Dysbiosis Malaria and Hypertension: The Mechanistic Links

Abstract

According to new research, dysbiosis is a crucial link between chronic non-communicable diseases and infectious diseases. This review examines how malaria-induced dysbiosis and hypertension may exacerbate gut dysbiosis and summarizes the current understanding of the mechanisms underlying this relationship. Reduced microbial diversity, fewer bacteria that produce short-chain fatty acids (SCFAs), and elevated levels of pro-hypertensive metabolites such as trimethylamine-N-oxide (TMAO) and lipopolysaccharides (LPS) are the hallmarks of dysbiosis in hypertension. These changes result in increased gut permeability, endothelial dysfunction, and systemic inflammation, all of which raise blood pressure. At the same time, parasite toxins from Plasmodium infection cause severe gut dysbiosis (e.g., hemozoin), systemic inflammation (TNF-α, IFN-γ), and related malnutrition. This dysbiosis linked to Malaria weakens the integrity of the gut barrier and impairs immune regulation, resulting in a leaky gut and a pro-inflammatory phenotype. We proposed that the dysbiotic state brought on by acute or recurrent Malaria may act as a latent risk factor, setting up the host environment for the emergence of hypertension via persistent barrier dysfunction, impaired SCFA signaling, and prolonged inflammation. This intersection implies that novel approaches to reducing the risk of hypertension in malaria-endemic populations may involve microbiome-targeted interventions.