Abstract
Neutrophils are innate immune response cells designed to kill invading microorganisms. One of the mechanisms neutrophils use to kill bacteria is generation of damaging reactive oxygen species (ROS) via the respiratory burst. However, during enteric salmonellosis, neutrophil-derived ROS actually facilitates Salmonella expansion and survival in the gut. This seeming paradox led us to hypothesize that Salmonella may possess mechanisms to influence the neutrophil respiratory burst. In this work, we used an in vitro Salmonella-neutrophil co-culture model to examine the impact of enteric infection relevant virulence factors on the respiratory burst of human neutrophils. We report that neutrophils primed with granulocyte-macrophage colony stimulating factor and suspended in serum containing complement produce a robust respiratory burst when stimulated with viable STm. The magnitude of the respiratory burst increases when STm are grown under conditions to induce the expression of the type-3 secretion system-1. STm mutants lacking the type-3 secretion system-1 induce less neutrophil ROS than the virulent WT. In addition, we demonstrate that flagellar motility is a significant agonist of the neutrophil respiratory burst. Together our data demonstrate that both the type-3 secretion system-1 and flagellar motility, which are established virulence factors in enteric salmonellosis, also appear to directly influence the magnitude of the neutrophil respiratory burst in response to STm in vitro.
Highlights
Non-typhoidal salmonellae are a leading cause of bacterial food-borne gastroenteritis with disease characterized by a marked neutrophilic intestinal inflammation [1, 2]
We found that normal human serum (NHS), containing complement, increased the magnitude of the Salmonella Typhimurium (STm)-induced intracellular neutrophil respiratory burst in granulocyte macrophage-colony stimulating factor (GM-CSF)-primed neutrophils (S1 Fig)
These data suggest that a robust in vitro intracellular respiratory burst in response to STm occurs in the presence of complement and when neutrophils are primed with GM-CSF
Summary
Non-typhoidal salmonellae are a leading cause of bacterial food-borne gastroenteritis with disease characterized by a marked neutrophilic intestinal inflammation [1, 2]. Salmonella invades non-phagocytic intestinal epithelial cells using the type-3 secretion system-1 (TTSS) encoded on Salmonella Pathogenicity Island-1 (SPI-1). The TTSS-1 secreted effector proteins are necessary for epithelial cell invasion, epithelial cell inflammatory signaling and neutrophil recruitment to the intestine [3,4,5]. Neutrophil recruitment is further enhanced by flagellin, which. Neutrophil respiratory burst and Salmonella study design, data collection and analysis, decision to publish, or preparation of the manuscript
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