As many as 1 in 5 women in the United States will report the occurrence of dyspareunia (pain with intercourse) over the past 30 days, while many women will experience vulvar or sexual pain at some point in their lifetime. For some, the pain is longstanding and difficult to resolve, largely because the causes of vulvar pain remain incompletely understood. Localized provoked vulvodynia (LPV) is the most common cause of chronic dyspareunia, and there is no curative therapy. Even surgical excision of a large portion of the vulvar tissue may not result in complete resolution of symptoms. Recent evidence shows inflammation plays a key role in vulvodynia; cells from painful areas are sensitive to low levels of microbial inflammatory stimuli that normally would not provoke a response (e.g. subclinical yeast infection). Investigating the inflammatory underpinnings of LPV will improve our understanding of the connections between microbial sensing, inflammation, and pain and could lead to the development of more efficacious mechanism-based therapies for LPV and other chronic inflammatory diseases.
With the goal of improving mechanistic understanding of vulvodynia while also furthering our overall understanding of chronic inflammatory disease mechanisms, this Frontiers Research Topic seeks to better define the relationship between innate immune sensing systems and pro-nociceptive proinflammatory mediator production and the role that microbes may play in this interaction. Several proinflammatory mediators are associated with and elevated in chronic pain conditions, but the reason for this is not completely clear. Recent work in the vulvodynia field has revealed a disproportionately strong inflammatory response to low abundance inflammatory signals (e.g. > 100 yeast cells) that is linked to pain. Translational research examining the connection between aberrant inflammatory signaling and chronic inflammation and pain in the context of women’s health is direly needed. Cross-disciplinary, innovative, and team science approaches drawing on clinical and laboratory expertise are strongly encouraged. Conditions outside women’s health looking at highly conserved systems (e.g. pattern recognition receptors) are also of interest.
In this Topic, we seek articles that
1) Explore the influence of microbes and innate immunity on the production of pro-nociceptive proinflammatory signals in vulvodynia;
2) Explore how microbes interact with innate sensing and the mechanisms by which they initiate inflammatory responses in vulvodynia and other vulvar conditions;
3) Explore the role of the vulvovaginal microbiota in vulvar disease, specifically in vulvodynia and chronic pain;
4) Identify aberrant proinflammatory signaling regimes associated with pain, loss of function, and chronic or unresolved inflammation; and
5) Identify or test, novel methods or treatments that could overcome aberrant and pain-inducing proinflammatory signaling in vulvodynia and beyond.
We welcome all forms of submissions accepted by the journal: Original Research Articles, Review Articles, Method Articles, Brief Research Reports, Mini-Review Articles, General Commentaries, Perspectives, and Hypothesis & Theories.
As many as 1 in 5 women in the United States will report the occurrence of dyspareunia (pain with intercourse) over the past 30 days, while many women will experience vulvar or sexual pain at some point in their lifetime. For some, the pain is longstanding and difficult to resolve, largely because the causes of vulvar pain remain incompletely understood. Localized provoked vulvodynia (LPV) is the most common cause of chronic dyspareunia, and there is no curative therapy. Even surgical excision of a large portion of the vulvar tissue may not result in complete resolution of symptoms. Recent evidence shows inflammation plays a key role in vulvodynia; cells from painful areas are sensitive to low levels of microbial inflammatory stimuli that normally would not provoke a response (e.g. subclinical yeast infection). Investigating the inflammatory underpinnings of LPV will improve our understanding of the connections between microbial sensing, inflammation, and pain and could lead to the development of more efficacious mechanism-based therapies for LPV and other chronic inflammatory diseases.
With the goal of improving mechanistic understanding of vulvodynia while also furthering our overall understanding of chronic inflammatory disease mechanisms, this Frontiers Research Topic seeks to better define the relationship between innate immune sensing systems and pro-nociceptive proinflammatory mediator production and the role that microbes may play in this interaction. Several proinflammatory mediators are associated with and elevated in chronic pain conditions, but the reason for this is not completely clear. Recent work in the vulvodynia field has revealed a disproportionately strong inflammatory response to low abundance inflammatory signals (e.g. > 100 yeast cells) that is linked to pain. Translational research examining the connection between aberrant inflammatory signaling and chronic inflammation and pain in the context of women’s health is direly needed. Cross-disciplinary, innovative, and team science approaches drawing on clinical and laboratory expertise are strongly encouraged. Conditions outside women’s health looking at highly conserved systems (e.g. pattern recognition receptors) are also of interest.
In this Topic, we seek articles that
1) Explore the influence of microbes and innate immunity on the production of pro-nociceptive proinflammatory signals in vulvodynia;
2) Explore how microbes interact with innate sensing and the mechanisms by which they initiate inflammatory responses in vulvodynia and other vulvar conditions;
3) Explore the role of the vulvovaginal microbiota in vulvar disease, specifically in vulvodynia and chronic pain;
4) Identify aberrant proinflammatory signaling regimes associated with pain, loss of function, and chronic or unresolved inflammation; and
5) Identify or test, novel methods or treatments that could overcome aberrant and pain-inducing proinflammatory signaling in vulvodynia and beyond.
We welcome all forms of submissions accepted by the journal: Original Research Articles, Review Articles, Method Articles, Brief Research Reports, Mini-Review Articles, General Commentaries, Perspectives, and Hypothesis & Theories.
