Toll-like receptors and signalling in spermatogenesis and testicular responses to inflammation - a perspective

    Research output: Contribution to journalArticleResearchpeer-review

    49 Citations (Scopus)

    Abstract

    It is self-evident that infection and inflammation in the reproductive tract can inhibit male fertility, but the observation that fertility may also be compromised by systemic inflammation and disease is more difficult to explain. Recent studies implicating microbial pattern-recognition receptors, such as the Toll-like receptors (TLRs), as well as inflammatory cytokines and their signalling pathways, in testicular function have cast new light on this mysterious link between infection/inflammation and testicular dysfunction. It is increasingly evident that signalling pathways normally involved in controlling inflammation play fundamental roles in regulating Sertoli cell activity and responses to reproductive hormones, in addition to promoting immune responses within the testis. Many of the negative effects of inflammation on spermatogenesis may be attributed to elevated production of inflammation-related gene products within the circulation and the testis, which subsequently exert disruptive effects on spermatogenic cell development and survival, as well as the ability of the Sertoli cells to provide support for spermatogenesis. These interactions have important implications for testicular dysfunction and disease, and may eventually provide new opportunities for therapeutic interventions.
    Original languageEnglish
    Pages (from-to)130 - 141
    Number of pages12
    JournalJournal of Reproductive Immunology
    Volume88
    Issue number2
    DOIs
    Publication statusPublished - 2011

    Cite this

    @article{74cb3464428b4f1ab70ae4eabb93bfa7,
    title = "Toll-like receptors and signalling in spermatogenesis and testicular responses to inflammation - a perspective",
    abstract = "It is self-evident that infection and inflammation in the reproductive tract can inhibit male fertility, but the observation that fertility may also be compromised by systemic inflammation and disease is more difficult to explain. Recent studies implicating microbial pattern-recognition receptors, such as the Toll-like receptors (TLRs), as well as inflammatory cytokines and their signalling pathways, in testicular function have cast new light on this mysterious link between infection/inflammation and testicular dysfunction. It is increasingly evident that signalling pathways normally involved in controlling inflammation play fundamental roles in regulating Sertoli cell activity and responses to reproductive hormones, in addition to promoting immune responses within the testis. Many of the negative effects of inflammation on spermatogenesis may be attributed to elevated production of inflammation-related gene products within the circulation and the testis, which subsequently exert disruptive effects on spermatogenic cell development and survival, as well as the ability of the Sertoli cells to provide support for spermatogenesis. These interactions have important implications for testicular dysfunction and disease, and may eventually provide new opportunities for therapeutic interventions.",
    author = "Mark Hedger",
    year = "2011",
    doi = "10.1016/j.jri.2011.01.010",
    language = "English",
    volume = "88",
    pages = "130 -- 141",
    journal = "Journal of Reproductive Immunology",
    issn = "0165-0378",
    publisher = "Elsevier",
    number = "2",

    }

    Toll-like receptors and signalling in spermatogenesis and testicular responses to inflammation - a perspective. / Hedger, Mark.

    In: Journal of Reproductive Immunology, Vol. 88, No. 2, 2011, p. 130 - 141.

    Research output: Contribution to journalArticleResearchpeer-review

    TY - JOUR

    T1 - Toll-like receptors and signalling in spermatogenesis and testicular responses to inflammation - a perspective

    AU - Hedger, Mark

    PY - 2011

    Y1 - 2011

    N2 - It is self-evident that infection and inflammation in the reproductive tract can inhibit male fertility, but the observation that fertility may also be compromised by systemic inflammation and disease is more difficult to explain. Recent studies implicating microbial pattern-recognition receptors, such as the Toll-like receptors (TLRs), as well as inflammatory cytokines and their signalling pathways, in testicular function have cast new light on this mysterious link between infection/inflammation and testicular dysfunction. It is increasingly evident that signalling pathways normally involved in controlling inflammation play fundamental roles in regulating Sertoli cell activity and responses to reproductive hormones, in addition to promoting immune responses within the testis. Many of the negative effects of inflammation on spermatogenesis may be attributed to elevated production of inflammation-related gene products within the circulation and the testis, which subsequently exert disruptive effects on spermatogenic cell development and survival, as well as the ability of the Sertoli cells to provide support for spermatogenesis. These interactions have important implications for testicular dysfunction and disease, and may eventually provide new opportunities for therapeutic interventions.

    AB - It is self-evident that infection and inflammation in the reproductive tract can inhibit male fertility, but the observation that fertility may also be compromised by systemic inflammation and disease is more difficult to explain. Recent studies implicating microbial pattern-recognition receptors, such as the Toll-like receptors (TLRs), as well as inflammatory cytokines and their signalling pathways, in testicular function have cast new light on this mysterious link between infection/inflammation and testicular dysfunction. It is increasingly evident that signalling pathways normally involved in controlling inflammation play fundamental roles in regulating Sertoli cell activity and responses to reproductive hormones, in addition to promoting immune responses within the testis. Many of the negative effects of inflammation on spermatogenesis may be attributed to elevated production of inflammation-related gene products within the circulation and the testis, which subsequently exert disruptive effects on spermatogenic cell development and survival, as well as the ability of the Sertoli cells to provide support for spermatogenesis. These interactions have important implications for testicular dysfunction and disease, and may eventually provide new opportunities for therapeutic interventions.

    UR - http://www.ncbi.nlm.nih.gov/pubmed/21333360

    U2 - 10.1016/j.jri.2011.01.010

    DO - 10.1016/j.jri.2011.01.010

    M3 - Article

    VL - 88

    SP - 130

    EP - 141

    JO - Journal of Reproductive Immunology

    JF - Journal of Reproductive Immunology

    SN - 0165-0378

    IS - 2

    ER -