Candidalysin Drives Epithelial Signaling, Neutrophil Recruitment, and Immunopathology at the Vaginal Mucosa
Unlike other forms of candidiasis, vulvovaginal candidiasis, caused primarily by the fungal pathogen , is a disease of immunocompetent and otherwise healthy women. Despite its prevalence, the fungal factors responsible for initiating symptomatic infection remain poorly understood. One of the hallmar...
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| Vydané v: | Infection and immunity Ročník 86; číslo 2 |
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| Hlavní autori: | , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | English |
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01.02.2018
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| ISSN: | 1098-5522, 1098-5522 |
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| Abstract | Unlike other forms of candidiasis, vulvovaginal candidiasis, caused primarily by the fungal pathogen
, is a disease of immunocompetent and otherwise healthy women. Despite its prevalence, the fungal factors responsible for initiating symptomatic infection remain poorly understood. One of the hallmarks of vaginal candidiasis is the robust recruitment of neutrophils to the site of infection, which seemingly do not clear the fungus, but rather exacerbate disease symptomatology. Candidalysin, a newly discovered peptide toxin secreted by
hyphae during invasion, drives epithelial damage, immune activation, and phagocyte attraction. Therefore, we hypothesized that Candidalysin is crucial for vulvovaginal candidiasis immunopathology. Anti-
immune responses are anatomical-site specific, as effective gastrointestinal, oral, and vaginal immunities are uniquely compartmentalized. Thus, we aimed to identify the immunopathologic role of Candidalysin and downstream signaling events at the vaginal mucosa. Microarray analysis of
-infected human vaginal epithelium
revealed signaling pathways involved in epithelial damage responses, barrier repair, and leukocyte activation. Moreover, treatment of A431 vaginal epithelial cells with Candidalysin induced dose-dependent proinflammatory cytokine responses (including interleukin 1α [IL-1α], IL-1β, and IL-8), damage, and activation of c-Fos and mitogen-activated protein kinase (MAPK) signaling, consistent with fungal challenge. Mice intravaginally challenged with
strains deficient in Candidalysin exhibited no differences in colonization compared to isogenic controls. However, significant decreases in neutrophil recruitment, damage, and proinflammatory cytokine expression were observed with these strains. Our findings demonstrate that Candidalysin is a key hypha-associated virulence determinant responsible for the immunopathogenesis of
vaginitis. |
|---|---|
| AbstractList | Unlike other forms of candidiasis, vulvovaginal candidiasis, caused primarily by the fungal pathogen Candida albicans, is a disease of immunocompetent and otherwise healthy women. Despite its prevalence, the fungal factors responsible for initiating symptomatic infection remain poorly understood. One of the hallmarks of vaginal candidiasis is the robust recruitment of neutrophils to the site of infection, which seemingly do not clear the fungus, but rather exacerbate disease symptomatology. Candidalysin, a newly discovered peptide toxin secreted by C. albicans hyphae during invasion, drives epithelial damage, immune activation, and phagocyte attraction. Therefore, we hypothesized that Candidalysin is crucial for vulvovaginal candidiasis immunopathology. Anti-Candida immune responses are anatomical-site specific, as effective gastrointestinal, oral, and vaginal immunities are uniquely compartmentalized. Thus, we aimed to identify the immunopathologic role of Candidalysin and downstream signaling events at the vaginal mucosa. Microarray analysis of C. albicans-infected human vaginal epithelium in vitro revealed signaling pathways involved in epithelial damage responses, barrier repair, and leukocyte activation. Moreover, treatment of A431 vaginal epithelial cells with Candidalysin induced dose-dependent proinflammatory cytokine responses (including interleukin 1α [IL-1α], IL-1β, and IL-8), damage, and activation of c-Fos and mitogen-activated protein kinase (MAPK) signaling, consistent with fungal challenge. Mice intravaginally challenged with C. albicans strains deficient in Candidalysin exhibited no differences in colonization compared to isogenic controls. However, significant decreases in neutrophil recruitment, damage, and proinflammatory cytokine expression were observed with these strains. Our findings demonstrate that Candidalysin is a key hypha-associated virulence determinant responsible for the immunopathogenesis of C. albicans vaginitis.Unlike other forms of candidiasis, vulvovaginal candidiasis, caused primarily by the fungal pathogen Candida albicans, is a disease of immunocompetent and otherwise healthy women. Despite its prevalence, the fungal factors responsible for initiating symptomatic infection remain poorly understood. One of the hallmarks of vaginal candidiasis is the robust recruitment of neutrophils to the site of infection, which seemingly do not clear the fungus, but rather exacerbate disease symptomatology. Candidalysin, a newly discovered peptide toxin secreted by C. albicans hyphae during invasion, drives epithelial damage, immune activation, and phagocyte attraction. Therefore, we hypothesized that Candidalysin is crucial for vulvovaginal candidiasis immunopathology. Anti-Candida immune responses are anatomical-site specific, as effective gastrointestinal, oral, and vaginal immunities are uniquely compartmentalized. Thus, we aimed to identify the immunopathologic role of Candidalysin and downstream signaling events at the vaginal mucosa. Microarray analysis of C. albicans-infected human vaginal epithelium in vitro revealed signaling pathways involved in epithelial damage responses, barrier repair, and leukocyte activation. Moreover, treatment of A431 vaginal epithelial cells with Candidalysin induced dose-dependent proinflammatory cytokine responses (including interleukin 1α [IL-1α], IL-1β, and IL-8), damage, and activation of c-Fos and mitogen-activated protein kinase (MAPK) signaling, consistent with fungal challenge. Mice intravaginally challenged with C. albicans strains deficient in Candidalysin exhibited no differences in colonization compared to isogenic controls. However, significant decreases in neutrophil recruitment, damage, and proinflammatory cytokine expression were observed with these strains. Our findings demonstrate that Candidalysin is a key hypha-associated virulence determinant responsible for the immunopathogenesis of C. albicans vaginitis. Unlike other forms of candidiasis, vulvovaginal candidiasis, caused primarily by the fungal pathogen , is a disease of immunocompetent and otherwise healthy women. Despite its prevalence, the fungal factors responsible for initiating symptomatic infection remain poorly understood. One of the hallmarks of vaginal candidiasis is the robust recruitment of neutrophils to the site of infection, which seemingly do not clear the fungus, but rather exacerbate disease symptomatology. Candidalysin, a newly discovered peptide toxin secreted by hyphae during invasion, drives epithelial damage, immune activation, and phagocyte attraction. Therefore, we hypothesized that Candidalysin is crucial for vulvovaginal candidiasis immunopathology. Anti- immune responses are anatomical-site specific, as effective gastrointestinal, oral, and vaginal immunities are uniquely compartmentalized. Thus, we aimed to identify the immunopathologic role of Candidalysin and downstream signaling events at the vaginal mucosa. Microarray analysis of -infected human vaginal epithelium revealed signaling pathways involved in epithelial damage responses, barrier repair, and leukocyte activation. Moreover, treatment of A431 vaginal epithelial cells with Candidalysin induced dose-dependent proinflammatory cytokine responses (including interleukin 1α [IL-1α], IL-1β, and IL-8), damage, and activation of c-Fos and mitogen-activated protein kinase (MAPK) signaling, consistent with fungal challenge. Mice intravaginally challenged with strains deficient in Candidalysin exhibited no differences in colonization compared to isogenic controls. However, significant decreases in neutrophil recruitment, damage, and proinflammatory cytokine expression were observed with these strains. Our findings demonstrate that Candidalysin is a key hypha-associated virulence determinant responsible for the immunopathogenesis of vaginitis. |
| Author | Willems, Hubertine M E Richardson, Jonathan P Peters, Brian M Shoaie, Saeed Palmer, Glen E Hube, Bernhard Barker, Katherine S Moyes, David L Naglik, Julian R Tan, Shir Lynn |
| Author_xml | – sequence: 1 givenname: Jonathan P surname: Richardson fullname: Richardson, Jonathan P organization: King's College London, Division of Mucosal and Salivary Biology, London, United Kingdom – sequence: 2 givenname: Hubertine M E surname: Willems fullname: Willems, Hubertine M E organization: University of Tennessee Health Science Center, Department of Clinical Pharmacy, Memphis, Tennessee, USA – sequence: 3 givenname: David L surname: Moyes fullname: Moyes, David L organization: King's College London, Centre for Host-Microbiome Interactions, London, United Kingdom – sequence: 4 givenname: Saeed surname: Shoaie fullname: Shoaie, Saeed organization: King's College London, Centre for Host-Microbiome Interactions, London, United Kingdom – sequence: 5 givenname: Katherine S surname: Barker fullname: Barker, Katherine S organization: University of Tennessee Health Science Center, Department of Clinical Pharmacy, Memphis, Tennessee, USA – sequence: 6 givenname: Shir Lynn surname: Tan fullname: Tan, Shir Lynn organization: King's College London, Division of Mucosal and Salivary Biology, London, United Kingdom – sequence: 7 givenname: Glen E surname: Palmer fullname: Palmer, Glen E organization: University of Tennessee Health Science Center, Department of Clinical Pharmacy, Memphis, Tennessee, USA – sequence: 8 givenname: Bernhard surname: Hube fullname: Hube, Bernhard organization: Friedrich-Schiller-University Jena, Jena, Germany – sequence: 9 givenname: Julian R surname: Naglik fullname: Naglik, Julian R email: julian.naglik@kcl.ac.uk, brian.peters@uthsc.edu organization: King's College London, Division of Mucosal and Salivary Biology, London, United Kingdom julian.naglik@kcl.ac.uk brian.peters@uthsc.edu – sequence: 10 givenname: Brian M surname: Peters fullname: Peters, Brian M email: julian.naglik@kcl.ac.uk, brian.peters@uthsc.edu organization: University of Tennessee Health Science Center, Department of Clinical Pharmacy, Memphis, Tennessee, USA julian.naglik@kcl.ac.uk brian.peters@uthsc.edu |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/29109176$$D View this record in MEDLINE/PubMed |
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| Keywords | Candidalysin immunopathogenesis vulvovaginal Candida mucosal pathogens epithelial cells mycology vaginitis mucosal immunity |
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| Snippet | Unlike other forms of candidiasis, vulvovaginal candidiasis, caused primarily by the fungal pathogen
, is a disease of immunocompetent and otherwise healthy... Unlike other forms of candidiasis, vulvovaginal candidiasis, caused primarily by the fungal pathogen Candida albicans, is a disease of immunocompetent and... |
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| Title | Candidalysin Drives Epithelial Signaling, Neutrophil Recruitment, and Immunopathology at the Vaginal Mucosa |
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