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Pathogenic Escherichia coli: Pathogenesis, Virulence and Control Strategies

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Microbiology".

Deadline for manuscript submissions: closed (30 December 2022) | Viewed by 22215

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Prof. Dr. Eric Cox

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Guest Editor

Laboratory of Immunology, Department of Parasitology, Virology & Immunology, Ghent University, 9000 Ghent, Belgium
Interests: mucosal immunity; E. coli; ETEC; STEC; EHEC; toxoplasmosis; Chlamydia sp.; food allergy; vaccines
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Dr. Pengpeng Xia

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College of Veterinary Medicine (Institute of Comparative Medicine), Yangzhou University, Yangzhou 225009, China
Interests: Escherichia coli; nutritional immunity; host-pathogen interaction; receptor; diarrhea; mucosal immunity; vaccines
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Pathogenic Escherichia coli (E. coli) is the leading cause of intestinal and extraintestinal diseases in humans and livestock. The classification of numerous pathogenic E. coli categories or pathotypes is based on the production of virulence factors and the presence or severity of certain symptoms that they cause. To invade host cells, bacteria have gradually developed a variety of mechanisms to survive or take advantage of benefits within intracellular niches during the infection process. Thus, even though bacteria share similar virulence features, they might have a distinctive pathogenic mechanism. Additionally, the molecular biology of the interplay between host and pathogenic E. coli is relatively poorly understood. This Special Issue aims to present the latest findings in this field and will cover all topics concerning the pathogenesis, virulence, and control strategies of pathogenic E. coli, including but not limited to: the immunomodulatory effect of metal ions and nutritional immunity, the regulatory effect of small non-coding RNA in pathogenic E. coli infections, new materials for preventing pathogenic E. coli infections, new methods for the detection and identification of pathogenic E. coli, and receptors for the host–pathogen interaction.

Prof. Dr. Eric Cox
Dr. Pengpeng Xia
Guest Editors

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Keywords

Escherichia coli
nutritional immunity
enterotoxin
fimbriae
flagellum
host–pathogen interaction
receptor
secretion system
small non-coding RNA
bacterial infections
detection methods

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Published Papers (9 papers)

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Research

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11 pages, 1425 KiB

Open AccessArticle

Safety and Immunogenicity of a Chimeric Subunit Vaccine against Shiga Toxin-Producing Escherichia coli in Pregnant Cows

by Roberto M. Vidal, David A. Montero, Felipe Del Canto, Juan C. Salazar, Carolina Arellano, Alhejandra Alvarez, Nora L. Padola, Hernán Moscuzza, Analía Etcheverría, Daniel Fernández, Victoria Velez, Mauro García, Rocío Colello, Marcelo Sanz and Angel Oñate

Int. J. Mol. Sci. 2023, 24(3), 2771; https://doi.org/10.3390/ijms24032771 - 1 Feb 2023

Cited by 3 | Viewed by 2508

Abstract

Shiga toxin-producing Escherichia coli (STEC) is a zoonotic pathogen that causes gastroenteritis and Hemolytic Uremic Syndrome. Cattle are the main animal reservoir, excreting the bacteria in their feces and contaminating the environment. In addition, meat can be contaminated by releasing the intestinal content during slaughtering. Here, we evaluated the safety and immunogenicity of a vaccine candidate against STEC that was formulated with two chimeric proteins (Chi1 and Chi2), which contain epitopes of the OmpT, Cah and Hes proteins. Thirty pregnant cows in their third trimester of gestation were included and distributed into six groups (n = 5 per group): four groups were administered intramuscularly with three doses of the formulation containing 40 µg or 100 µg of each protein plus the Quil-A or Montanide™ Gel adjuvants, while two control groups were administered with placebos. No local or systemic adverse effects were observed during the study, and hematological parameters and values of blood biochemical indicators were similar among all groups. Furthermore, all vaccine formulations triggered systemic anti-Chi1/Chi2 IgG antibody levels that were significantly higher than the control groups. However, specific IgA levels were generally low and without significant differences among groups. Notably, anti-Chi1/Chi2 IgG antibody levels in the serum of newborn calves fed with colostrum from their immunized dams were significantly higher compared to newborn calves fed with colostrum from control cows, suggesting a passive immunization through colostrum. These results demonstrate that this vaccine is safe and immunogenic when applied to pregnant cows during the third trimester of gestation. Full article

(This article belongs to the Special Issue Pathogenic Escherichia coli: Pathogenesis, Virulence and Control Strategies)

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15 pages, 2173 KiB

Open AccessArticle

A Novel Role of the Two-Component System Response Regulator UvrY in Enterohemorrhagic Escherichia coli O157:H7 Pathogenicity Regulation

by Pan Wu, Qian Wang, Qian Yang, Xiaohui Feng, Xingmei Liu, Hongmin Sun, Jun Yan, Chenbo Kang, Bin Liu, Yutao Liu and Bin Yang

Int. J. Mol. Sci. 2023, 24(3), 2297; https://doi.org/10.3390/ijms24032297 - 24 Jan 2023

Cited by 3 | Viewed by 2607

Abstract

Enterohemorrhagic Escherichia coli (EHEC) O157:H7 is an important human pathogen causing severe diseases, such as hemorrhagic colitis and lethal hemolytic uremic syndrome. The signal-sensing capability of EHEC O157:H7 at specific host colonization sites via different two-component systems (TCSs) is closely related to its pathogenicity during infection. However, the types of systems involved and the regulatory mechanisms are not fully understood. Here, we investigated the function of the TCS BarA/UvrY regulator UvrY in the pathogenicity regulation of EHEC O157:H7. Our results showed that UvrY acts as a positive regulator of EHEC O157:H7 for cellular adherence and mouse colonization through the transcriptional activation of the locus for enterocyte effacement (LEE) pathogenic genes. Furthermore, this regulation is mediated by the LEE island master regulator, Ler. Our results highlight the significance of UvrY in EHEC O157:H7 pathogenicity and underline the unknown importance of BarA/UvrY in colonization establishment and intestinal adaptability during infection. Full article

(This article belongs to the Special Issue Pathogenic Escherichia coli: Pathogenesis, Virulence and Control Strategies)

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18 pages, 7761 KiB

Open AccessArticle

Persistence Infection of TGEV Promotes Enterococcus faecalis Infection on IPEC-J2 Cells

by Zhenzhen Guo, Chenxin Zhang, Jiajun Dong, Yabin Wang, Hui Hu and Liying Chen

Int. J. Mol. Sci. 2023, 24(1), 450; https://doi.org/10.3390/ijms24010450 - 27 Dec 2022

Cited by 2 | Viewed by 1843

Abstract

Transmissible gastroenteritis virus (TGEV) is a coronavirus causing diarrhea with high incidence in swine herds. Its persistent infection might lead to epithelial-mesenchymal transition (EMT) of swine intestinal epithelial cells, followed by subsequent infections of other pathogens. Enterococcus faecalis (E. faecalis) is a member of the enteric microorganisms and an opportunistic pathogen. There is no report of secondary E. faecalis infection to TGEV, even though they both target to the intestinal tracts. To investigate the interactions between TGEV and E. faecalis, we set up an in vitro infection model by the swine IPEC-J2 cells. Dynamic changes of cell traits, including EMT and cell motility, were evaluated through qPCR, Western blot, electronic microscopy, scratch test, Transwell migration test and invasion test, respectively. The adhesion and invasion tests of E. faecalis were taken to verify the impact of the preceding TGEV infection. The cell morphology and molecular marker evaluation results showed that the TGEV persistent infection induced EMT on IPEC-J2 cells; increased cellular motility and invasion potential were also observed. Spontaneously, the expression levels of fibronectin (FN) and the membrane protein integrin-α5, which are dominant bacterial receptors on IPEC-J2 cells, were upgraded. It indicated that the bacteria E. faecalis adhered to IPEC-J2 cells through the FN receptor, and then invaded the cells by binding with the integrin-α5, suggesting that both molecules were critical for the adhesion and invasion of E. faecalis to IPEC-J2 cells. Additionally, it appeared that E. faecalis alone might trigger certain EMT phenomena, implying a vicious circle might occur. Generally, bacterial and viral co-infections are frustrating yet common in both human and veterinary medicines, and our observations on enteric TGEV and E. faecalis interactions, especially the diversity of bacterial invasion strategies, might provide new insights into the mechanisms of E. faecalis pathogenicity. Full article

(This article belongs to the Special Issue Pathogenic Escherichia coli: Pathogenesis, Virulence and Control Strategies)

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19 pages, 6735 KiB

Open AccessArticle

RyhB in Avian Pathogenic Escherichia coli Regulates the Expression of Virulence-Related Genes and Contributes to Meningitis Development in a Mouse Model

by Xia Meng, Yanfei Chen, Peili Wang, Mengping He, Yuxing Shi, Yuxin Lai, Guoqiang Zhu and Heng Wang

Int. J. Mol. Sci. 2022, 23(24), 15532; https://doi.org/10.3390/ijms232415532 - 8 Dec 2022

Cited by 3 | Viewed by 1789

Abstract

Avian pathogenic Escherichia coli (APEC) is an important member of extraintestinal pathogenic Escherichia coli (ExPEC). It shares similar pathogenic strategies with neonatal meningitis E. coli (NMEC) and may threaten human health due to its potential zoonosis. RyhB is a small non-coding RNA that regulates iron homeostasis in E. coli. However, it is unclear whether RyhB regulates meningitis occurrence. To investigate the function of RyhB in the development of meningitis, we constructed the deletion mutant APEC XM∆ryhB and the complemented mutant APEC XM∆ryhB/pryhB, established a mouse meningitis model and evaluated the role of RyhB in virulence of APEC. The results showed that the deletion of ryhB decreased biofilm formation, adhesion to the brain microvascular endothelial cell line bEnd.3 and serum resistance. RNA-seq data showed that the expression of multiple virulence-related genes changed in the ryhB deletion mutant in the presence of duck serum. Deletion of ryhB reduced the clinical symptoms of mice, such as opisthotonus, diarrhea and neurological signs, when challenged with APEC. Compared with the mice infected with the wild-type APEC, fewer histopathological lesions were observed in the brain of mice infected with the ryhB deletion mutant APEC XM∆ryhB. The bacterial loads in the tissues and the relative expression of cytokines (IL-1β, IL-6, and TNF-α) in the brain significantly decreased when challenged with the APEC XM∆ryhB. The expressions of tight junction proteins (claudin-5, occludin and ZO-1) were not reduced in the brain of mice infected with APEC XM∆ryhB; that is, the blood-brain barrier permeability of mice was not significantly damaged. In conclusion, RyhB contributes to the pathogenicity of APEC XM in the meningitis-causing process by promoting biofilm formation, adhesion to endothelial cells, serum resistance and virulence-related genes expression. Full article

(This article belongs to the Special Issue Pathogenic Escherichia coli: Pathogenesis, Virulence and Control Strategies)

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18 pages, 5574 KiB

Open AccessArticle

Effect and Mechanism Analysis of Pig FUT8 Gene on Resistance to Escherichia coli F18 Infection

by Lisi Wu, Yifu Wang, Shenglong Wu, Zhengchang Wu and Wenbin Bao

Int. J. Mol. Sci. 2022, 23(23), 14713; https://doi.org/10.3390/ijms232314713 - 25 Nov 2022

Cited by 1 | Viewed by 1588

Abstract

Post-weaning diarrhea caused by enterotoxigenic Escherichia coli F18 (E. coli F18) causes significant economic losses for pig producers. Fucosyltransferase 8 (FUT8) is a glycosyltransferase that catalyzes core fucosylation; however, its role in mediating the resistance to E. coli F18 infection in pigs remains unknown. In this study, we systematically verified the relationship between FUT8 expression and E. coli resistance. The results showed that FUT8 was expressed in all detected tissues of Meishan piglets and that its expression was significantly increased in the duodenum and jejunum of E. coli F18-sensitive individuals when compared to E. coli F18-resistant individuals. FUT8 expression increased after exposure to E. coli F18 (p < 0.05) and decreased significantly after LPS induction for 6 h (p < 0.01). Then, the IPEC-J2 stable cell line with FUT8 interference was constructed, and FUT8 knockdown decreased the adhesion of E. coli F18ac to IPEC-J2 cells (p < 0.05). Moreover, we performed a comparative transcriptome study of IPEC-J2 cells after FUT8 knockdown via RNA-seq. In addition, further expression verification demonstrated the significant effect of FUT8 on the glycosphingolipid biosynthesis and Toll-like signaling pathways. Moreover, the core promoter of FUT8, which was located at −1213 bp to −673 bp, was identified via luciferase assay. Interestingly, we found a 1 bp C base insertion mutation at the −774 bp region, which could clearly inhibit the transcriptional binding activity of C/EBPα to an FUT8 promoter. Therefore, it is speculated that FUT8 acts in a critical role in the process of E. coli infection; furthermore, the low expression of FUT8 is conducive to the enhancement of E. coli resistance in piglets. Our findings revealed the mechanism of pig FUT8 in regulating E. coli resistance, which provided a theoretical basis for the screening of E. coli resistance in Chinese local pig breeds. Full article

(This article belongs to the Special Issue Pathogenic Escherichia coli: Pathogenesis, Virulence and Control Strategies)

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16 pages, 3069 KiB

Open AccessArticle

Comprehensive Analysis Revealed the Potential Roles of N⁶-Methyladenosine (m⁶A) Mediating E. coli F18 Susceptibility in IPEC-J2 Cells

by Zhengchang Wu, Yifu Wang, Tong Li, Li Yang, Jian Jin, Shenglong Wu and Wenbin Bao

Int. J. Mol. Sci. 2022, 23(21), 13602; https://doi.org/10.3390/ijms232113602 - 6 Nov 2022

Viewed by 2195

Abstract

Post-weaning diarrhea caused by enterotoxigenic Escherichia coli F18 (E. coli F18) causes significant economic losses for pig producers. N⁶-methyladenosine (m⁶A) is a highly abundant epitranscriptomic marker that has been found to be involved in regulating the resistance of host cells to pathogenic infection, but its potential role in E. coli F18-exposed intestinal porcine epithelial cells (IPEC-J2) remains undetermined. Here, we demonstrated that m⁶A and its regulators modulate E. coli F18 susceptibility. Briefly, we revealed that the Wilms’ tumor 1-associating protein (WTAP) expressions were markedly elevated in IPEC-J2 cells upon E. coli F18 exposure. WTAP are required for the regulation of E. coli F18 adhesion in IPEC-J2 cells. Additionally, WTAP knockdown significantly suppressed m⁶A level at N-acetyllactosaminide beta-1,6-N-acetylglucosaminyl-transferase (GCNT2) 3′UTR, resulting in the enhancement of TH N⁶-methyladenosine RNA binding protein 2 (YTHDF2)-mediated GCNT2 mRNA stability. Subsequently, the altered GCNT2 expressions could inhibit the glycosphingolipid biosynthesis, thus improving resistance to E. coli F18 infection in IPEC-J2. Collectively, our analyses highlighted the mechanism behind the m⁶A-mediated management of E. coli F18 susceptibility, which will aid in the development of novel approaches that protect against bacterial diarrhea in piglets. Full article

(This article belongs to the Special Issue Pathogenic Escherichia coli: Pathogenesis, Virulence and Control Strategies)

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12 pages, 1778 KiB

Open AccessArticle

The EcpD Tip Adhesin of the Escherichia coli Common Pilus Mediates Binding of Enteropathogenic E. coli to Extracellular Matrix Proteins

by Rajesh Mondal, Zeus Saldaña-Ahuactzi, Jorge Soria-Bustos, Andrew Schultz, Jorge A. Yañez-Santos, Ygnacio Martínez Laguna, María L. Cedillo-Ramírez and Jorge A. Girón

Int. J. Mol. Sci. 2022, 23(18), 10350; https://doi.org/10.3390/ijms231810350 - 8 Sep 2022

Cited by 1 | Viewed by 2191

Abstract

The attachment of enteropathogenic Escherichia coli (EPEC) to intestinal epithelial cells is facilitated by several adhesins; however, the individual host-cell receptors for pili-mediated adherence have not been fully characterized. In this study, we evaluated the hypothesis that the E. coli common pilus (ECP) tip adhesin protein EcpD mediates attachment of EPEC to several extracellular matrix (ECM) glycoproteins (fibronectin, laminin, collagens I and IV, and mucin). We found that the ΔecpA mutant, which lacks production of the EcpA filament but retains EcpD on the surface, adhered to these glycoproteins below the wild-type levels, while the ΔecpD mutant, which does not display EcpA or EcpD, bound significantly less to these host glycoproteins. In agreement, a purified recombinant EcpD subunit bound significantly more than EcpA to laminin, fibronectin, collagens I and IV, and mucin in a dose-dependent manner. These are compelling data that strongly suggest that ECP-producing EPEC may bind to host ECM glycoproteins and mucins through the tip adhesin protein EcpD. This study highlights the versatility of EPEC to bind to different host proteins and suggests that the interaction of ECP with the host’s ECM glycoproteins may facilitate colonization of the intestinal mucosal epithelium. Full article

(This article belongs to the Special Issue Pathogenic Escherichia coli: Pathogenesis, Virulence and Control Strategies)

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14 pages, 1644 KiB

Open AccessArticle

Intestinal Epithelial Cells Modulate the Production of Enterotoxins by Porcine Enterotoxigenic E. coli Strains

by Haixiu Wang, Eric Cox and Bert Devriendt

Int. J. Mol. Sci. 2022, 23(12), 6589; https://doi.org/10.3390/ijms23126589 - 13 Jun 2022

Cited by 1 | Viewed by 1881

Abstract

Enterotoxigenic Escherichia coli (ETEC) strains are one of the most common etiological agents of diarrhea in both human and farm animals. In addition to encoding toxins that cause diarrhea, ETEC have evolved numerous strategies to interfere with host defenses. These strategies most likely depend on the sensing of host factors, such as molecules secreted by gut epithelial cells. The present study tested whether the exposure of ETEC to factors secreted by polarized IPEC-J2 cells resulted in transcriptional changes of ETEC-derived virulence factors. Following the addition of host-derived epithelial factors, genes encoding enterotoxins, secretion-system-associated proteins, and the key regulatory molecule cyclic AMP (cAMP) receptor protein (CRP) were substantially modulated, suggesting that ETEC recognize and respond to factors produced by gut epithelial cells. To determine whether these factors were heat sensitive, the IEC-conditioned medium was incubated at 56 °C for 30 min. In most ETEC strains, heat treatment of the IEC-conditioned medium resulted in a loss of transcriptional modulation. Taken together, these data suggest that secreted epithelial factors play a role in bacterial pathogenesis by modulating the transcription of genes encoding key ETEC virulence factors. Further research is warranted to identify these secreted epithelial factors and how ETEC sense these molecules to gain a competitive advantage in the early engagement of the gut epithelium. Full article

(This article belongs to the Special Issue Pathogenic Escherichia coli: Pathogenesis, Virulence and Control Strategies)

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Review

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21 pages, 3854 KiB

Open AccessReview

Bacterial and Viral Co-Infection in the Intestine: Competition Scenario and Their Effect on Host Immunity

by Siqi Lian, Jiaqi Liu, Yunping Wu, Pengpeng Xia and Guoqiang Zhu

Int. J. Mol. Sci. 2022, 23(4), 2311; https://doi.org/10.3390/ijms23042311 - 19 Feb 2022

Cited by 15 | Viewed by 4113

Abstract

Bacteria and viruses are both important pathogens causing intestinal infections, and studies on their pathogenic mechanisms tend to focus on one pathogen alone. However, bacterial and viral co-infections occur frequently in clinical settings, and infection by one pathogen can affect the severity of infection by another pathogen, either directly or indirectly. The presence of synergistic or antagonistic effects of two pathogens in co-infection can affect disease progression to varying degrees. The triad of bacterial–viral–gut interactions involves multiple aspects of inflammatory and immune signaling, neuroimmunity, nutritional immunity, and the gut microbiome. In this review, we discussed the different scenarios triggered by different orders of bacterial and viral infections in the gut and summarized the possible mechanisms of synergy or antagonism involved in their co-infection. We also explored the regulatory mechanisms of bacterial–viral co-infection at the host intestinal immune interface from multiple perspectives. Full article

(This article belongs to the Special Issue Pathogenic Escherichia coli: Pathogenesis, Virulence and Control Strategies)

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