Abstract

Outer membrane vesicles (OMVs) play an important role in the persistence of Helicobacter pylori infection. Helicobacter OMVs carry a plethora of virulence factors, including catalase (KatA), an antioxidant enzyme that counteracts the host respiratory burst. We found KatA to be enriched and surface-associated in OMVs compared to bacterial cells. This conferred OMV-dependent KatA activity resulting in neutralization of H2O2 and NaClO, and rescue of surrounding bacteria from oxidative damage. The antioxidant activity of OMVs was abolished by deletion of KatA. In conclusion, enrichment of antioxidative KatA in OMVs is highly important for efficient immune evasion.

Highlights

  • Helicobacter pylori is a Gram-negative pathogen that commonly colonizes the gastric mucosa

  • Since most outer membrane (OM) proteins are located at the surface of vesicles (Bonnington and Kuehn, 2014), we wanted to investigate whether KatA localizes at the outer surface of H. pylori outer membrane vesicles (OMVs)

  • Further enumeration of antibody deposition revealed that more KatA was detected at the “blebbing areas” of wild type bacteria as compared to the “nonblebbing areas,” and this appearance was almost similar to the OMVs (Figure 1B)

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Summary

Introduction

Helicobacter pylori is a Gram-negative pathogen that commonly colonizes the gastric mucosa. In order to survive against the highly acidic gastric juice (pH 1.0–3.0), H. pylori uses a series of acidic acclimation systems that neutralize the surrounding acid. Other virulence mechanisms include expression of abundant molecules at the surface for attachment and manipulation of host extracellular matrix proteins and serum resistance (Parker and Keenan, 2012; Richter et al, 2016). H. pylori is equipped with antioxidant molecules such as catalase (KatA), catalase-like protein (KatB), alkyl hydroperoxide reductase (AhpC), and superoxide dismutase (SOD) to detoxify reactive oxygen species (ROS) released from host immune cells during the respiratory burst (Wang et al, 2006). H. pylori constitutively releases outer membrane vesicles (OMVs) from its outer membrane (OM)

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