| REVIEW ARTICLE |
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| Year : 2015 | Volume
: 8
| Issue : 1 | Page : 38-51 |
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Prostanoids and parasitic diseases
Amany M Eida MD
Department of Parasitology, Faculty of Medicine, Suez Canal University, Ismailia, Egypt
Correspondence Address:
Amany M Eida
Department of Parasitology, Faculty of Medicine, Suez Canal University, 41522, Ismailia
Egypt
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/1687-7942.163408
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The eicosanoid family includes prostanoids, leukotrienes, and other oxygenated derivatives. Prostanoids are a major class of the eicosanoid family derived from metabolism of arachidonic acid by the action of cyclooxygenase enzymes (COX). They are further subdivided into three main groups: prostaglandins (PGs), thromboxanes (TXs), and prostacyclins. PGs were first discovered as uterotonic substances in human seminal fluid in 1930. In the late 1950s to mid-1960s, their structures were studied and identified as being derived from unsaturated fatty acids. Prostanoids are produced by many cell types such as vascular endothelium, leukocytes, and the pathogens themselves. Prostanoid production is controlled by expression of different enzymes engaged in prostanoid biosynthesis, and by the distribution of different specific prostanoid synthases within those cells that determine their effect on the immune system. The production of prostanoids differs from one cell type to another; for example, dendritic cells predominately produce PG E 2 (PGE 2 ) and TXA 2 , whereas mastocytes produce PGD 2 . All inflammatory cells, including monocytes/macrophages, and neutrophils, are the main source of COX metabolites.
Produced in response to various physiological and pathological stimuli, PGs are noted as key participants in autoimmune immunopathology, infectious diseases, and cancer. Other reports have shown that PGIs are formed by endothelial and smooth muscle cells, and TXAs are formed by platelets and lungs; PGI 2 and some other PGs are produced by interactions between cells using enzymes in adjacent cells; for example, platelet-produced PGH 2 is converted to PGI 2 in the vascular epithelium.
PGs secreted in the saliva of blood-sucking arthropods increase local blood flow and maintain the supply for feeding; they were also reported to increase immune suppression, allowing prolongation of attachment by ticks. Progressive studies demonstrated that, besides insects, pathogenic fungi, protozoa, and parasitic worms produce PGs.
This review focuses on induced efforts to study prostanoids and their relation to different parasitic diseases.
Abbreviations
AA: Arachidonic acid; COXs: Cyclooxygenase enzymes; CyPG: Cyclopentanone; DC: Dendritic cell; GST: Glutathione-S-transferase; GA: Glycyrrhizic acid; MAP: Mitogen-activated protein; MIF: Macrophage migration inhibitory factor; NO: Nitric oxide; PBMC: Peripheral blood mononuclear cells; PG: Prostaglandin; PG12: Prostacyclin; PGE2: Prostaglandin E2; PL: Phospholipase; PPAR: Peroxisome proliferator-activated receptors; TGF: Transforming growth factor; TNF: Tumor necrosis factor; TP: Thromboxan receptor; TX: Thromboxane. |
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