RpoE Facilitates Stress-Resistance, Invasion, and Pathogenicity of <i>Escherichia coli</i> K1
<i>Escherichia coli</i> K1 is the most common Gram-negative bacterium that causes neonatal meningitis; thus, a better understanding of its pathogenic molecular mechanisms is critical. However, the mechanisms by which <i>E. coli</i> K1 senses the signals of the host and expres...
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| Format: | Article |
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MDPI AG
2022-04-01
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| Series: | Microorganisms |
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| Online Access: | https://www.mdpi.com/2076-2607/10/5/879 |
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| author | Yu Fan Jing Bai Daoyi Xi Bin Yang |
| author_facet | Yu Fan Jing Bai Daoyi Xi Bin Yang |
| author_sort | Yu Fan |
| collection | DOAJ |
| description | <i>Escherichia coli</i> K1 is the most common Gram-negative bacterium that causes neonatal meningitis; thus, a better understanding of its pathogenic molecular mechanisms is critical. However, the mechanisms by which <i>E. coli</i> K1 senses the signals of the host and expresses toxins for survival are poorly understood. As an extracytoplasmic function sigma factor, RpoE controls a wide range of pathogenesis-associated pathways in response to environmental stress. We found that the Δ<i>rpoE</i> mutant strain reduced the binding and invasion rate in human brain microvascular endothelial cells (HBMECs) in vitro, level of bacteremia, and percentage of meningitis in vivo. To confirm the direct targets of RpoE in vivo, we performed qRT-PCR and ChIP-qPCR on known toxic genes. RpoE was found to regulate pathogenic target genes, namely, <i>ompA</i>, <i>cnf1</i>, <i>fimB</i>, <i>ibeA</i>, <i>kpsM</i>, and <i>kpsF</i> directly and <i>fimA</i>, <i>aslA</i>, and <i>traJ</i> indirectly. The expression of these genes was upregulated when <i>E. coli</i> K1 was cultured with antibacterial peptides, whereas remained unchanged in the presence of the Δ<i>rpoE</i> mutant strain. Moreover, RpoE reduced IL-6 and IL-8 levels in <i>E. coli</i> K1-infected HBMECs. Altogether, these findings demonstrate that RpoE mediates the host adaptation capacity of <i>E. coli</i> K1 via a regulatory mechanism on virulence factors. |
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| id | doaj.art-5d1ccd5daac147a49a07557f5d57e109 |
| institution | Directory Open Access Journal |
| issn | 2076-2607 |
| language | English |
| last_indexed | 2024-03-10T03:23:03Z |
| publishDate | 2022-04-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Microorganisms |
| spelling | doaj.art-5d1ccd5daac147a49a07557f5d57e1092023-11-23T12:14:23ZengMDPI AGMicroorganisms2076-26072022-04-0110587910.3390/microorganisms10050879RpoE Facilitates Stress-Resistance, Invasion, and Pathogenicity of <i>Escherichia coli</i> K1Yu Fan0Jing Bai1Daoyi Xi2Bin Yang3The Key Laboratory of Molecular Microbiology and Technology, Ministry of Education, Nankai University, Tianjin 300457, ChinaThe Key Laboratory of Molecular Microbiology and Technology, Ministry of Education, Nankai University, Tianjin 300457, ChinaTianjin Institute of Industrial Biotechnology, Chinese Academy of Sciences, Tianjin 300308, ChinaThe Key Laboratory of Molecular Microbiology and Technology, Ministry of Education, Nankai University, Tianjin 300457, China<i>Escherichia coli</i> K1 is the most common Gram-negative bacterium that causes neonatal meningitis; thus, a better understanding of its pathogenic molecular mechanisms is critical. However, the mechanisms by which <i>E. coli</i> K1 senses the signals of the host and expresses toxins for survival are poorly understood. As an extracytoplasmic function sigma factor, RpoE controls a wide range of pathogenesis-associated pathways in response to environmental stress. We found that the Δ<i>rpoE</i> mutant strain reduced the binding and invasion rate in human brain microvascular endothelial cells (HBMECs) in vitro, level of bacteremia, and percentage of meningitis in vivo. To confirm the direct targets of RpoE in vivo, we performed qRT-PCR and ChIP-qPCR on known toxic genes. RpoE was found to regulate pathogenic target genes, namely, <i>ompA</i>, <i>cnf1</i>, <i>fimB</i>, <i>ibeA</i>, <i>kpsM</i>, and <i>kpsF</i> directly and <i>fimA</i>, <i>aslA</i>, and <i>traJ</i> indirectly. The expression of these genes was upregulated when <i>E. coli</i> K1 was cultured with antibacterial peptides, whereas remained unchanged in the presence of the Δ<i>rpoE</i> mutant strain. Moreover, RpoE reduced IL-6 and IL-8 levels in <i>E. coli</i> K1-infected HBMECs. Altogether, these findings demonstrate that RpoE mediates the host adaptation capacity of <i>E. coli</i> K1 via a regulatory mechanism on virulence factors.https://www.mdpi.com/2076-2607/10/5/879HBMECsbacteremiameningitis<i>E. coli</i> K1RpoEantibacterial peptides |
| spellingShingle | Yu Fan Jing Bai Daoyi Xi Bin Yang RpoE Facilitates Stress-Resistance, Invasion, and Pathogenicity of <i>Escherichia coli</i> K1 Microorganisms HBMECs bacteremia meningitis <i>E. coli</i> K1 RpoE antibacterial peptides |
| title | RpoE Facilitates Stress-Resistance, Invasion, and Pathogenicity of <i>Escherichia coli</i> K1 |
| title_full | RpoE Facilitates Stress-Resistance, Invasion, and Pathogenicity of <i>Escherichia coli</i> K1 |
| title_fullStr | RpoE Facilitates Stress-Resistance, Invasion, and Pathogenicity of <i>Escherichia coli</i> K1 |
| title_full_unstemmed | RpoE Facilitates Stress-Resistance, Invasion, and Pathogenicity of <i>Escherichia coli</i> K1 |
| title_short | RpoE Facilitates Stress-Resistance, Invasion, and Pathogenicity of <i>Escherichia coli</i> K1 |
| title_sort | rpoe facilitates stress resistance invasion and pathogenicity of i escherichia coli i k1 |
| topic | HBMECs bacteremia meningitis <i>E. coli</i> K1 RpoE antibacterial peptides |
| url | https://www.mdpi.com/2076-2607/10/5/879 |
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