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The cultured and wild specimens of the Nile tilapia (Oreochromis niloticus) are often infected by different hazardous as helminths; protozoa and arthropod which cause various degrees of diseases in such fish. The aim of this study was to record the most common protozoan parasites in the Nile tilapia in Egypt, and also assessment of the immunological changes through analyzing two genes (Tumor Necrosis Factor alpha, TNF-α; and Interlukin-1β, IL- 1β) in the infected fishes using qRT-PCR. Therefore, each fish individual was examined carefully, and smears were prepared from each organ; stained with Giemsa dye and examined under a light microscope. qRT-PCR was performed on infected tissues (skin and gills) by various collected parasites. Four trichodinid species (Trichodinella heterodentata, T. centrostrigeata, T. epizootica, Paratrichodina Africana,) were isolated and identified; also two Myxobolus spp. (M. tilapiae and M. heterosporous) were fully described. In skin, TNF-α in M. tilapiae and mixed groups were nearly similar and were significantly higher than Trichodina spp. group. IL-1β of M. tilapiae group was significantly lower than that of the mixed group; Trichodina spp. and control groups. In gills, TNF-α of the mixed group showed the significantly highest value. IL-1β was nearly same in all groups. We conclude that the skin is nearly higher in upregulation of the two studied genes comparing to the gills analysis, since it is considered as the first barrier in fish and contains many immunological defined cells.


Nile tilapia Tumor Necrosis Factor alpha Interlukin-1β Real-time Polymerase Chain Reaction.

Article Details

Author Biography

Marwa Mohamed Attia, Department of Parasitology, Faculty of Veterinary Medicine, Cairo University, 12211 Giza, Egypt.

Parasitology department
How to Cite
YOUNIS, N. A., Attia, M. M., & SALEH, N. M. (2021). Analysis of TNF alpha and Interlukin-1β genes in Oreochromis niloticus: inflammatory responses induced by Myxobolus spp. and Trichodina spp. Iranian Journal of Ichthyology, 8(1), 30–40.


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