What is the Mechanism of Mediated Hyper Sensitivity (Anaphylaxis)?


The first step in the development of Anaphylactic or Type I hypersensitivity is sensitization.

Exposure to allergen for the first time does not generate any clinical symptoms, but initiates the biosynthesis and release of humoral IgE Abs.

Generally basophils are found in circulation and mast cells are distributed in connective tissues, including capillaries. Both basophils and mast cells contain different pharmacologically potent components in vesicles.


Since mast cells and basophils are having receptors for FC region of IgE Abs, they bind to the membranes of both mast cells and basophils.

In subsequent exposures to the same allergen, the allergen molecule interacts with the IgE antibodies bound to the mast cells and basophils. The antigen antibody complex then triggers the release of pharmacological substances from basophils and mast cells.

The released pharmacological substances responsible for Type I hypersensitivity reactions are histamines, certonins, leucotrines, prostaglandins, eosinophil chemotactic factor of anaphylaxis, (ECFA), platelet activating factor, heparin, kinin, etc. The released biological products induce characteristic clinical symptoms of Type I hypersensitivity in atopic persons.



Histamine is the abundant and fast acting substance of all pharmacological substances.

It induces smooth muscle contractions, release of mucus, vasodilation and increased capillary permeability. The target areas for the action of histamines are respiratory tract, uterus etc.

Action of histamine on respiratory tract results in suffocation, leading to anoxic conditions.

Under the influence of histamine, uterus shows inappropriate contractions and these contractions may cause abortion in pregnant women. Histamines release also causes less toxic conditions for instance edema (excess fluid accumulation) in the tissue due to increased capillary permeability.


Extensive loss of fluid in the tissue due to vasodilatation may cause circulatory shock through reduced supply of oxygen and nutrients.

Serotonin (5-Hydroxytryptamine)

In addition to histamine, serotonin is another substance that acts as a chemoeffector of smooth muscles and it also increases the respiratory rate, heart rate and causes vasoconstriction leading to a raise in blood pressure.

It appears to have little effect on vascular permeability but stimulates further release of histamine.



These are slow reacting substances of anaphylaxis and are very potent muscle spasmogens.

They act as chemotactic substances for neutrophils, and eosinophils to attract them towards the site of reaction.

Other actions of leucotrines are similar to the actions of histamine and serotonin but at a slower level.


Prostaglandins (PGS):

They are a family of complex lipids with a wide range of activities. They act as vasodilators, brancho constrictors and regulators of blood coagulation.

Platelet Activating Factors (PAFS)

It provokes aggregation of platelets and release of their contents, especially serotonin.

Eosinophil Chemotactic Factor (ECF)

ECF attracts eosinophils and neutrophils to the site of mast cell degranulation, to prevent their movement from the site of inflammation and to desensitize them. This reaction overturns some of the deleterious effects of anaphylaxis.

Other Biologically Active Factors:

As the mast cell granules are modified lysosomes they contain some hydrolytic enzymes. Heparin is one of the substances released from the mast cells and basophils during allergic reactions.

Since it is anticoagulant in character, coagulation of blood in anaphylactic condition may be stopped or delayed.

Kenin is another substance released in small quantities. It is a small peptide and it enhances capillary permeability, mucous secretions and leucocyte migration from blood vessels in to the tissues.

The collective action of all the substances released from mast cells and basophils are responsible for the cause of anaphylactic reactions.

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