| ORIGINAL ARTICLE |
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| Year : 2019 | Volume
: 2
| Issue : 2 | Page : 64-68 |
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Relationship between parasitic infection of Toxoplasma gondii, IL-2, TNF-α tryptophan and CD4+ count
Mathew Folaranmi Olaniyan1, Temitayo Afolabi2, Nwachi Ogbona Idume3
1 Department of Medical Laboratory Science, Edo University, Iyamho, Edo, Nigeria
2 Department of Medical Laboratory Science, Achievers University, Owo, Ondo, Nigeria
3 Department of Education, Medical Laboratory Science Council of Nigeria, Abuja, Nigeria
Correspondence Address:
Mathew Folaranmi Olaniyan
Department of Medical Laboratory Science, Achievers University, Owo, Ondo
Nigeria
 Source of Support: None, Conflict of Interest: None
DOI: 10.4103/JNSM.JNSM_50_18
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Study Background: Toxoplasma gondii a protozoan and zoonotic infection can stimulate innate and adaptive immune responses. Aims and Objectives: This work was designed to determine relationship between parasitic infection of T. gondii, interleukin-2 (IL-2), tumor necrosis factor-alpha (TNF-α), and Tryptophan and CD4+ count. Materials and Methods: A total of 150 individuals aged 21–73 years (male: 100 and female: 50) were recruited from Saki-West, Saki-East, and ATISBO local governments of Nigeria. Plasma TNF-α, IL-2, Tryptophan, anti-hepatitis C virus (anti-HCV), hepatitis B surface antigen (HBsAg), anti-HIV, Plasmodium, and T. gondii infections were determined in each of the subjects. The results were used to group the subjects into: Control (n = 104; individuals not infected with T. gondii noninfected, Plasmodium spp., HIV or HCV); T. gondii mono-infected patients (n = 9) and patients with T. gondii co-infection with Plasmodium spp., HIV, HBV, or HCV. Plasma TNF-α, IL-2, anti-HCV, HBsAg, and anti-HIV were determined by enzyme-Linked Immunosorbent Assay. Plasmodium spp., was identified by thick blood film-Giemsa staining technique. Plasma tryptophan was determined by fluorometry. Results: Of 150 subjects recruited for the work, the results obtained showed a frequency of occurrence of 69.3% (104) T. gondii noninfected control not infected with Plasmodium spp., HIV, HBV, and HCV; 8.0% (9) T. gondii-infected patients not infected with Plasmodium spp., HIV and HCV; 22% (33) were infected with at least one of the Plasmodium spp., HIV, HBV, and HCV; 2.7% (4) T. gondii patients co-infected with at least one of the Plasmodium spp., HIV, HBV, and HCV. There was a significant decrease in plasma tryptophan in T. gondii mono- and co-infection including T. gondii noninfected individuals but infected with at least Plasmodium spp., HIV, HBV, and HCV compared with the control [P < 0.05]. There was a significant decrease in CD4 count in T. gondii noninfected individuals but infected with at least one of the Plasmodium spp., HIV, HBV, and HCV and T. gondii co-infection compared with T. gondii mono-infection; controls and also in T. gondii noninfected individuals but infected with at least one of the Plasmodium spp., HIV, HBV, and HCV compared to T. gondii confection (P < 0.05). There was a significant increase in plasma TNF-α in T. gondii mono-infected patients compared with the controls; T. gondii noninfected individuals but infected with at least one of the Plasmodium spp., HIV, HBV, and HCV compared to controls; T. gondii confection compared to controls; T. gondii mono-infected patients compared to T. gondii noninfected individuals but infected with at least one of the Plasmodium spp., HIV, HBV, and HCV; T. gondii mono-infected patients compared to T. gondii co-infection and T. gondii noninfected individuals but infected with at least one of the Plasmodium spp., HIV, HBV, and HCV compared to T. gondii confection (P < 0.05). Conclusion: T. gondii and its coinfection with HIV, HCV, and HBV caused a significant immunological alterations in the plasma values of IL-2, TNF-α, Tryptophan, and blood CD4+ count.
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