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The Host Protein Calprotectin Modulates the Type IV Secretion System via Zinc Sequestration
Helicobacter pylori is a bacterium that colonizes the stomach and causes gastric diseases. Some strains of H. pylori possess a secretion system that has the capacity to inject a cancer-causing protein into host cells. The activity of this secretion system contributes to the development of inflammation and is linked to the development of gastric cancer. Here, we show that the host protein calprotectin, which has the ability to bind and sequester nutrient metals from invading pathogens, can directly repress H. pylori secretory activity and the production of secretion-associated pili in a zinc-dependent manner. H. pylori-infected animals lacking calprotectin trend toward having more gastric inflammation and a significantly lower bacterial burden than infected animals that express calprotectin; these differences are not observed when animals are infected with a strain of H. pylori that lacks an active secretion system. Thus, a better understanding of how nutritional immunity modulates this secretion system could help us develop novel antimicrobial therapeutic strategies targeting secretory processes in H. pylori.
Vyšlo v časopise: The Host Protein Calprotectin Modulates the Type IV Secretion System via Zinc Sequestration. PLoS Pathog 10(10): e32767. doi:10.1371/journal.ppat.1004450
Kategorie: Research Article
prolekare.web.journal.doi_sk: https://doi.org/10.1371/journal.ppat.1004450Souhrn
Helicobacter pylori is a bacterium that colonizes the stomach and causes gastric diseases. Some strains of H. pylori possess a secretion system that has the capacity to inject a cancer-causing protein into host cells. The activity of this secretion system contributes to the development of inflammation and is linked to the development of gastric cancer. Here, we show that the host protein calprotectin, which has the ability to bind and sequester nutrient metals from invading pathogens, can directly repress H. pylori secretory activity and the production of secretion-associated pili in a zinc-dependent manner. H. pylori-infected animals lacking calprotectin trend toward having more gastric inflammation and a significantly lower bacterial burden than infected animals that express calprotectin; these differences are not observed when animals are infected with a strain of H. pylori that lacks an active secretion system. Thus, a better understanding of how nutritional immunity modulates this secretion system could help us develop novel antimicrobial therapeutic strategies targeting secretory processes in H. pylori.
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