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  1. Article ; Online: Author Correction: Pathogenesis, epidemiology and control of Group A Streptococcus infection.

    Brouwer, Stephan / Rivera-Hernandez, Tania / Curren, Bodie F / Harbison-Price, Nichaela / De Oliveira, David M P / Jespersen, Magnus G / Davies, Mark R / Walker, Mark J

    Nature reviews. Microbiology

    2023  Volume 21, Issue 9, Page(s) 619

    Language English
    Publishing date 2023-07-03
    Publishing country England
    Document type Published Erratum
    ZDB-ID 2139054-X
    ISSN 1740-1534 ; 1740-1526
    ISSN (online) 1740-1534
    ISSN 1740-1526
    DOI 10.1038/s41579-023-00939-6
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5865: Show issues Location:
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  2. Article ; Online: Pathogenesis, epidemiology and control of Group A Streptococcus infection.

    Brouwer, Stephan / Rivera-Hernandez, Tania / Curren, Bodie F / Harbison-Price, Nichaela / De Oliveira, David M P / Jespersen, Magnus G / Davies, Mark R / Walker, Mark J

    Nature reviews. Microbiology

    2023  Volume 21, Issue 7, Page(s) 431–447

    Abstract: Streptococcus pyogenes (Group A Streptococcus; GAS) is exquisitely adapted to the human host, resulting in asymptomatic infection, pharyngitis, pyoderma, scarlet fever or invasive diseases, with potential for triggering post-infection immune sequelae. ... ...

    Abstract Streptococcus pyogenes (Group A Streptococcus; GAS) is exquisitely adapted to the human host, resulting in asymptomatic infection, pharyngitis, pyoderma, scarlet fever or invasive diseases, with potential for triggering post-infection immune sequelae. GAS deploys a range of virulence determinants to allow colonization, dissemination within the host and transmission, disrupting both innate and adaptive immune responses to infection. Fluctuating global GAS epidemiology is characterized by the emergence of new GAS clones, often associated with the acquisition of new virulence or antimicrobial determinants that are better adapted to the infection niche or averting host immunity. The recent identification of clinical GAS isolates with reduced penicillin sensitivity and increasing macrolide resistance threatens both frontline and penicillin-adjunctive antibiotic treatment. The World Health Organization (WHO) has developed a GAS research and technology road map and has outlined preferred vaccine characteristics, stimulating renewed interest in the development of safe and effective GAS vaccines.
    MeSH term(s) Humans ; Anti-Bacterial Agents/pharmacology ; Anti-Bacterial Agents/therapeutic use ; Macrolides/pharmacology ; Macrolides/therapeutic use ; Drug Resistance, Bacterial ; Streptococcal Infections/drug therapy ; Streptococcal Infections/epidemiology ; Streptococcal Infections/prevention & control ; Streptococcus pyogenes/genetics ; Penicillins/therapeutic use
    Chemical Substances Anti-Bacterial Agents ; Macrolides ; Penicillins
    Language English
    Publishing date 2023-03-09
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2139054-X
    ISSN 1740-1534 ; 1740-1526
    ISSN (online) 1740-1534
    ISSN 1740-1526
    DOI 10.1038/s41579-023-00865-7
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Long-lived regulatory T cells generated during severe bronchiolitis in infancy influence later progression to asthma.

    Lynch, Jason P / Werder, Rhiannon B / Curren, Bodie F / Sikder, Md Al Amin / Ullah, Ashik / Sebina, Ismail / Rashid, Ridwan B / Zhang, Vivian / Upham, John W / Hill, Geoff R / Steptoe, Raymond J / Phipps, Simon

    Mucosal immunology

    2020  Volume 13, Issue 4, Page(s) 652–664

    Abstract: The type-2 inflammatory response that promotes asthma pathophysiology occurs in the absence of sufficient immunoregulation. Impaired regulatory T cell (Treg) function also predisposes to severe viral bronchiolitis in infancy, a major risk factor for ... ...

    Abstract The type-2 inflammatory response that promotes asthma pathophysiology occurs in the absence of sufficient immunoregulation. Impaired regulatory T cell (Treg) function also predisposes to severe viral bronchiolitis in infancy, a major risk factor for asthma. Hence, we hypothesized that long-lived, aberrantly programmed Tregs causally link viral bronchiolitis with later asthma. Here we found that transient plasmacytoid dendritic cell (pDC) depletion during viral infection in early-life, which causes the expansion of aberrant Tregs, predisposes to allergen-induced or virus-induced asthma in later-life, and is associated with altered airway epithelial cell (AEC) responses and the expansion of impaired, long-lived Tregs. Critically, the adoptive transfer of aberrant Tregs (unlike healthy Tregs) to asthma-susceptible mice failed to prevent the development of viral-induced or allergen-induced asthma. Lack of protection was associated with increased airway epithelial cytoplasmic-HMGB1 (high-mobility group box 1), a pro-type-2 inflammatory alarmin, and granulocytic inflammation. Aberrant Tregs expressed lower levels of CD39, an ectonucleotidase that hydrolyzes extracellular ATP, a known inducer of alarmin release. Using cultured mouse AECs, we identify that healthy Tregs suppress allergen-induced HMGB1 translocation whereas this ability is markedly impaired in aberrant Tregs. Thus, defective Treg programming in infancy has durable consequences that underlie the association between bronchiolitis and subsequent asthma.
    MeSH term(s) Allergens/immunology ; Animals ; Asthma/etiology ; Asthma/metabolism ; Asthma/pathology ; Biomarkers ; Bronchiolitis/etiology ; Bronchiolitis/metabolism ; Bronchiolitis/pathology ; Cytokines/metabolism ; Disease Models, Animal ; Disease Progression ; Disease Susceptibility ; HMGB1 Protein/metabolism ; Immunization ; Mice ; Protein Transport ; Severity of Illness Index ; T-Lymphocyte Subsets/immunology ; T-Lymphocyte Subsets/metabolism ; T-Lymphocytes, Regulatory/immunology ; T-Lymphocytes, Regulatory/metabolism
    Chemical Substances Allergens ; Biomarkers ; Cytokines ; HMGB1 Protein
    Language English
    Publishing date 2020-02-17
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2411370-0
    ISSN 1935-3456 ; 1933-0219
    ISSN (online) 1935-3456
    ISSN 1933-0219
    DOI 10.1038/s41385-020-0268-8
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Detection of Streptococcus pyogenes M1

    Davies, Mark R / Keller, Nadia / Brouwer, Stephan / Jespersen, Magnus G / Cork, Amanda J / Hayes, Andrew J / Pitt, Miranda E / De Oliveira, David M P / Harbison-Price, Nichaela / Bertolla, Olivia M / Mediati, Daniel G / Curren, Bodie F / Taiaroa, George / Lacey, Jake A / Smith, Helen V / Fang, Ning-Xia / Coin, Lachlan J M / Stevens, Kerrie / Tong, Steven Y C /
    Sanderson-Smith, Martina / Tree, Jai J / Irwin, Adam D / Grimwood, Keith / Howden, Benjamin P / Jennison, Amy V / Walker, Mark J

    Nature communications

    2023  Volume 14, Issue 1, Page(s) 1051

    Abstract: A new variant of Streptococcus pyogenes serotype M1 (designated ' ... ...

    Abstract A new variant of Streptococcus pyogenes serotype M1 (designated 'M1
    MeSH term(s) Humans ; Streptococcus pyogenes/genetics ; Scarlet Fever/epidemiology ; Superantigens ; Bacterial Proteins/genetics ; United Kingdom ; Exotoxins/genetics ; Mutation ; Australia ; Streptococcal Infections
    Chemical Substances Superantigens ; Bacterial Proteins ; Exotoxins
    Language English
    Publishing date 2023-02-24
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-023-36717-4
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article: The Influence of the Microbiome on Early-Life Severe Viral Lower Respiratory Infections and Asthma-Food for Thought?

    Lynch, Jason P / Sikder, Md Al Amin / Curren, Bodie F / Werder, Rhiannon B / Simpson, Jennifer / Cuív, Páraic Ó / Dennis, Paul G / Everard, Mark L / Phipps, Simon

    Frontiers in immunology

    2017  Volume 8, Page(s) 156

    Abstract: Severe viral lower respiratory infections are a major cause of infant morbidity. In developing countries, respiratory syncytial virus (RSV)-bronchiolitis induces significant mortality, whereas in developed nations the disease represents a major risk ... ...

    Abstract Severe viral lower respiratory infections are a major cause of infant morbidity. In developing countries, respiratory syncytial virus (RSV)-bronchiolitis induces significant mortality, whereas in developed nations the disease represents a major risk factor for subsequent asthma. Susceptibility to severe RSV-bronchiolitis is governed by gene-environmental interactions that affect the host response to RSV infection. Emerging evidence suggests that the excessive inflammatory response and ensuing immunopathology, typically as a consequence of insufficient immunoregulation, leads to long-term changes in immune cells and structural cells that render the host susceptible to subsequent environmental incursions. Thus, the initial host response to RSV may represent a tipping point in the balance between long-term respiratory health or chronic disease (e.g., asthma). The composition and diversity of the microbiota, which in humans stabilizes in the first year of life, critically affects the development and function of the immune system. Hence, perturbations to the maternal and/or infant microbiota are likely to have a profound impact on the host response to RSV and susceptibility to childhood asthma. Here, we review recent insights describing the effects of the microbiota on immune system homeostasis and respiratory disease and discuss the environmental factors that promote microbial dysbiosis in infancy. Ultimately, this knowledge will be harnessed for the prevention and treatment of severe viral bronchiolitis as a strategy to prevent the onset and development of asthma.
    Language English
    Publishing date 2017-02-16
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2606827-8
    ISSN 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2017.00156
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Targeting the P2Y

    Werder, Rhiannon B / Ullah, Md Ashik / Rahman, Muhammed Mahfuzur / Simpson, Jennifer / Lynch, Jason P / Collinson, Natasha / Rittchen, Sonja / Rashid, Ridwan B / Sikder, Md Al Amin / Handoko, Herlina Y / Curren, Bodie F / Sebina, Ismail / Hartel, Gunter / Bissell, Alec / Ngo, Sylvia / Yarlagadda, Tejasri / Hasnain, Sumaira Z / Lu, Wenying / Sohal, Sukhwinder S /
    Martin, Megan / Bowler, Simon / Burr, Lucy D / Martinez, Laurent O / Robaye, Bernard / Spann, Kirsten / Ferreira, Manuel A R / Phipps, Simon

    American journal of respiratory and critical care medicine

    2021  Volume 205, Issue 3, Page(s) 300–312

    Abstract: Rationale: ...

    Abstract Rationale:
    MeSH term(s) Animals ; Asthma/immunology ; Asthma/metabolism ; Asthma/physiopathology ; Biomarkers/metabolism ; Case-Control Studies ; Disease Progression ; Enzyme-Linked Immunosorbent Assay ; Epithelial Cells/metabolism ; HMGB1 Protein/metabolism ; Humans ; Immunohistochemistry ; Interleukin-33/metabolism ; Mice ; Mice, Inbred C57BL ; Receptors, Purinergic P2/metabolism
    Chemical Substances Biomarkers ; HMGB1 Protein ; HMGB1 protein, human ; HMGB1 protein, mouse ; IL33 protein, human ; Il33 protein, mouse ; Interleukin-33 ; P2RY13 protein, human ; P2ry13 protein, mouse ; Receptors, Purinergic P2
    Language English
    Publishing date 2021-12-19
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1180953-x
    ISSN 1535-4970 ; 0003-0805 ; 1073-449X
    ISSN (online) 1535-4970
    ISSN 0003-0805 ; 1073-449X
    DOI 10.1164/rccm.202009-3686OC
    Database MEDical Literature Analysis and Retrieval System OnLINE

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