Leukotriene E4

Leukotriene E₄

Names
Systematic IUPAC name (5S,6R,7E,9E,11Z,14Z)-6-({(2R)-2-Amino-2-carboxyethyl}sulfanyl)-5-hydroxyicosa-7,9,11,14-tetraenoic acid
Identifiers
CAS Number	75715-89-8^Y
3D model (JSmol)	Interactive image
Abbreviations	LTE4
ChEBI	CHEBI:15650
ChemSpider	4444402
KEGG	C05952
MeSH	Leukotriene+E4
PubChem CID	5280749
UNII	8EYT8ATL7G^Y
CompTox Dashboard (EPA)	DTXSID20897510
InChI InChI=1S/C23H37NO5S/c1-2-3-4-5-6-7-8-9-10-11-12-13-16-21(30-18-19(24)23(28)29)20(25)15-14-17-22(26)27/h6-7,9-13,16,19-21,25H,2-5,8,14-15,17-18,24H2,1H3,(H,26,27)(H,28,29)/b7-6-,10-9-,12-11+,16-13+/t19?,20-,21+/m0/s1 Key: OTZRAYGBFWZKMX-MPWKMEBCSA-N
SMILES CCCCC/C=C\C/C=C\C=C\C=C\[C@H]([C@H](CCCC(=O)O)O)SCC(C(=O)O)N
Properties
Chemical formula	C23H37NO5S
Molar mass	439.61 g·mol^−1
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa). Infobox references

Leukotriene E₄ (LTE₄) is a cysteinyl leukotriene involved in inflammation. It is known to be produced by several types of white blood cells, including eosinophils, mast cells, tissue macrophages, and basophils, and recently was also found to be produced by platelets adhering to neutrophils.^[1] It is formed from the sequential conversion of LTC₄ to LTD₄ and then to LTE₄, which is the final and most stable cysteinyl leukotriene.^[2] Compared to the short half lives of LTC₄ and LTD₄, LTE₄ is relatively stable and accumulates in breath condensation, in plasma, and in urine, making it the dominant cysteinyl leukotriene detected in biologic fluids.^[3] Therefore, measurements of LTE₄, especially in the urine, are commonly monitored in clinical research studies.

Increased production and excretion of LTE₄ has been linked to several respiratory diseases, and urinary LTE₄ levels are increased during severe asthma attacks and are especially high in people with aspirin-exacerbated respiratory disease.^[4]

Studies have suggested that LTE₄ works through its own distinct receptor, and although one has not yet been discovered, research is ongoing to isolate and characterize an LTE₄-specific receptor.^[5][6]

Eicosanoid synthesis (leukotrienes at right)

References

1. Laidlaw TM, Kidder MS, Bhattacharyya N, Xing W, Shen S, Milne GL, Castells MC, Chhay H, Boyce JA (2012). "Cysteinyl leukotriene overproduction in aspirin exacerbated respiratory disease is driven by platelet-adherent leukocytes". Blood. 119 (16): 3790–3798. doi:10.1182/blood-2011-10-384826. PMC 3335383. PMID 22262771.
2. Lee CW, Lewis RA, Corey EJ, Austen KF (1983). "Conversion of leukotriene D4 to leukotriene E4 by a dipeptidase released from the specific granule of human polymorphonuclear leucocytes". Immunology. 48 (1): 27–35. PMC 1453997. PMID 6293969.
3. Sala A, Voelkel N, Maclouf J, Murphy RC (1990). "Leukotriene E4 elimination and metabolism in normal human subjects". J Biol Chem. 265 (35): 21771–21778. doi:10.1016/S0021-9258(18)45807-3. hdl:2434/180227. PMID 2174886.
4. Lee TH, Christie PE (1993). "Leukotrienes and aspirin induced asthma". Thorax. 48 (12): 1189–1190. doi:10.1136/thx.48.12.1189. PMC 464963. PMID 8303620.
5. Maekawa A, Kanaoka Y, Xing W; Kanaoka; Xing; Austen (2008). "Functional recognition of a distinct receptor preferential for leukotriene E4 in mice lacking the cysteinyl leukotriene 1 and 2 receptors". Proc. Natl. Acad. Sci. USA. 105 (43): 16695–16700. Bibcode:2008PNAS..10516695M. doi:10.1073/pnas.0808993105. PMC 2575482. PMID 18931305.
6. Paruchuri, S; Tashimo, H; Feng, C; Maekawa, A; Xing, W; Jiang, Y; Kanaoka, Y; Conley, P; Boyce, JA (2009). "Leukotriene E4-induced pulmonary inflammation is mediated by the P2Y12 receptor". The Journal of Experimental Medicine. 206 (11): 2543–55. doi:10.1084/jem.20091240. PMC 2768854. PMID 19822647.