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  1. Article: Tamm-Horsfall protein augments neutrophil NETosis during urinary tract infection.

    Mercado-Evans, Vicki / Chew, Claude / Serchejian, Camille / Saltzman, Alexander / Mejia, Marlyd E / Zulk, Jacob J / Cornax, Ingrid / Nizet, Victor / Patras, Kathryn A

    bioRxiv : the preprint server for biology

    2024  

    Abstract: Urinary neutrophils are a hallmark of urinary tract infection (UTI), yet the mechanisms governing their activation, function, and efficacy in controlling infection remain incompletely understood. Tamm-Horsfall glycoprotein (THP), the most abundant ... ...

    Abstract Urinary neutrophils are a hallmark of urinary tract infection (UTI), yet the mechanisms governing their activation, function, and efficacy in controlling infection remain incompletely understood. Tamm-Horsfall glycoprotein (THP), the most abundant protein in urine, uses terminal sialic acids to bind an inhibitory receptor and dampen neutrophil inflammatory responses. We hypothesized that neutrophil modulation is an integral part of THP-mediated host protection. In a UTI model, THP-deficient mice showed elevated urinary tract bacterial burdens, increased neutrophil recruitment, and more severe tissue histopathological changes compared to WT mice. Furthermore, THP-deficient mice displayed impaired urinary NETosis during UTI. To investigate the impact of THP on NETosis, we coupled
    Language English
    Publishing date 2024-02-05
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2024.02.01.578501
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Gestational diabetes augments group B Streptococcus infection by disrupting maternal immunity and the vaginal microbiota.

    Mercado-Evans, Vicki / Mejia, Marlyd E / Zulk, Jacob J / Ottinger, Samantha / Hameed, Zainab A / Serchejian, Camille / Marunde, Madelynn G / Robertson, Clare M / Ballard, Mallory B / Ruano, Simone H / Korotkova, Natalia / Flores, Anthony R / Pennington, Kathleen A / Patras, Kathryn A

    Nature communications

    2024  Volume 15, Issue 1, Page(s) 1035

    Abstract: Group B Streptococcus (GBS) is a pervasive perinatal pathogen, yet factors driving GBS dissemination in utero are poorly defined. Gestational diabetes mellitus (GDM), a complication marked by dysregulated immunity and maternal microbial dysbiosis, ... ...

    Abstract Group B Streptococcus (GBS) is a pervasive perinatal pathogen, yet factors driving GBS dissemination in utero are poorly defined. Gestational diabetes mellitus (GDM), a complication marked by dysregulated immunity and maternal microbial dysbiosis, increases risk for GBS perinatal disease. Using a murine GDM model of GBS colonization and perinatal transmission, we find that GDM mice display greater GBS in utero dissemination and subsequently worse neonatal outcomes. Dual-RNA sequencing reveals differential GBS adaptation to the GDM reproductive tract, including a putative glycosyltransferase (yfhO), and altered host responses. GDM immune disruptions include reduced uterine natural killer cell activation, impaired recruitment to placentae, and altered maternofetal cytokines. Lastly, we observe distinct vaginal microbial taxa associated with GDM status and GBS invasive disease status. Here, we show a model of GBS dissemination in GDM hosts that recapitulates several clinical aspects and identifies multiple host and bacterial drivers of GBS perinatal disease.
    MeSH term(s) Pregnancy ; Female ; Humans ; Animals ; Mice ; Diabetes, Gestational ; Infectious Disease Transmission, Vertical ; Microbiota ; Cytokines ; Vagina/microbiology ; Streptococcus ; Streptococcus agalactiae ; Streptococcal Infections/microbiology
    Chemical Substances Cytokines
    Language English
    Publishing date 2024-02-03
    Publishing country England
    Document type Journal Article
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-024-45336-6
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: Heterogeneity of the group B streptococcal type VII secretion system and influence on colonization of the female genital tract.

    Spencer, Brady L / Job, Alyx M / Robertson, Clare M / Hameed, Zainab A / Serchejian, Camille / Wiafe-Kwakye, Caitlin S / Mendonça, Jéssica C / Apolonio, Morgan A / Nagao, Prescilla E / Neely, Melody N / Korotkova, Natalia / Korotkov, Konstantin V / Patras, Kathryn A / Doran, Kelly S

    bioRxiv : the preprint server for biology

    2023  

    Abstract: Type VIIb secretion systems (T7SSb) in Gram-positive bacteria facilitate physiology, interbacterial competition, and/or virulence via EssC ATPase-driven secretion of small ɑ-helical proteins and toxins. Recently, we characterized T7SSb in group ... ...

    Abstract Type VIIb secretion systems (T7SSb) in Gram-positive bacteria facilitate physiology, interbacterial competition, and/or virulence via EssC ATPase-driven secretion of small ɑ-helical proteins and toxins. Recently, we characterized T7SSb in group B
    Language English
    Publishing date 2023-01-25
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2023.01.25.525443
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Heterogeneity of the group B streptococcal type VII secretion system and influence on colonization of the female genital tract.

    Spencer, Brady L / Job, Alyx M / Robertson, Clare M / Hameed, Zainab A / Serchejian, Camille / Wiafe-Kwakye, Caitlin S / Mendonça, Jéssica C / Apolonio, Morgan A / Nagao, Prescilla E / Neely, Melody N / Korotkova, Natalia / Korotkov, Konstantin V / Patras, Kathryn A / Doran, Kelly S

    Molecular microbiology

    2023  Volume 120, Issue 2, Page(s) 258–275

    Abstract: Type VIIb secretion systems (T7SSb) in Gram-positive bacteria facilitate physiology, interbacterial competition, and/or virulence via EssC ATPase-driven secretion of small ɑ-helical proteins and toxins. Recently, we characterized T7SSb in group B ... ...

    Abstract Type VIIb secretion systems (T7SSb) in Gram-positive bacteria facilitate physiology, interbacterial competition, and/or virulence via EssC ATPase-driven secretion of small ɑ-helical proteins and toxins. Recently, we characterized T7SSb in group B Streptococcus (GBS), a leading cause of infection in newborns and immunocompromised adults. GBS T7SS comprises four subtypes based on variation in the C-terminus of EssC and the repertoire of downstream effectors; however, the intraspecies diversity of GBS T7SS and impact on GBS-host interactions remains unknown. Bioinformatic analysis indicates that GBS T7SS loci encode subtype-specific putative effectors, which have low interspecies and inter-subtype homology but contain similar domains/motifs and therefore may serve similar functions. We further identify orphaned GBS WXG100 proteins. Functionally, we show that GBS T7SS subtype I and III strains secrete EsxA in vitro and that in subtype I strain CJB111, esxA1 appears to be differentially transcribed from the T7SS operon. Furthermore, we observe subtype-specific effects of GBS T7SS on host colonization, as CJB111 subtype I but not CNCTC 10/84 subtype III T7SS promotes GBS vaginal colonization. Finally, we observe that T7SS subtypes I and II are the predominant subtypes in clinical GBS isolates. This study highlights the potential impact of T7SS heterogeneity on host-GBS interactions.
    MeSH term(s) Infant, Newborn ; Female ; Humans ; Bacterial Proteins/genetics ; Bacterial Proteins/metabolism ; Type VII Secretion Systems/genetics ; Virulence ; Operon/genetics ; Genitalia, Female/metabolism ; Streptococcal Infections/microbiology ; Streptococcus agalactiae/genetics ; Streptococcus agalactiae/metabolism ; Vagina/metabolism ; Vagina/microbiology
    Chemical Substances Bacterial Proteins ; Type VII Secretion Systems
    Language English
    Publishing date 2023-06-26
    Publishing country England
    Document type Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 619315-8
    ISSN 1365-2958 ; 0950-382X
    ISSN (online) 1365-2958
    ISSN 0950-382X
    DOI 10.1111/mmi.15115
    Database MEDical Literature Analysis and Retrieval System OnLINE

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