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Biomolecules
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Advances in Molecular Pathology and Therapeutics of Bacterial Infections
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Advances in Molecular Pathology and Therapeutics of Bacterial Infections

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: closed (31 October 2020) | Viewed by 6774

Special Issue Editor

Prof. Dr. Maria Lina Bernardini

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Guest Editor
Department of Biology and Biotechnology, Sapienza University of Rome, Via dei Sardi 70, 00185 Rome, Italy
Interests: pathogenic bacteria; bacterial structures; innate immunity; cellular microbiology; vaccines

Special Issue Information

Dear Colleagues,

Since the end of the last century, the development of molecular biology and genetic tools has improved our understanding of the molecular mechanisms underlying the virulence of pathogenic bacteria. Studies about bacterial secretion systems and effector mechanisms have paved the way for cellular microbiology, unveiling the sophisticated strategies of bacterial pathogens. This could be dubbed as the golden age of bacterial pathogenesis studies. Our improved knowledge of host innate immunity and the corresponding pathogen immune evasion strategies has highlighted the still unexplored aspects of the relationship between host and pathogen. This ménage a deux soon became a ménage à trois upon discovery of the crucial role played by microbiota.  Despite the dramatic reduction in the incidence of infectious diseases, new bacterial pathogens are emerging and old illnesses, such as tuberculosis, bacteria-induced pneumoniae, and diarrheas, still result in global mortality. Treatment with conventional antibiotics has been hampered by the increased rate of antibiotic resistance that often results from multidrug- or pandrug-resistant bacterial strains. In this context, pharmaceutical industries have been reducing the development of new antibiotics. A scenario is thus arising of a future where many bacterial infections could become untreatable. As a result, alternative non-antibiotic approaches are being explored in order to develop novel reliable therapies.

In this Special Issue, we will provide an overview of state-of-the-art molecular mechanisms of bacterial pathogenesis and innovative therapeutic approaches to fight against bacterial infection.

Prof. Dr. Maria Lina Bernardini
Guest Editor

Keywords

  • pathogenic bacteria
  • emerging bacterial pathogens
  • molecular mechanisms of virulence
  • antibacterial therapies
  • novel antibacterial approaches
  • antibiotic resistance mechanisms

Published Papers (2 papers)

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20 pages, 6786 KiB  
Article
Chain-Selective Isotopic Labeling of the Heterodimeric Type III Secretion Chaperone, Scc4:Scc1, Reveals the Total Structural Rearrangement of the Chlamydia trachomatis Bi-Functional Protein, Scc4
by Thilini O. Ukwaththage, Samantha M. Keane, Li Shen and Megan A. Macnaughtan
Biomolecules 2020, 10(11), 1480; https://doi.org/10.3390/biom10111480 - 24 Oct 2020
Cited by 2 | Viewed by 2189
Abstract
Scc4 is an unusual bi-functional protein from Chlamydia trachomatis (CT) that functions as a type III secretion system (T3SS) chaperone and an RNA polymerase (RNAP)-binding protein. Both functions require interactions with protein partners during specific stages of the CT developmental cycle. [...] Read more.
Scc4 is an unusual bi-functional protein from Chlamydia trachomatis (CT) that functions as a type III secretion system (T3SS) chaperone and an RNA polymerase (RNAP)-binding protein. Both functions require interactions with protein partners during specific stages of the CT developmental cycle. As a T3SS chaperone, Scc4 binds Scc1 during the late stage of development to form a heterodimer complex, which chaperones the essential virulence effector, CopN. During the early-middle stage of development, Scc4 regulates T3SS gene expression by binding the σ66-containing RNAP holoenzyme. In order to study the structure and association mechanism of the Scc4:Scc1 T3SS chaperone complex using nuclear magnetic resonance (NMR) spectroscopy, we developed an approach to selectively label each chain of the Scc4:Scc1 complex with the 15N-isotope. The approach allowed one protein to be visible in the NMR spectrum at a time, which greatly reduced resonance overlap and permitted comparison of the backbone structures of free and bound Scc4. 1H,15N-heteronuclear single quantum coherence spectra of the 15N-Scc4:Scc1 and Scc4:15N-Scc1 complexes showed a total structural rearrangement of Scc4 upon binding Scc1 and a dynamic region isolated to Scc1, respectively. Development of the chain-selective labeling approach revealed that the association of Scc4 and Scc1 requires partial denaturation of Scc1 to form the high affinity complex, while low affinity interactions occurred between the isolated proteins under non-denaturing conditions. These results provide new models for Scc4′s functional switching mechanism and Scc4:Scc1 association in CT. Full article
(This article belongs to the Special Issue Advances in Molecular Pathology and Therapeutics of Bacterial Infections)
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23 pages, 7806 KiB  
Article
Autophagy Inhibits Grass Carp Reovirus (GCRV) Replication and Protects Ctenopharyngodon idella Kidney (CIK) Cells from Excessive Inflammatory Responses after GCRV Infection
by Pengfei Chu, Libo He, Rong Huang, Lanjie Liao, Yongming Li, Zuoyan Zhu, Wei Hu and Yaping Wang
Biomolecules 2020, 10(9), 1296; https://doi.org/10.3390/biom10091296 - 8 Sep 2020
Cited by 28 | Viewed by 4192
Abstract
Autophagy is an essential and highly conserved process in mammals, which is critical to maintaining physiological homeostasis, including cell growth, development, repair, and survival. However, the understanding of autophagy in fish virus replication is limited. In this study, we found that grass carp [...] Read more.
Autophagy is an essential and highly conserved process in mammals, which is critical to maintaining physiological homeostasis, including cell growth, development, repair, and survival. However, the understanding of autophagy in fish virus replication is limited. In this study, we found that grass carp reovirus (GCRV) infection stimulated autophagy in the spleen of grass carp (Ctenopharyngodon idella). Moreover, both Western blot (WB) analysis and fluorescent tracer tests showed that GCRV infection induced the enhancement of autophagy activation in Ctenopharyngodon idella kidney (CIK) cells. Autophagy inducer rapamycin and autophagy inhibitor 3-MA pretreatment can inhibit and promote the proliferation of GCRV, respectively. In addition, grass carp autophagy-related gene 5 (CiATG5)-induced autophagy, as well as rapamycin, showed effects on GCRV replication in CIK cells. Transcriptome analysis revealed that the total number of differentially expressed genes (DEGs) in CiATG5 overexpression groups was less than that of the control during GCRV infection. Enrichment analysis showed that CiATG5 overexpression induced the enhancement of autophagy, lysosome, phagosome, and apoptosis in the early stage of GCRV infection, which led to the clearance of viruses. In the late stage, steroid biosynthesis, DNA replication, terpenoid backbone biosynthesis, and carbon metabolism were upregulated, which contributed to cell survival. Moreover, signaling pathways involved in the immune response and cell death were downregulated in CiATG5 overexpression groups. Further study showed that CiATG5 repressed the expression of inflammatory response genes, including cytokines and type I interferons. Taken together, the results demonstrate that autophagy represses virus replication and attenuates acute inflammatory responses to protect cells. Full article
(This article belongs to the Special Issue Advances in Molecular Pathology and Therapeutics of Bacterial Infections)
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