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Molecular Mechanisms of Infection for Pathogenic Bacteria 2.0

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 (25 March 2024) | Viewed by 2287

Special Issue Editor


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Guest Editor

Special Issue Information

Dear Colleagues,

This Special Issue is a continuation of our previous Special Issue entitled Molecular Mechanisms of Infection for Pathogenic Bacteria.

The molecular mechanisms of infection for pathogenic bacteria can be now more easily characterized in terms of genomic and proteomic approaches. Pathogenic bacteria are diverse in their gene sets. Many virulence factors are maintained on a virulence plasmid and were acquired through horizontal gene transfer. Others were integrated into the chromosome by bacteriophages or transposable elements. Although the gain of traits is important in the evolution of a pathogen, the loss of certain genes is necessary to become fully pathogenic. We are beginning to dissect the interactions between virulence factors from pathogenic bacteria and host cell components. Several pathogenic molecules have been shown to hijack and manipulate host–cell processes for the benefit of the bacterium. Detailed knowledge of the molecular mechanisms of microbial pathogenicity is necessary in order to develop new strategies against infectious diseases and thus lower their impact on human health and social development. In this Special Issue, we will focus on these molecules, which represent infection mechanisms specially developed by pathogenic bacteria, either by increasing their virulence or by compromising the host defense.

Prof. Dr. Juan M. Tomás
Guest Editor

Manuscript Submission Information

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Keywords

  • bacterial pathogen
  • infection
  • molecules
  • host defense
  • infectious diseases
  • human health
  • infection models
  • virulence factors

Published Papers (3 papers)

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Research

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17 pages, 3694 KiB  
Article
EspP2 Regulates the Adhesion of Glaesserella parasuis via Rap1 Signaling Pathway
by Xinwei Tang, Shiyu Xu, Zhen Yang, Kang Wang, Ke Dai, Yiwen Zhang, Bangdi Hu, Yu Wang, Sanjie Cao, Xiaobo Huang, Qigui Yan, Rui Wu, Qin Zhao, Senyan Du, Xintian Wen and Yiping Wen
Int. J. Mol. Sci. 2024, 25(8), 4570; https://doi.org/10.3390/ijms25084570 - 22 Apr 2024
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Abstract
Different levels of EspP2 expression are seen in strains of Glaesserella parasuis with high and low pathogenicity. As a potential virulence factor for G. parasuis, the pathogenic mechanism of EspP2 in infection of host cells is not clear. To begin to elucidate [...] Read more.
Different levels of EspP2 expression are seen in strains of Glaesserella parasuis with high and low pathogenicity. As a potential virulence factor for G. parasuis, the pathogenic mechanism of EspP2 in infection of host cells is not clear. To begin to elucidate the effect of EspP2 on virulence, we used G. parasuis SC1401 in its wild-type form and SC1401, which was made EspP2-deficient. We demonstrated that EspP2 causes up-regulation of claudin-1 and occludin expression, thereby promoting the adhesion of G. parasuis to host cells; EspP2-deficiency resulted in significantly reduced adhesion of G. parasuis to cells. Transcriptome sequencing analysis of EspP2-treated PK15 cells revealed that the Rap1 signaling pathway is stimulated by EspP2. Blocking this pathway diminished occludin expression and adhesion. These results indicated that EspP2 regulates the adhesion of Glaesserella parasuis via Rap1 signaling pathway. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Infection for Pathogenic Bacteria 2.0)
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14 pages, 6685 KiB  
Article
H9N2 Avian Influenza Virus Downregulates FcRY Expression in Chicken Macrophage Cell Line HD11 by Activating the JNK MAPK Pathway
by Zhijian Sun, Wenjie Zhang, Jian Li, Kang Yang, Yanhao Zhang and Zili Li
Int. J. Mol. Sci. 2024, 25(5), 2650; https://doi.org/10.3390/ijms25052650 - 24 Feb 2024
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Abstract
The H9N2 avian influenza virus causes reduced production performance and immunosuppression in chickens. The chicken yolk sac immunoglobulins (IgY) receptor (FcRY) transports from the yolk into the embryo, providing offspring with passive immunity to infection against common poultry pathogens. FcRY is expressed in [...] Read more.
The H9N2 avian influenza virus causes reduced production performance and immunosuppression in chickens. The chicken yolk sac immunoglobulins (IgY) receptor (FcRY) transports from the yolk into the embryo, providing offspring with passive immunity to infection against common poultry pathogens. FcRY is expressed in many tissues/organs of the chicken; however, there are no reports investigating FcRY expression in chicken macrophage cells, and how H9N2-infected HD11 cells (a chicken macrophage-like cell line) regulate FcRY expression remains uninvestigated. This study used the H9N2 virus as a model pathogen to explore the regulation of FcRY expression in avian macrophages. FcRY was highly expressed in HD11 cells, as shown by reverse transcription polymerase chain reactions, and indirect immunofluorescence indicated that FcRY was widely expressed in HD11 cells. HD11 cells infected with live H9N2 virus exhibited downregulated FcRY expression. Transfection of eukaryotic expression plasmids encoding each viral protein of H9N2 into HD11 cells revealed that nonstructural protein (NS1) and matrix protein (M1) downregulated FcRY expression. In addition, the use of a c-jun N-terminal kinase (JNK) activator inhibited the expression of FcRY, while a JNK inhibitor antagonized the downregulation of FcRY expression by live H9N2 virus, NS1 and M1 proteins. Finally, a dual luciferase reporter system showed that both the M1 protein and the transcription factor c-jun inhibited FcRY expression at the transcriptional level. Taken together, the transcription factor c-jun was a negative regulator of FcRY, while the live H9N2 virus, NS1, and M1 proteins downregulated the FcRY expression through activating the JNK signaling pathway. This provides an experimental basis for a novel mechanism of immunosuppression in the H9N2 avian influenza virus. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Infection for Pathogenic Bacteria 2.0)
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Review

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13 pages, 1409 KiB  
Review
Remarkable Phenotypic Virulence Factors of Microsporum canis and Their Associated Genes: A Systematic Review
by Tania Vite-Garín, Norma Angélica Estrada-Cruz, Rigoberto Hernández-Castro, Claudia Erika Fuentes-Venado, Paola Berenice Zarate-Segura, María Guadalupe Frías-De-León, Macario Martínez-Castillo, Erick Martínez-Herrera and Rodolfo Pinto-Almazán
Int. J. Mol. Sci. 2024, 25(5), 2533; https://doi.org/10.3390/ijms25052533 - 22 Feb 2024
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Abstract
Microsporum canis is a widely distributed dermatophyte, which is among the main etiological agents of dermatophytosis in humans and domestic animals. This fungus invades, colonizes and nourishes itself on the keratinized tissues of the host through various virulence factors. This review will bring [...] Read more.
Microsporum canis is a widely distributed dermatophyte, which is among the main etiological agents of dermatophytosis in humans and domestic animals. This fungus invades, colonizes and nourishes itself on the keratinized tissues of the host through various virulence factors. This review will bring together the known information about the mechanisms, enzymes and their associated genes relevant to the pathogenesis processes of the fungus and will provide an overview of those virulence factors that should be better studied to establish effective methods of prevention and control of the disease. Public databases using the MeSH terms “Microsporum canis”, “virulence factors” and each individual virulence factor were reviewed to enlist a series of articles, from where only original works in English and Spanish that included relevant information on the subject were selected. Out of the 147 articles obtained in the review, 46 were selected that reported virulence factors for M. canis in a period between 1988 and 2023. The rest of the articles were discarded because they did not contain information on the topic (67), some were written in different languages (3), and others were repeated in two or more databases (24) or were not original articles (7). The main virulence factors in M. canis are keratinases, fungilisins and subtilisins. However, less commonly reported are biofilms or dipeptidylpeptidases, among others, which have been little researched because they vary in expression or activity between strains and are not considered essential for the infection and survival of the fungus. Although it is known that they are truly involved in resistance, infection and metabolism, we recognize that their study could strengthen the knowledge of the pathogenesis of M. canis with the aim of achieving effective treatments, as well as the prevention and control of infection. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Infection for Pathogenic Bacteria 2.0)
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