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Background Emerging evidence suggests that while standard antimalarial and antityphoidal treatments are effective against the pathogens, they may also influence host immune responses, with potential implications on recovery and clinical outcomes. This piece of work was designed to evaluate the effects of standard antimalarial and antibiotic therapies on selected immune biomarkers in patients with malaria and typhoid fever.Methods In this prospective observational cohort study conducted at the Obala District Hospital, Yaoundé, Cameroon, we performed a comparative analysis of cytokine concentrations in 55 patients receiving antimalarial and/or antibiotic treatment and 15 healthy controls. Inflammatory cytokines were measured in 70 participants at admission (baseline) and in 50 out of the 70 patients at day 5 post-treatment using ELISA. An exploratory data analysis was performed using GraphPad Prism while correlation analysis between cytokine levels and recovery time was performed using SPSS at 95% CI (p<0.05).Results By day 5 (±2) of treatment, just over half of the patients had achieved clinical recovery, with the highest recovery observed in the antimalarial group and the lowest in the antityphoidal group. Treatment was associated with significant changes in inflammatory cytokine expression. At baseline, patients with malaria–typhoid coinfection exhibited marked overexpression of pro-inflammatory cytokines, particularly interleukin (IL)-2, tumour necrosis factor (TNF)-α and interferon (IFN)-γ, compared with healthy controls. Antimalarial therapy was associated with increased IL-2 and IL-1β levels and reduced IL-10, while antibiotic treatment promoted upregulation of IL-1β, IL-2 and TNF-α. Combination therapy resulted in decreased IL-10 and IFN-γ alongside increased TNF-α. Pro-inflammatory cytokines positively correlated with longer recovery time, whereas anti-inflammatory responses showed treatment-specific associations, with higher IL-10 linked to shorter recovery in patients with typhoid.Conclusion Antimalarial and antityphoidal therapies modulate cytokines levels in complex ways, with elevated pro-inflammatory responses linked to delayed recovery. These findings emphasise the need for personalised treatment strategies guided by patients’ immune profiles.