Host immune responses to mono-infections of Plasmodium spp., hepatitis B virus, and Mycobacterium tuberculosis as evidenced by blood complement 3, complement 5, tumor necrosis factor-α and interleukin-10: Host immune responses to mono‑infections of Plasmodium spp., hepatitis B virus, and Mycobacterium tuberculosis

Mathew Folaranmi Olaniyan; Tolulope Busayo Ojediran; Ferdinand Uwaifo; Mufutau Mosunmade Azeez

Authors

Mathew Folaranmi Olaniyan Department of Medical Laboratory Science, Edo University, Iyamho, Nigeria
Tolulope Busayo Ojediran Department of Medical Laboratory Science, Edo University, Iyamho, Nigeria
Ferdinand Uwaifo Department of Medical Laboratory Science, Edo University, Iyamho, Nigeria
Mufutau Mosunmade Azeez Department of Medical Laboratory Science, Lead City University, Ibadan, Nigeria

Keywords:

Complements, cytokines, hepatitis B virus, Mycobacterium tuberculosis Plasmodium spp

Abstract

Background: Mono-infections of Plasmodium spp., hepatitis B virus (HBV), and Mycobacterium tuberculosis could elicit activation of complements for innate immunity leading to inflammatory responses. Objective: This work was designed to determine host immune responses to mono-infections of Plasmodium spp., HBV, and M. tuberculosis in blood complement 3 (C3), complement 5 (C5), tumor necrosis factor-alpha (TNF-α), and interleukin 10 (IL-10). Materials and Methods: Of 200 volunteers 66 Plasmodium spp., mono-infected, 28 HBV mono-infected, 12 M. tuberculosis mono-infected and 62 noninfected volunteers were studied as test and controls. ELISA was used to determine HBV, hepatitis C virus (HCV), HIV, plasma C3, C5, IL-10, and TNF-α while Plasmodium spp., was identified by Geimsha thick-film microscopy and M. tuberculosis by immunofluorescence microscopy. Results: The results obtained in the 200 volunteers showed. 69% (138) were infected with one or more of Plasmodium, HBV, HCV, HIV, and M. tuberculosis; 31% (62) were not infected; 16% (32) had co-infections of at least two of Plasmodium, HBV, HCV, HIV, and M. tuberculosis; 33% (66) were Plasmodium spp., mono-infected 14% (28) were HBV mono-infected while 6% (12) were M. tuberculosis. mono-infected. There was a significant increase in the plasma C3 in M. tuberculosis mono-infection compared with Plasmodium mono-infection; HBV mono-infection and control (P < 0.05). There was a significant increase in the plasma C3 in Plasmodium mono-infection compared with HBV mono-infection and control (P < 0.05) There was a significant decrease in the plasma C3 in the results obtained in HBV mono-infection compared with the control (P < 0.05). There was a significant increase in the plasma C5 in M. tuberculosis mono-infection compared with Plasmodium mono-infection; HBV mono-infection and control (P < 0.05). There was a significant increase in the plasma C5 in Plasmodium mono-infection compared with HBV mono-infection (P < 0.05). There was a significant decrease in plasma IL-10 and increased plasma TNF-α in Plasmodium, M. tuberculosis, and HBV mono-infections compared with the control (P < 0.05). There was also a significant increase in plasma TNF-α in M. tuberculosis mono-infection compared with Plasmodium mono-infection (P < 0.05). Conclusion: There was an evidence of host immune responses as evidenced by a significant increase in plasma C3, C5, and TNF-α including a decrease in IL-10 in mono-infections of Plasmodium spp., HBV and M. tuberculosis.

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Host immune responses to mono-infections of Plasmodium spp., hepatitis B virus, and Mycobacterium tuberculosis as evidenced by blood complement 3, complement 5, tumor necrosis factor-α and interleukin-10