Concurrent Toxoplasma gondii infection and neuroinflammation in traumatic brain injury patients in a referral hospital in Douala Cameroon

Abstract Studies on murine models show that Toxoplasma gondii infection reduces cerebral microvascular perfusion and induces neuroinflammation by activating cerebral endothelial cells, which could affect traumatic brain injury (TBI) outcomes. Whether TBI inflammatory profile and outcomes differ in persons with concurrent latent infection with Toxoplasma gondii has not yet been elucidated in TBI patients, constituting the core of this study. Understanding the impact of chronic T. gondii infection on neuroinflammation after TBI may ensure better management and prognosis of TBI. This study aimed to investigate the inflammatory profile in TBI patients and investigate the influence of concurrent T. gondii infection on inflammatory markers and TBI outcomes. The level of inflammatory markers interleukin (IL)-1β, IL-6, IL-10, interferon-gamma (INF-ɣ), Tumour necrosis factor-alpha (TNF-α), and Toxoplasma gondii infection were detected in serum obtained < 24 h post-injury. Glasgow Outcome Scale-Extended (GOSE) was used to evaluate the 6-month outcome post-discharge. The Wilcoxon and Kruskal-Wallis’s rank sum tests were used to compare concentrations of inflammatory markers to T. gondii infection and TBI outcome. T. gondii infection was detected in 33% (52/160) of TBI cases. There was a significant increase ( p < 0.001) in the concentrations of all inflammatory markers (IM) in TBI patients compared with the healthy controls. Higher levels of IL-6, INF-ɣ, and TNF-α were associated with mortality. Findings from this study show an increase in IM levels for all the T. gondii-positive TBI cases, which were significant for IL-1β ( P < 0.001) and TNF-α ( P < 0.001). IL-1β and TNF-α, had significantly greater density values, above 30pg/mL and 90pg/mL, respectively, in TBI patients infected with T. gondii , compared to greater density values, below 30 pg/mL and 90 pg/mL, respectively, for TBI patients seronegative to T. gondii. Concurrent T. gondii infection in TBI significantly influenced the inflammation profile of patients. Further multicenter studies with larger sample sizes will provide more insights into T. gondii induced neuropathology and prognostication in TBI care.