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. 2021 Jun 11;11(6):552–562. doi: 10.1016/j.jtcme.2021.06.001

Table 5.

Mediators of inflammation involved in the inflammatory symptoms most affected by Kan Jang (adapted from Panossian & Wikman, 2012).17

Cell Mediator Target tissue, cells Effect Inflammatory symptoms
must cell, eosinophils, histamine
PAF leukotrienes
Vessels Vascular permeability increases
Vasodilatation-blood stream decreases
Leukocyte extravasation increases
Sneezing edema
reddening's/warming
Neurons Activation of nociceptors Pain
Airway epithelium Airway sensory nerve endings Cough
macrophages IL-1,
IL-6,
TNFa,
Brain fatigue,
headache,
malaise,
anorexia
sleep disturbance
Hypothalamus Interact with the vagus nerve endings to signal the temperature control center fever
prostaglandins Skin blood vessels Vasoconstriction chilliness
Skeletal muscle Effects on peripheral pain receptors muscle ache, pain
Muscles Catabolism weight loss
Leukotrienes Fat tissue Lipolysis
Neutrophils
Monocytes
Chemotaxis, phagocytosis. nasal discharge
mucous secretion
PAF Bacteria, virus Phagocytosis
Immune system Immune defense all symptoms
prostaglandins bradykinin Nerve endings in the airway Pain mediated by the cranial nerves Supplying the nasopharynx and pharynx. sore throat
blood plasma globulins Bradykinin large veins in the nasal epithelium Vasodilation nasal congestion