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  1. Article ; Online: Murine Soft Tissue Infection Model to Study Group A Streptococcus (GAS) Pathogenesis in Necrotizing Fasciitis.

    Ravins, Miriam / Ambalavanan, Poornima / Biswas, Debabrata / Tan, Rachel Ying Min / Lim, Kimberly Xuan Zhen / Kaufman, Yael / Anand, Aparna / Sharma, Abhinay / Hanski, Emanuel

    Methods in molecular biology (Clifton, N.J.)

    2022  Volume 2427, Page(s) 185–200

    Abstract: Group A streptococcus (GAS) necrotizing fasciitis (NF) causes high morbidity and mortality despite prompt intravenous administration of antibiotics, surgical soft-tissue debridement, and supportive treatment in the intensive care unit. Since there is no ... ...

    Abstract Group A streptococcus (GAS) necrotizing fasciitis (NF) causes high morbidity and mortality despite prompt intravenous administration of antibiotics, surgical soft-tissue debridement, and supportive treatment in the intensive care unit. Since there is no effective vaccine against GAS infections, a comprehensive understanding of NF pathogenesis is required to design more efficient treatments. To increase our understanding of NF pathogenesis, we need a reliable animal model that mirrors, at least in part, the infectious process in humans. This chapter describes a reliable murine model of human NF that mimics the histopathology observed in humans, namely the destruction of soft tissue, a paucity of infiltrating neutrophils, and the presence of many gram-positive cocci at the center of the infection.
    MeSH term(s) Animals ; Anti-Bacterial Agents/pharmacology ; Anti-Bacterial Agents/therapeutic use ; Fasciitis, Necrotizing/drug therapy ; Fasciitis, Necrotizing/pathology ; Mice ; Soft Tissue Infections/drug therapy ; Streptococcal Infections ; Streptococcus pyogenes
    Chemical Substances Anti-Bacterial Agents
    Language English
    Publishing date 2022-05-26
    Publishing country United States
    Document type Journal Article
    ISSN 1940-6029
    ISSN (online) 1940-6029
    DOI 10.1007/978-1-0716-1971-1_16
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Dominant Negative TRAF3 Variant With Recurrent

    Liew, Mei Fong / Lim, Hui Fang / Liang, Mui Cheng / Lim, Ives / Tan, Zhaohong / Tan, Rachel Ying Min / Sam, Qi Hui / Soe, Win Mar / Tay, Sen Hee / Xu, Shengli / Chang, Matthew Wook / Foo, Roger / Soong, Tuck Wah / Ravikumar, Sharada / Chai, Louis Yi Ann

    Open forum infectious diseases

    2022  Volume 9, Issue 8, Page(s) ofac379

    Abstract: Host factors leading to pulmonary nontuberculous mycobacteria (PNTM) disease are poorly understood compared with disseminated NTM disease, which is linked to the interleukin 12-interferon gamma signaling pathway. We investigated the tumor necrosis factor ...

    Abstract Host factors leading to pulmonary nontuberculous mycobacteria (PNTM) disease are poorly understood compared with disseminated NTM disease, which is linked to the interleukin 12-interferon gamma signaling pathway. We investigated the tumor necrosis factor receptor associated factor 3 (TRAF3) R338W variant in a patient with recurrent PNTM infection, demonstrating TRAF3- and TNF-α-deficient phenotypes via ex vivo immune and cloning-transfection cellular studies.
    Language English
    Publishing date 2022-08-03
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2757767-3
    ISSN 2328-8957
    ISSN 2328-8957
    DOI 10.1093/ofid/ofac379
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Unfolded protein response inhibitors cure group A streptococcal necrotizing fasciitis by modulating host asparagine.

    Anand, Aparna / Sharma, Abhinay / Ravins, Miriam / Biswas, Debabrata / Ambalavanan, Poornima / Lim, Kimberly Xuan Zhen / Tan, Rachel Ying Min / Johri, Atul Kumar / Tirosh, Boaz / Hanski, Emanuel

    Science translational medicine

    2021  Volume 13, Issue 605

    Abstract: Group A streptococcus (GAS) is among the top 10 causes of mortality from an infectious disease, producing mild to invasive life-threatening manifestations. Necrotizing fasciitis (NF) is characterized by a rapid GAS spread into fascial planes followed by ... ...

    Abstract Group A streptococcus (GAS) is among the top 10 causes of mortality from an infectious disease, producing mild to invasive life-threatening manifestations. Necrotizing fasciitis (NF) is characterized by a rapid GAS spread into fascial planes followed by extensive tissue destruction. Despite prompt treatments of antibiotic administration and tissue debridement, mortality from NF is still high. Moreover, there is no effective vaccine against GAS, and early diagnosis of NF is problematic because its clinical presentations are not specific. Thus, there is a genuine need for effective treatments against GAS NF. Previously, we reported that GAS induces endoplasmic reticulum (ER) stress to gain asparagine from the host. Here, we demonstrate that GAS-mediated asparagine induction and release occur through the PERK-eIF2α-ATF4 branch of the unfolded protein response. Inhibitors of PERK or integrated stress response (ISR) blocked the formation and release of asparagine by infected mammalian cells, and exogenously added asparagine overcame this inhibition. Moreover, in a murine model of NF, we show that the inhibitors minimized mortality when mice were challenged with a lethal dose of GAS and reduced bacterial counts and lesion size when mice were challenged with a sublethal dose. Immunohistopathology studies demonstrated that PERK/ISR inhibitors protected mice by enabling neutrophil infiltration into GAS-infected fascia and reducing the pro-inflammatory response that causes tissue damage. Inhibitor treatment was also effective in mice when started at 12 hours after infection. We conclude that host metabolic alteration induced by PERK or ISR inhibitors is a promising therapeutic strategy to treat highly invasive GAS infections.
    MeSH term(s) Animals ; Asparagine ; Fasciitis, Necrotizing/drug therapy ; Mice ; Streptococcal Infections/drug therapy ; Streptococcus pyogenes ; Unfolded Protein Response
    Chemical Substances Asparagine (7006-34-0)
    Language English
    Publishing date 2021-08-04
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2518854-9
    ISSN 1946-6242 ; 1946-6234
    ISSN (online) 1946-6242
    ISSN 1946-6234
    DOI 10.1126/scitranslmed.abd7465
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: LL-37-mediated activation of host receptors is critical for defense against group A streptococcal infection.

    Biswas, Debabrata / Ambalavanan, Poornima / Ravins, Miriam / Anand, Aparna / Sharma, Abhinay / Lim, Kimberly Xuan Zhen / Tan, Rachel Ying Min / Lim, Hwee Ying / Sol, Asaf / Bachrach, Gilad / Angeli, Veronique / Hanski, Emanuel

    Cell reports

    2021  Volume 34, Issue 9, Page(s) 108766

    Abstract: Group A Streptococcus (GAS) causes diverse human diseases, including life-threatening soft-tissue infections. It is accepted that the human antimicrobial peptide LL-37 protects the host by killing GAS. Here, we show that GAS extracellular protease ScpC N- ...

    Abstract Group A Streptococcus (GAS) causes diverse human diseases, including life-threatening soft-tissue infections. It is accepted that the human antimicrobial peptide LL-37 protects the host by killing GAS. Here, we show that GAS extracellular protease ScpC N-terminally cleaves LL-37 into two fragments of 8 and 29 amino acids, preserving its bactericidal activity. At sub-bactericidal concentrations, the cleavage inhibits LL-37-mediated neutrophil chemotaxis, shortens neutrophil lifespan, and eliminates P2X7 and EGF receptors' activation. Mutations at the LL-37 cleavage site protect the peptide from ScpC-mediated splitting, maintaining all its functions. The mouse LL-37 ortholog CRAMP is neither cleaved by ScpC nor does it activate P2X7 or EGF receptors. Treating wild-type or CRAMP-null mice with sub-bactericidal concentrations of the non-cleavable LL-37 analogs promotes GAS clearance that is abolished by the administration of either P2X7 or EGF receptor antagonists. We demonstrate that LL-37-mediated activation of host receptors is critical for defense against GAS soft-tissue infections.
    MeSH term(s) Animals ; Anti-Bacterial Agents/pharmacology ; Antimicrobial Cationic Peptides/metabolism ; Antimicrobial Cationic Peptides/pharmacology ; Bacterial Proteins/metabolism ; Cathelicidins/genetics ; Cathelicidins/metabolism ; Cell Line ; Disease Models, Animal ; ErbB Receptors/metabolism ; Female ; Host-Pathogen Interactions ; Humans ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Knockout ; Neutrophils/drug effects ; Neutrophils/metabolism ; Neutrophils/microbiology ; Receptors, Purinergic P2X7/metabolism ; Serine Endopeptidases/metabolism ; Signal Transduction ; Streptococcal Infections/drug therapy ; Streptococcal Infections/genetics ; Streptococcal Infections/metabolism ; Streptococcal Infections/microbiology ; Streptococcus pyogenes/enzymology ; Streptococcus pyogenes/genetics ; Streptococcus pyogenes/pathogenicity ; Substrate Specificity ; Mice
    Chemical Substances Anti-Bacterial Agents ; Antimicrobial Cationic Peptides ; Bacterial Proteins ; Camp protein, mouse ; Cathelicidins ; P2rx7 protein, mouse ; Receptors, Purinergic P2X7 ; EGFR protein, mouse (EC 2.7.10.1) ; ErbB Receptors (EC 2.7.10.1) ; Serine Endopeptidases (EC 3.4.21.-)
    Language English
    Publishing date 2021-03-03
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2649101-1
    ISSN 2211-1247 ; 2211-1247
    ISSN (online) 2211-1247
    ISSN 2211-1247
    DOI 10.1016/j.celrep.2021.108766
    Database MEDical Literature Analysis and Retrieval System OnLINE

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