ecstatichamster
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Progesterone-Based Therapy Protects Against Influenza by Promoting Lung Repair and Recovery in Females
Over 100 million women use progesterone therapies worldwide. Despite having immunomodulatory and repair properties, their effects on the outcome of viral diseases outside of the reproductive tract have not been evaluated. Administration of exogenous progesterone (at concentrations that mimic the luteal phase) to progesterone-depleted adult female mice conferred protection from both lethal and sublethal influenza A virus (IAV) infection. Progesterone treatment altered the inflammatory environment of the lungs, but had no effects on viral load. Progesterone treatment promoted faster recovery by increasing TGF-β, IL-6, IL-22, numbers of regulatory Th17 cells expressing CD39, and cellular proliferation, reducing protein leakage into the airway, improving pulmonary function, and upregulating the epidermal growth factor amphiregulin (AREG) in the lungs. Administration of rAREG to progesterone-depleted females promoted pulmonary repair and improved the outcome of IAV infection. Progesterone-treatment of AREG-deficient females could not restore protection, indicating that progesterone-mediated induction of AREG caused repair in the lungs and accelerated recovery from IAV infection. Repair and production of AREG by damaged respiratory epithelial cell cultures in vitro was increased by progesterone. Our results illustrate that progesterone is a critical host factor mediating production of AREG by epithelial cells and pulmonary tissue repair following infection, which has important implications for women’s health.
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Problem
Influenza infection severity may be mediated by estradiol and/or progesterone.
Method of Study
An exploratory study was designed to evaluate 17‐β‐estradiol and progesterone on influenza infection and examine immune‐mediated response in a mouse model. Inoculation with placebo or mouse‐adapted H1N1 influenza virus occurred. Treatment groups included 17‐β‐estradiol, progesterone, ovariectomy, and pregnancy. Mice were assessed for morbidity and mortality. Toll‐like receptor gene studies and airspace cell differentials were performed.
Results
Onset of morbidity was earlier and morbidity duration greater for progesterone. Absence of morbidity/mortality and overall survival was greater for 17‐β‐estradiol. Airspace cell differentials suggest improved immune cell recruitment for 17‐β‐estradiol. Pregnant mouse data demonstrate significant mortality during the period of increased progesterone. Select immune cell markers demonstrate patterns of regulation that may promote proper immune response to influenza infection for 17‐β‐estradiol.
Conclusion
Estradiol may play a protective and progesterone a detrimental role in the pathophysiology of influenza infection.
Progesterone-Based Therapy Protects Against Influenza by Promoting Lung Repair and Recovery in Females
Over 100 million women use progesterone therapies worldwide. Despite having immunomodulatory and repair properties, their effects on the outcome of viral diseases outside of the reproductive tract have not been evaluated. Administration of exogenous progesterone (at concentrations that mimic the luteal phase) to progesterone-depleted adult female mice conferred protection from both lethal and sublethal influenza A virus (IAV) infection. Progesterone treatment altered the inflammatory environment of the lungs, but had no effects on viral load. Progesterone treatment promoted faster recovery by increasing TGF-β, IL-6, IL-22, numbers of regulatory Th17 cells expressing CD39, and cellular proliferation, reducing protein leakage into the airway, improving pulmonary function, and upregulating the epidermal growth factor amphiregulin (AREG) in the lungs. Administration of rAREG to progesterone-depleted females promoted pulmonary repair and improved the outcome of IAV infection. Progesterone-treatment of AREG-deficient females could not restore protection, indicating that progesterone-mediated induction of AREG caused repair in the lungs and accelerated recovery from IAV infection. Repair and production of AREG by damaged respiratory epithelial cell cultures in vitro was increased by progesterone. Our results illustrate that progesterone is a critical host factor mediating production of AREG by epithelial cells and pulmonary tissue repair following infection, which has important implications for women’s health.
It's bad:
Error - Cookies Turned Off
Problem
Influenza infection severity may be mediated by estradiol and/or progesterone.
Method of Study
An exploratory study was designed to evaluate 17‐β‐estradiol and progesterone on influenza infection and examine immune‐mediated response in a mouse model. Inoculation with placebo or mouse‐adapted H1N1 influenza virus occurred. Treatment groups included 17‐β‐estradiol, progesterone, ovariectomy, and pregnancy. Mice were assessed for morbidity and mortality. Toll‐like receptor gene studies and airspace cell differentials were performed.
Results
Onset of morbidity was earlier and morbidity duration greater for progesterone. Absence of morbidity/mortality and overall survival was greater for 17‐β‐estradiol. Airspace cell differentials suggest improved immune cell recruitment for 17‐β‐estradiol. Pregnant mouse data demonstrate significant mortality during the period of increased progesterone. Select immune cell markers demonstrate patterns of regulation that may promote proper immune response to influenza infection for 17‐β‐estradiol.
Conclusion
Estradiol may play a protective and progesterone a detrimental role in the pathophysiology of influenza infection.