Melatonin reduces the severity of experimental amoebiasis

The effect of melatonin was investigated in models of experimental amoebiasis in hamsters and rats by evaluating the area of necrosis induced by E. histolytica. The activity of melatonin on the interactions between leukocytes and amoebae was determined by examining leukophagocytosis. For in vitro tests, polymorphonuclear and mononuclear human blood leucocytes were incubated with E. histolytica trophozoites.The areas of amoebic necrosis were significantly reduced in animals treated with melatonin. Melatonin treatment increased leukophagocytosis but was associated with a greater number of dead amoebae.These results suggest that melatonin may play a beneficial role in the control of amoebic lesions, raising the possibility that this drug may be used as an adjuvant in anti-amoebic therapy.Melatonin [N-acetyl-5-methoxytryptamine] is an indoleamine synthesised from tryptophan. The physiological properties of melatonin are not limited to its neuroendocrine role in controlling circadian rhythms [1]; several other actions have been discovered. Melatonin has been shown to increase innate and acquired immunity [2], to activate the bone marrow and lymph nodes [3], to enhance NK cell activity [4,5] and antibody-dependent cell cytotoxicity [6], to increase T cell proliferation in vivo and in vitro [7,8] and to activate monocytes [9,10] and neutrophils [11].Melatonin can stimulate innate immune cells, primarily leukocytes, which represents an important anti-bacterial mechanism [12,13]; however, very little is known about its influence on protozoan infections.Entamoeba histolytica is an enteric protozoan parasite that infects 500 million people, causes amoebiasis in 50 million and kills 100 000 individuals annually, thus constituting a serious health public problem [14]. The disease is widely distributed worldwide, but its incidence is highest in places with insufficient basic sanitation. Several aspects of this host parasite relationship, such as parasite virulence and host suscep