We have located links that may give you full text access.
Blocking CXCR1/2 attenuates experimental periodontitis by suppressing neutrophils recruitment.
International Immunopharmacology 2024 January 5
Periodontitis (PD) is a common chronic oral inflammatory disease that cause alveolar bone loss. Current strategies for bone regeneration achieve limited results in PD. The aberrant host osteoimmunity to pathogenic bacteria is responsible for the destruction of alveolar bone in PD. We aimed to investigate the distinctive activity of immune cells in PD to create more effective and precise therapeutic approaches for treating PD. In this study, we revealed that neutrophils in the inflamed alveolar bone of PD patients expressed higher levels of CXCR1/2 and had a stronger pro-inflammatory capacity and chemotactic ability than that in healthy individuals. Suppressing the recruitment of neutrophils to inflamed sites with the CXCR1/2 inhibitor reparixin reduced alveolar bone loss in PD mice. In this study, we not only revealed that neutrophils exhibit a heterogeneously stronger pro-inflammatory capacity in the inflamed alveolar bone of PD patients but also provided a precise therapeutic treatment for PD involving the suppression of neutrophil recruitment.
Full text links
Related Resources
Trending Papers
Autoimmune Hemolytic Anemias: Classifications, Pathophysiology, Diagnoses and Management.International Journal of Molecular Sciences 2024 April 13
Executive Summary: State-of-the-Art Review: Unintended Consequences: Risk of Opportunistic Infections Associated with Long-term Glucocorticoid Therapies in Adults.Clinical Infectious Diseases 2024 April 11
Clinical practice guidelines on the management of status epilepticus in adults: A systematic review.Epilepsia 2024 April 13
Finerenone: From the Mechanism of Action to Clinical Use in Kidney Disease.Pharmaceuticals 2024 March 27
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app
All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.
By using this service, you agree to our terms of use and privacy policy.
Your Privacy Choices
You can now claim free CME credits for this literature searchClaim now
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app