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Analysis of Pro-Inflammatory Cytokines Response Among Typhoid Patients Co-Infection with Plasmodium falciparum In Khartoum State -Sudan

Domaine:

healthcare
Créateur:
IbrAbdQutSal
Éditeur:
Ide
Hôte:
Background: Typhoid fever and malaria remain among the most prevalent infectious diseases in developing countries, contributing to significant morbidity and mortality. Pro-inflammatory cytokines such as interleukin-6 (IL-6) and interleukin-8 (IL-8) play a critical role in the immune response to these infections. While elevated levels of these cytokines are associated with immune clearance, their dysregulation has also been implicated in severe disease outcomes. This study aimed to investigate the levels of IL-6 and IL-8 among typhoid patients co-infected with Plasmodium falciparum in Khartoum State, Sudan. Materials and Methods: A total of 140 blood samples were collected from typhoid patients, malaria patients, co-infected individuals, and healthy controls. Blood films and immunochromatographic tests were used to confirm malaria, while culture and Widal tests were employed to diagnose typhoid. Plasma cytokine levels were measured using a sandwich ELISA. Data were statistically analyzed using chi-square and t-tests. Results: IL-6 levels were significantly higher in typhoid (133.3 pg/mL) and malaria patients (107 pg/mL) compared to healthy controls (37.6 pg/mL). In contrast, co-infected patients had significantly lower IL-6 levels (17.02 pg/mL) than controls (p < 0.0064). Similarly, IL-8 levels were significantly elevated in typhoid (165±7.1 pg/mL) and malaria (184±5.1 pg/mL) patients compared to controls (17±5.9 pg/mL). However, IL-8 levels in co-infected patients (15±7.1 pg/mL) showed a non-significant decline (p = 0.861). Conclusion: The findings suggest that co-infection with P. falciparum may downregulate the pro-inflammatory cytokine response typically observed in mono-infections. This immune modulation could affect clinical outcomes and diagnostic markers. Further studies are recommended to explore the underlying mechanisms of cytokine regulation in co-infections.

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