IL-17A is secreted from Th17 cells, a discovery leading to revision of the mechanism underlying the role of Th1/Th2 in the immune response. Strong evidence suggests that immune responses associated with inflammation are involved in the pathogenesis of endometriosis. In the present study, we first demonstrated that the presence of Th17 cells in peritoneal fluid of endometriotic women by flow cytometric analysis and IL-17A-positive cells in endometriotic tissues by immunohistochemistry. To investigate the role of IL-17A in the development of endometriosis, we then studied the effect of IL-17A on IL-8 production, cyclooxygensase-2 expression, and cell proliferation of cultured endometriotic stromal cells (ESCs). IL-17A enhanced IL-8 secretion from ESCs in a dose-dependent manner. The IL-17A-induced secretion of IL-8 from ESCs was suppressed by anti-IL-17 receptor A antibodies or inhibitors of p38 MAPK, p42/44 MAPK, and stress-activated protein kinase/c-Jun N-terminal kinase. Addition of TNFalpha synergistically increased IL-17A-induced IL-8 secretion from ESCs. IL-17A also enhanced the expression of cyclooxygensase-2 mRNA and proliferation of ESCs. IL-17A may play a role in the development of endometriosis by stimulating inflammatory responses and proliferation of ESCs.
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http://dx.doi.org/10.1210/en.2007-0749 | DOI Listing |
Alzheimers Dement
December 2024
Institute of Public and Preventative Health, Augusta, GA, USA.
Background: Physiological changes, including metabolic and cellular aging, as well as increased inflammation, occur in people living with dementia (PWD). While there is existing evidence in other populations suggesting that exercise may improve physiological outcomes, their impact in PWD remains unclear. This randomized controlled trial (RCT) aimed to assess the effects of exercise on serum levels of metabolic aging, cellular aging, and inflammatory blood biomarkers relative to usual care alone in PWD.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
UNICAMP, Campinas, Brazil; Sao Leopoldo Mandic Araras School of Medicine, Araras, Brazil; USP - University of Sao Paulo, Ribeirao Preto, Brazil.
Background: Neuroinflammation can be considered a risk factor for the onset or progression of Alzheimer's dementia. In a neuroinflammatory process, the death of neurons may accelerate, favoring the progression of Alzheimer's disease. The release of pro-inflammatory proteins can, for example, cause synaptic dysfunction and impede neurogenesis.
View Article and Find Full Text PDFBackground: People living with dementia (PWD) have upregulated inflammatory pathways, exaggerated metabolic aging, and cellular aging. They also have declines in physical function and heightened fall-risk. Understanding the physiologic factors that influence physical decline and fall-risk in PWD is vital to assess and prevent adverse health outcomes, such as future falls.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
The Pennsylvania State University, University Park, PA, USA.
Background: Inflammation is a risk factor for cognitive decline, mild cognitive impairment (MCI), and Alzheimer's disease (AD). While past research in laboratory settings suggests that inflammation relates to cognitive decline and MCI status, more research is needed to examine such associations in everyday life. The present work addressed this gap by examining MCI and gender stratified links between circulating inflammatory biomarkers and self-reported prospective memory (PM; i.
View Article and Find Full Text PDFBackground: Patients with rapid progressive Alzheimer disease and related dementias (rpAD/ADRD) develop dementia within 1 year or incapacitation within 2 years of symptom onset. We previously showed that selected CSF biomarkers of neuronal injury (NfL, VILIP-1), AD neuropathology (p-tau181), and neuroinflammation (GFAP, MCP-1, sTREM2) measured at presentation associated with etiologic diagnoses and reliably differentiated patients with treatment-responsive causes of rapid progressive dementia. However, no differences were identified between CSF biomarkers in patients with rapid and typical progressive forms of AD/ADRD, leaving key questions unanswered concerning the mechanisms that drive rpAD/ADRD.
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