Danielle J. Glynn
University of Adelaide
20 Papers
17 Citations
Danielle J. Glynn is an academic researcher from University of Adelaide. The author has contributed to research in topics: Biology & Cytokine. The author has an hindex of 8, co-authored 19 publications. Previous affiliations of Danielle J. Glynn include Flinders University.
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Papers
TLR4 Signaling Is a Major Mediator of the Female Tract Response to Seminal Fluid in Mice
TL;DR: Evidence is provided that TLR4 contributes to seminal fluid modulation of the periconception immune environment by activating microbial or endogenous components of seminal fluid and being implicated as a key element of the female tract response to seminal fluids at the outset of pregnancy in mice.
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Inflammatory mediators in mastitis and lactation insufficiency
TL;DR: An alternate paradigm to the widely held notion that breast inflammation is driven principally by infectious bacterial pathogens is presented, and it is suggested there may be other therapeutic strategies, apart from the currently utilised antimicrobial agents, that could be employed to prevent and treat mastitis in women.
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CCL2-driven inflammation increases mammary gland stromal density and cancer susceptibility in a transgenic mouse model
Xuan Sun,Danielle J. Glynn,Leigh J. Hodson,Cecilia Huo,Kara L. Britt,Erik W. Thompson,Erik W. Thompson,Lucy Woolford,Andreas Evdokiou,Jeffrey W. Pollard,Sarah A. Robertson,Wendy V. Ingman +11 more
TL;DR: Overexpression of CCL2 in the mammary epithelium resulted in an increased number of macrophages, increased density of stroma and collagen and elevated mRNA encoding matrix remodelling enzymes lysyl oxidase (LOX) and tissue inhibitor of matrix metalloproteinases (TIMP).
Toll-Like Receptor 4 Regulates Lipopolysaccharide-Induced Inflammation and Lactation Insufficiency in a Mouse Model of Mastitis
TL;DR: It is demonstrated that inflammatory pathways activated in the host are critically important in mastitis disease progression and suggests that lactation insufficiency associated with mastitis may be a consequence of TLR4-mediated inflammation, rather than the bacterial infection itself.
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Interferon-gamma inhibits seminal plasma induction of colony-stimulating factor 2 in mouse and human reproductive tract epithelial cells.
TL;DR: IFNG in seminal plasma acts to suppress TGFB-mediated induction of CSF2 expression in female reproductive tract epithelia, thereby potently inhibiting the female immune response to seminal fluid after coitus, raising the prospect that IFNG in the male partner's seminal fluid impairs immune adaptation for pregnancy following coitus in women.