Helicobacter pylori are spiral and rod-shaped Gram-negative bacteria [1] that colonize the gastric mucosa of about half of the world’s population [2]. This bacterium has been associated with several gastric diseases such as chronic gastritis, peptic ulcer and gastric cancer [3]. Contamination is usually acquired in childhood [4,5], probably by ingesting food or water contaminated with fecal matter [6,7], and, once established, H. pylori has no significant bacterial competitors [8]. In order to protect itself from the bulk acidic pH of the stomach, H. pylori uses its flagellar motility to cross the mucus layer that covers and protects the gastric cells and reach the gastric epithelium where the pH is more neutral. To achieve this, H. pylori surface-bound ureases catalyze the hydrolysis of urea to generate ammonia and bicarbonate, neutralizing the acidic pH of its microenvironment.
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Furthermore, ammonia and bicarbonate have also been described as chemotactic agents [10], increasing the number of H. pylori close to the surface of the epithelium. H. pylori infection treatment is based on a combination of at least two antibiotics and a proton pump inhibitor [11]. These therapies have shown an eradication rate of 75% in patients [12]. Strategies to improve the efficacy of the treatments involve drug protection from the highly acidic gastric fluids by encapsulating the drugs in chitosan microstructures
Furthermore, ammonia and bicarbonate have also been described as chemotactic agents [10], increasing the number of H. pylori close to the surface of the epithelium. H. pylori infection treatment is based on a combination of at least two antibiotics and a proton pump inhibitor [11]. These therapies have shown an eradication rate of 75% in patients [12]. Strategies to improve the efficacy of the treatments involve drug protection from the highly acidic gastric fluids by encapsulating the drugs in chitosan microstructures