Transcriptomic Analysis of Campylobacter jejuni Following Exposure to Gaseous Chlorine Dioxide Reveals an Oxidative Stress Response

Gaseous chlorine dioxide (ClO<sub>2</sub>) is a potent antimicrobial agent used to control microbial contamination in food and water. This study evaluates the bactericidal activity of gaseous ClO<sub>2</sub> released from a sodium chlorite (NaClO<sub>2</sub>) pad against <i>Campylobacter jejuni</i>. Exposure to a low concentration (0.4 mg/L) of dissolved ClO<sub>2</sub> for 2 h resulted in a >93% reduction of <i>C. jejuni</i>, highlighting the bacterium's extreme sensitivity to gaseous ClO<sub>2</sub>. To elucidate the molecular mechanism of ClO<sub>2</sub>-induced bactericidal action, transcriptomic analysis was conducted using RNA sequencing (RNA-seq). The results indicate that <i>C. jejuni</i> responds to ClO<sub>2</sub>-induced oxidative stress by upregulating genes involved in reactive oxygen species (ROS) detoxification (<i>sodB</i>, <i>ahpC</i>, <i>katA</i>, <i>msrP</i>, and <i>trxB</i>), iron transport (<i>ceuBCD</i>, <i>cfbpABC</i>, and <i>chuBCD</i>), phosphate transport (<i>pstSCAB</i>), and DNA repair (<i>rdgB</i> and <i>mutY</i>). Reverse transcription-quantitative PCR (RT-qPCR) validated the increased expression of oxidative stress response genes but not general stress response genes (<i>spoT</i>, <i>dnaK</i>, and <i>groES</i>). These findings provide insights into the antimicrobial mechanism of ClO<sub>2</sub>, demonstrating that oxidative damage to essential cellular components results in bacterial cell death.

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Journal
International Journal of Molecular Sciences
Published
2025-04-01
DOI
https://doi.org/10.3390/ijms26073254
Citations
2
Primary Topic
Salmonella and Campylobacter epidemiology
Type
article
Field-Weighted Citation Impact
2.32
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article

Transcriptomic Analysis of Campylobacter jejuni Following Exposure to Gaseous Chlorine Dioxide Reveals an Oxidative Stress Response

Joseph A. Capobianco, Tony Z. Jin, Shing Yip Lee, Gretchen E. Dykes et al.
2 citations
International Journal of Molecular Sciences
Salmonella and Campylobacter epidemiology
2.32
article

Transcriptomic Analysis of Campylobacter jejuni Following Exposure to Gaseous Chlorine Dioxide Reveals an Oxidative Stress Response

Joseph A. Capobianco, Tony Z. Jin, Shing Yip Lee, Gretchen E. Dykes, Yiping He, Xuetong Fan, Sue Reed
article en
2 citations

Abstract

Gaseous chlorine dioxide (ClO<sub>2</sub>) is a potent antimicrobial agent used to control microbial contamination in food and water. This study evaluates the bactericidal activity of gaseous ClO<sub>2</sub> released from a sodium chlorite (NaClO<sub>2</sub>) pad against <i>Campylobacter jejuni</i>. Exposure to a low concentration (0.4 mg/L) of dissolved ClO<sub>2</sub> for 2 h resulted in a >93% reduction of <i>C. jejuni</i>, highlighting the bacterium's extreme sensitivity to gaseous ClO<sub>2</sub>. To elucidate the molecular mechanism of ClO<sub>2</sub>-induced bactericidal action, transcriptomic analysis was conducted using RNA sequencing (RNA-seq). The results indicate that <i>C. jejuni</i> responds to ClO<sub>2</sub>-induced oxidative stress by upregulating genes involved in reactive oxygen species (ROS) detoxification (<i>sodB</i>, <i>ahpC</i>, <i>katA</i>, <i>msrP</i>, and <i>trxB</i>), iron transport (<i>ceuBCD</i>, <i>cfbpABC</i>, and <i>chuBCD</i>), phosphate transport (<i>pstSCAB</i>), and DNA repair (<i>rdgB</i> and <i>mutY</i>). Reverse transcription-quantitative PCR (RT-qPCR) validated the increased expression of oxidative stress response genes but not general stress response genes (<i>spoT</i>, <i>dnaK</i>, and <i>groES</i>). These findings provide insights into the antimicrobial mechanism of ClO<sub>2</sub>, demonstrating that oxidative damage to essential cellular components results in bacterial cell death.

International Journal of Molecular SciencesVol. 26(7)
Agricultural Research Service (US), United States Department of Agriculture (US), Eastern Regional Research Center (US)
Openalex Percentile: Top 14%
Salmonella and Campylobacter epidemiology
2.32
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