Leukotrienes are a family of eicosanoid inflammatory mediators produced in leukocytes by the oxidation of arachidonic acid by the enzyme arachidonate 5-lipoxygenase.

Leukotrienes are present in leukocytes, and other immune cells.

Leukotrienes use lipid signaling to convey autocrine signaling and paracrine signaling to regulate immune responses.

Leukotriene production is usually accompanied by the production of histamine and prostaglandins, which are inflammatory mediators.

Leukotrienes trigger contractions in the smooth muscles lining the bronchioles.

Overproduction of leukotrienes are a major cause of inflammation in asthma and allergic rhinitis.

Leukotriene antagonists are used to treat these disorders.

LTC4, LTD4, LTE4 and LTF4, called cysteinyl leukotrienes due to the presence of the amino acid cysteine in their structure, and make up the slow-reacting substance of anaphylaxis (SRS-A).

Leukotriene B4 is synthesized in vivo from LTA4 by the enzyme LTA4 hydrolase

Leukotriene B4 has at its primary function is to recruit neutrophils to areas of tissue damage.

Leukotriene B4 helps promote the production of inflammatory cytokines by various immune cells.

Leukotrienes are synthesized from arachidonic acid by arachidonate 5-lipoxygenase.

Prostaglandins and leukotrienes enhance vascular permeability and recruit leukocytes.

The lipoxygenase pathway is active in leukocytes and other immunocompetent cells, including mast cells, eosinophils, neutrophils, monocytes, and basophils.

The cysteinyl-leukotrienes act at their cell-surface receptors CysLT1 and CysLT2 on target cells to contract bronchial and vascular smooth muscle, to increase permeability of small blood vessels, to enhance secretion of mucus in the airway and gut, and to recruit leukocytes to sites of inflammation.

Both LTB4 and the cysteinyl-leukotrienes (LTC4, LTD4, LTE4) are partly degraded in local tissues, and ultimately become inactive metabolites in the liver.

Leukotrienes are involved in asthmatic and allergic reactions and act to sustain inflammatory reactions.

Several leukotriene receptor antagonists such as montelukast and zafirlukast are used to treat asthma.

Important agents in the inflammatory response, with some having a chemotactic effect on migrating neutrophils.

Leukotrienes associated with bronchoconstriction and increased vascular permeability.

Contribute to the pathophysiology of asthma, especially in patients with aspirin-exacerbated respiratory disease and cause or potentiate the following symptoms:

airflow obstruction

increased secretion of mucus

mucosal accumulation


infiltration of inflammatory cells in the airway wall

Cysteinyl leukotriene receptors CYSLTR1 and CYSLTR2 are present on mast cells, eosinophil, and endothelial cells, and can stimulate proinflammatory activities such as endothelial cell adherence and chemokine production by mast cells.

Cysteinyl leukotriene receptors induce asthma and other inflammatory disorders, thereby reducing the airflow to the alveoli.

The levels of cysteinyl leukotrienes correlate with disease severity.

Cysteinyl leukotrienes may also play a role in adverse drug reactions in general and in contrast medium induced adverse reactions in particular.

In excess, the cysteinyl leukotrienes can induce anaphylactic shock.

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