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Salmonella Pathophysiology and Host-Bacteria Relationship
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Salmonella Pathophysiology and Host-Bacteria Relationship

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 (27 February 2024) | Viewed by 4540

Special Issue Editor

Prof. Dr. John Hwa Lee

E-Mail Website
Guest Editor
College of Veterinary Medicine, Jeonbuk National University, Iksan 54596, Republic of Korea
Interests: veterinary vaccines; delivery systems; Salmonella vectored vaccines; Salmonella in cancer therapy; oral mRNA vaccine; Salmonella pathophysiology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Salmonella is a group of Gram-negative bacteria that account for varied pathogy in the host depending on the serovars. Typhoidal and non-typhoidal Salmonella (NTS) interact with the host defense machinery and elicit  varied immune responses in humans. NTS serovars cause a local intestinal immune response in the gut mucosa resulting in self-limiting diarrhea. Bacteremia is rare in NTS infection but can occur in immunocompromised individuals and infants in sub-saharan regions. On the other hand, Typhoidal serovars do not cause acute diarrhea or induce neutrophil migration into the gut lumen. After circumventing the acidic environment in the stomach, the bacteria prevents neutrophil infiltration resulting from activation of TLRs, and enters the circulation via immune cells to establish systemic infection. Host-pathogen interaction in salmonellosis using patient records, murine models, and whole genome sequencing have provided new insights. The genome of Typhoidal servovars harbor many inactivated or disrupted genes compared to the NTS serovas. This may partly contribute to serovar-specific disease outcome in the host. A better understanding of the Salmonella pathogenesis will help develop potential therapeutic strategies.

This Special Issue invites original research articles, communications, and reviews that describe the Salmonella pathophysiology, its virulence machinery and ability to interact and circumvent host immune response machinery to establish sucessful infection. We look forward to receiving your contributions.

Prof. Dr. John Hwa Lee
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Salmonella
  • Salmonella serovars
  • virulence factors
  • host immune response
  • human health
  • animal health and productivity
  • infection models

Published Papers (5 papers)

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Research

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15 pages, 2914 KiB  
Article
Deciphering the Interrelationship of arnT Involved in Lipid-A Alteration with the Virulence of Salmonella Typhimurium
by Chandran Sivasankar, Khristine Kaith Sison Lloren and John Hwa Lee
Int. J. Mol. Sci. 2024, 25(5), 2760; https://doi.org/10.3390/ijms25052760 - 27 Feb 2024
Viewed by 582
Abstract
The lipopolysaccharide (LPS) that resides on the outermost surface and protects Gram-negative bacteria from host defenses is one of the key components leading to Salmonella infection, particularly the endotoxic lipid A domain of LPS. Lipid A modifications have been associated with several genes [...] Read more.
The lipopolysaccharide (LPS) that resides on the outermost surface and protects Gram-negative bacteria from host defenses is one of the key components leading to Salmonella infection, particularly the endotoxic lipid A domain of LPS. Lipid A modifications have been associated with several genes such as the arnT that encodes 4-amino-4-deoxy-L-arabinose transferase, which can be critical for bacteria to resist cationic antimicrobial peptides and interfere with host immune recognition. However, the association of arnT with virulence is not completely understood. Thus, this study aimed to elucidate the interrelationship of the major lipid A modification gene arnT with Salmonella Typhimurium virulence. We observed that the arnT-deficient S. Typhimurium (JOL2943), compared to the wild type (JOL401), displayed a significant decrease in several virulence phenotypes such as polymyxin B resistance, intracellular survival, swarming, and biofilm and extracellular polymeric substance (EPS) production. Interestingly, the cell-surface hydrophobicity, adhesion, and invasion characteristics remained unaffected. Additionally, LPS isolated from the mutant induced notably lower levels of endotoxicity-related cytokines in RAW and Hela cells and mice, particularly IL-1β with a nine-fold decrease, than WT. In terms of in vivo colonization, JOL2943 showed diminished presence in internal organs such as the spleen and liver by more than 60%, while ileal infectivity remained similar to JOL401. Overall, the arnT deletion rendered the strain less virulent, with low endotoxicity, maintained gut infectivity, and reduced colonization in internal organs. With these ideal characteristics, it can be further explored as a potential attenuated Salmonella strain for therapeutics or vaccine delivery systems. Full article
(This article belongs to the Special Issue Salmonella Pathophysiology and Host-Bacteria Relationship)
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15 pages, 3583 KiB  
Article
Phosphate (Pi) Transporter PIT1 Induces Pi Starvation in Salmonella-Containing Vacuole in HeLa Cells
by Wen Yang, Yingxing Feng, Jun Yan, Chenbo Kang, Ting Yao, Hongmin Sun and Zhihui Cheng
Int. J. Mol. Sci. 2023, 24(24), 17216; https://doi.org/10.3390/ijms242417216 - 07 Dec 2023
Viewed by 762
Abstract
Salmonella enterica serovar Typhimurium (S. Typhimurium), an important foodborne pathogen, causes diarrheal illness and gastrointestinal diseases. S. Typhimurium survives and replicates in phagocytic and non-phagocytic cells for acute or chronic infections. In these cells, S. Typhimurium resides within Salmonella [...] Read more.
Salmonella enterica serovar Typhimurium (S. Typhimurium), an important foodborne pathogen, causes diarrheal illness and gastrointestinal diseases. S. Typhimurium survives and replicates in phagocytic and non-phagocytic cells for acute or chronic infections. In these cells, S. Typhimurium resides within Salmonella-containing vacuoles (SCVs), in which the phosphate (Pi) concentration is low. S. Typhimurium senses low Pi and expresses virulence factors to modify host cells. However, the mechanism by which host cells reduce the Pi concentration in SCVs is not clear. In this study, we show that through the TLR4-MyD88-NF-κB signaling pathway, S. Typhimurium upregulates PIT1, which in turn transports Pi from SCVs into the cytosol and results in Pi starvation in SCVs. Immunofluorescence and western blotting analysis reveal that after the internalization of S. Typhimurium, PIT1 is located on SCV membranes. Silencing or overexpressing PIT1 inhibits or promotes Pi starvation, Salmonella pathogenicity island-2 (SPI-2) gene expression, and replication in SCVs. The S. Typhimurium ΔmsbB mutant or silenced TLR4-MyD88-NF-κB pathway suppresses the expression of the SPI-2 genes and promotes the fusion of SCVs with lysosomes. Our results illustrate that S. Typhimurium exploits the host innate immune responses as signals to promote intracellular replication, and they provide new insights for the development of broad-spectrum therapeutics to combat bacterial infections. Full article
(This article belongs to the Special Issue Salmonella Pathophysiology and Host-Bacteria Relationship)
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19 pages, 3136 KiB  
Article
Evaluation of the Antimicrobial Activity of a Formulation Containing Ascorbic Acid and Eudragit FS 30D Microparticles for the Controlled Release of a Curcumin–Boric Acid Solid Dispersion in Turkey Poults Infected with Salmonella enteritidis: A Therapeutic Model
by Daniel Hernandez-Patlan, Bruno Solis-Cruz, Juan D. Latorre, Jesus A. Maguey-Gonzalez, Inkar Castellanos-Huerta, Eric Beyssac, Ghislain Garrait, Alma Vázquez-Durán, Raquel López-Arellano, Abraham Méndez-Albores, Billy M. Hargis and Guillermo Tellez-Isaias
Int. J. Mol. Sci. 2023, 24(22), 16186; https://doi.org/10.3390/ijms242216186 - 10 Nov 2023
Viewed by 752
Abstract
The selection of components within a formulation or for treatment must stop being arbitrary and must be focused on scientific evidence that supports the inclusion of each one. Therefore, the objective of the present study was to obtain a formulation based on ascorbic [...] Read more.
The selection of components within a formulation or for treatment must stop being arbitrary and must be focused on scientific evidence that supports the inclusion of each one. Therefore, the objective of the present study was to obtain a formulation based on ascorbic acid (AA) and Eudragit FS 30D microparticles containing curcumin–boric acid (CUR–BA) considering interaction studies between the active components carried out via Fourier transform infrared spectrometry (FTIR) and differential scanning calorimetry (DSC) to minimize antagonistic effects, and comprehensively and effectively treat turkey poults infected with Salmonella enteritidis (S. enteritidis). The DSC and FTIR studies clearly demonstrated the interactions between AA, BA, and CUR. Consequently, the combination of AA with CUR and/or BA should be avoided, but not CUR and BA. Furthermore, the Eudragit FS 30D microparticles containing CUR–BA (SD CUR–BA MP) showed a limited release of CUR–BA in an acidic medium, but they were released at a pH 6.8–7.0, which reduced the interactions between CUR–BA and AA. Finally, in the S. enteritidis infection model, turkey poults treated with the combination of AA and SD CUR–BA MP presented lower counts of S. enteritidis in cecal tonsils after 10 days of treatment. These results pointed out that the use of an adequate combination of AA and CUR–BA as an integral treatment of S. enteritidis infections could be a viable option to replace the indiscriminate use of antibiotics. Full article
(This article belongs to the Special Issue Salmonella Pathophysiology and Host-Bacteria Relationship)
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17 pages, 2976 KiB  
Article
A Potential Adhesin/Invasin STM0306 Participates in Host Cell Inflammation Induced by Salmonella enterica Serovar Typhimurium
by Chong Ling, Shujie Liang, Yan Li, Qingyun Cao, Hui Ye, Changming Zhang, Zemin Dong, Dingyuan Feng, Weiwei Wang and Jianjun Zuo
Int. J. Mol. Sci. 2023, 24(9), 8170; https://doi.org/10.3390/ijms24098170 - 03 May 2023
Viewed by 1569
Abstract
Salmonella enterica serovar typhimurium (S. Typhimurium) is a common Gram-negative foodborne pathogenic bacterium that causes gastrointestinal disease in humans and animals. It is well known that adhesins and invasins play crucial roles in the infection mechanism of S. Typhimurium. S. Typhimurium STM0306 [...] Read more.
Salmonella enterica serovar typhimurium (S. Typhimurium) is a common Gram-negative foodborne pathogenic bacterium that causes gastrointestinal disease in humans and animals. It is well known that adhesins and invasins play crucial roles in the infection mechanism of S. Typhimurium. S. Typhimurium STM0306 has been denoted as a putative protein and its functions have rarely been reported. In this study, we constructed the STM0306 gene mutant strain of S. Typhimurium and purified the recombinant STM0306 from Escherichia coli. Deletion of the STM0306 gene resulted in reduced adhesion and invasion of S. Typhimurium to IPEC-J2, Caco-2, and RAW264.7 cells. In addition, STM0306 could bind to intestinal epithelial cells and induced F-actin modulation in IPEC-J2 cells. Furthermore, we found that STM0306 activated the nuclear factor kappa B (NF-κB) signaling pathway and increased the mRNA expression of pro-inflammatory cytokines such as IL-1β, TNF-α, as well as chemokine CXCL2, thus resulting in cellular inflammation in host cells. In vivo, the deletion of the STM0306 gene led to reduced pathogenicity of S. Typhimurium, as evidenced by lower fecal bacterial counts and reduced body weight loss in S. Typhimurium infected mice. In conclusion, the STM0306 of S. Typhimurium is an important adhesin/invasin involved in the pathogenic process and cellular inflammation of the host. Full article
(This article belongs to the Special Issue Salmonella Pathophysiology and Host-Bacteria Relationship)
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Review

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18 pages, 5296 KiB  
Review
Functional Divergence of the Paralog Salmonella Effector Proteins SopD and SopD2 and Their Contributions to Infection
by Mosopefoluwa T. Oke and Vanessa M. D’Costa
Int. J. Mol. Sci. 2024, 25(8), 4191; https://doi.org/10.3390/ijms25084191 - 10 Apr 2024
Viewed by 304
Abstract
Salmonella enterica is a leading cause of bacterial food-borne illness in humans and is responsible for millions of cases annually. A critical strategy for the survival of this pathogen is the translocation of bacterial virulence factors termed effectors into host cells, which primarily [...] Read more.
Salmonella enterica is a leading cause of bacterial food-borne illness in humans and is responsible for millions of cases annually. A critical strategy for the survival of this pathogen is the translocation of bacterial virulence factors termed effectors into host cells, which primarily function via protein–protein interactions with host proteins. The Salmonella genome encodes several paralogous effectors believed to have arisen from duplication events throughout the course of evolution. These paralogs can share structural similarities and enzymatic activities but have also demonstrated divergence in host cell targets or interaction partners and contributions to the intracellular lifecycle of Salmonella. The paralog effectors SopD and SopD2 share 63% amino acid sequence similarity and extensive structural homology yet have demonstrated divergence in secretion kinetics, intracellular localization, host targets, and roles in infection. SopD and SopD2 target host Rab GTPases, which represent critical regulators of intracellular trafficking that mediate diverse cellular functions. While SopD and SopD2 both manipulate Rab function, these paralogs display differences in Rab specificity, and the effectors have also evolved multiple mechanisms of action for GTPase manipulation. Here, we highlight this intriguing pair of paralog effectors in the context of host–pathogen interactions and discuss how this research has presented valuable insights into effector evolution. Full article
(This article belongs to the Special Issue Salmonella Pathophysiology and Host-Bacteria Relationship)
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