Abstract
Streptococcus suis is a zoonotic pathogen causing serious infections in swine and humans. Although metals are essential for life, excess amounts of metals are toxic to bacteria. Transcriptome-level data of the mechanisms for resistance to metal toxicity in S. suis are available for no metals other than zinc. Herein, we explored the transcriptome-level changes in S. suis in response to ferrous iron and cobalt toxicity by RNA sequencing. Many genes were differentially expressed in the presence of excess ferrous iron and cobalt. Most genes in response to cobalt toxicity showed the same expression trends as those in response to ferrous iron toxicity. qRT-PCR analysis of the selected genes confirmed the accuracy of RNA sequencing results. Bioinformatic analysis of the differentially expressed genes indicated that ferrous iron and cobalt have similar effects on the cellular processes of S. suis. Ferrous iron treatment resulted in down-regulation of several oxidative stress tolerance-related genes and up-regulation of the genes in an amino acid ABC transporter operon. Expression of several genes in the arginine deiminase system was down-regulated after ferrous iron and cobalt treatment. Collectively, our results suggested that S. suis alters the expression of multiple genes to respond to ferrous iron and cobalt toxicity.
Highlights
Streptococcus suis causes meningitis, septicemia, pneumonia, endocarditis, and arthritis in pigs, leading to major economic losses worldwide [1]
To better understand the mechanisms of S. suis in response to ferrous iron and cobalt toxicity, the transcription profiles of S. suis following treatment with ferrous iron and cobalt were compared with that treatment with water by RNA sequencing analysis
The experiment was performed in three conditions, i.e., ferrous iron treatment (Fe), cobalt treatment (Co), and water treatment, with three biological replications for each condition
Summary
Streptococcus suis causes meningitis, septicemia, pneumonia, endocarditis, and arthritis in pigs, leading to major economic losses worldwide [1]. It can be transmitted to humans by skin lesions or via the gastrointestinal tract, and is responsible for serious diseases such as meningitis and streptococcal toxic shock-like syndrome [2,3]. Serotype 2 is the most prevalent serotype involved in both human and swine infections in most countries [5]. S. suis caused more than 1600 human deaths worldwide by 2013 [5]. In China, two large outbreaks of S. suis infection in humans occurred in 1998 and 2005, leading to 240 cases with 53 deaths in total [6]. Sporadic cases of human infection of S
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