Abstract

Small non-coding RNA RyhB is a key regulator of iron homeostasis in bacteria by sensing iron availability in the environment. Although RyhB is known to influence bacterial virulence by interacting with iron metabolism related regulators, its interaction with virulence genes, especially the Type III secretion system (T3SS), has not been reported. Here, we demonstrate that two RyhB paralogs of Salmonella enterica serovar Enteritidis upregulate Type III secretion system (T3SS) effectors, and consequently affect Salmonella invasion into intestinal epithelial cells. Specifically, we found that RyhB-1 modulate Salmonella response to stress condition of iron deficiency and hypoxia, and stress in simulated intestinal environment (SIE). Under SIE culture conditions, both RyhB-1 and RyhB-2 are drastically induced and directly upregulate the expression of T3SS effector gene sipA by interacting with its 5′ untranslated region (5′ UTR) via an incomplete base-pairing mechanism. In addition, the RyhB paralogs upregulate the expression of T3SS effector gene sopE. By regulating the invasion-related genes, RyhBs in turn affect the ability of S. Enteritidis to adhere to and invade into intestinal epithelial cells. Our findings provide evidence that RyhBs function as critical virulence factors by directly regulating virulence-related gene expression. Thus, inhibition of RyhBs may be a potential strategy to attenuate Salmonella.

Highlights

  • Salmonella is an important zoonotic pathogen that causes foodborne enteritis, which is frequently reported worldwide

  • We identified target genes of RyhB paralogs via a simulated intestinal environment (SIE) model in vitro and demonstrated that both RyhBs upregulated the expression of Salmonella T3SS effector genes sipA and sopE, thereby affecting the ability of Salmonella Enteritidis to invade intestinal epithelial cells

  • The results showed that ryhB-1 and ryhB-2 (GenBank accession numbers: MW583716 and MW583717) in SE50336, shared 99% and 100% identity to the two ryhB paralogs in S

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Summary

Introduction

Salmonella is an important zoonotic pathogen that causes foodborne enteritis, which is frequently reported worldwide. During the process of infecting the intestine, Salmonella penetrates the mucosal layer and is internalized into the intestinal epithelium. This step is directed by the delivery of a series of effector proteins into host cells via. T3SS effectors SipA and SopE play a crucial role in Salmonella invasion of intestinal epithelial cells. SopE cooperates with host ADP ribosylation factor 1 (Arf1) activator (ARNO) to trigger Salmonella invasion [12]. Both SipA and SopE can disrupt tight junctions that likely lead to polymorphonuclear leukocyte (PMN) transmigration [8, 13]. The regulation of T3SS effector production by noncoding small RNA has not yet been reported

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