuals diagnosed with moderate to severe ME have been noted to have higher amounts of dysfunctional mast cells in circulation[8].

Fibromyalgia[edit | edit source]

Over expression of mast cells has been observed in the skin of patients with fibromyalgia.[9]

Notable studies[edit | edit source]

Learn more[edit | edit source]

See also[edit | edit source]

References[edit | edit source]

  1. 1.0 1.1 1.2 "Mast cell: a multifunctional master cell". 2016. 
  2. Tettamanti, L (2018). "Different signals induce mast cell inflammatory activity: inhibitory effect of Vitamin E". J biol regul homeost agents. 
  3. Kronauer, C (2007). "Influence of UVB, UVA and UVA1 Irradiation on Histamine Release from Human Basophils and Mast Cells In Vitro in the Presence and Absence of Antioxidants". Photochemistry and Photobiology. 
  4. Fairweather, D (2005). "Viruses as adjuvants for autoimmunity: evidence from Coxsackievirus-induced myocarditis". Rev Med Virol. 
  5. "The gut-brain axis: interactions between enteric microbiota, central and enteric nervous systems". Ann Gasteroenterol. 2015. 
  6. Milner, Joshua, Dr. "Research Update: POTS, EDS, MCAS Genetics." 2015 Dysautonomia International Conference & CME. Washington DC. Dysautonomia International Research Update: POTS, EDS, MCAS Genetics. Web. <>
  7. Cheung, Ingrid (February 2015). "A New Disease Cluster: Mast Cell Activation Syndrome, Postural Orthostatic Tachycardia Syndrome, and Ehlers-Danlos Syndrome". The Journal of Allergy and Clinical Immunology. 
  8. 8.0 8.1 Nguyen, T.; Johnston, S.; Chacko, A.; Gibson, D.; Cepon, J.; Smith, D.; Staines, D.; Marshall-Gradisnik, S. (2017), "Novel characterisation of mast cell phenotypes from peripheral blood mononuclear cells in chronic fatigue syndrome/myalgic encephalomyelitis patients", Asian Pac J Allergy Immunol, 35 (2): 75-81, doi:10.12932/AP0771 
  9. Ang, DC (2015). "Mast Cell Stabilizer (Ketotifen) in Fibromyalgia: Phase 1 Randomized Controlled Clinical Trial". The clinical journal of pain. 

The information provided at this site is not intended to diagnose or treat any illness.

From MEpedia, a crowd-sourced encyclopedia of ME and CFS science and history