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LL-37 Triggers Antimicrobial Activity in Human Platelets
Francisco Javier Sánchez-Peña1, María de Los Ángeles Romero-Tlalolini2, Honorio Torres-Aguilar3
1Departamento de Biomedicina Experimental, Facultad de Medicina y Cirugía de la Universidad Autónoma "Benito Juárez" de Oaxaca, Oaxaca 68120, México.
Abstract:
Platelets play a crucial role in hemostasis and the immune response, mainly by recognizing signals associated with vascular damage. However, it has recently been discovered that the antimicrobial peptide LL-37 activates platelets in functions related to thrombus formation and inflammation. Therefore, this work aims to evaluate the effect of LL-37 on the activation of antimicrobial functions of human platelets. Our results show that platelets treated with LL-37 increase the surface expression of receptors (Toll-like receptors (TLRs) 2 and -4, CD32, CD206, Dectin-1, CD35, LOX-1, CD41, CD62P, and αIIbβ3 integrins) for the recognition of microorganisms, and molecules related to antigen presentation to T lymphocytes (CD80, CD86, and HLA-ABC) secrete the antimicrobial molecules: bactericidal/permeability-increasing protein (BPI), azurocidin, human neutrophil peptide (HNP) -1, and myeloperoxidase. They also translate azurocidin, and have enhanced binding to Escherichia coli, Staphylococcus aureus, and Candida albicans. Furthermore, the supernatant of LL-37-treated platelets can inhibit E. coli growth, or platelets can employ their LL-37 to inhibit microbial growth. In conclusion, these findings demonstrate that LL-37 participates in the antimicrobial function of human platelets.
Insights
The antimicrobial peptide LL-37 activates human platelets, enhancing their ability to recognize and bind microbes. LL-37 also stimulates platelets to release antimicrobial molecules, boosting the immune response against bacterial and fungal infections.
Area of Science:
- Immunology
- Hematology
- Microbiology
Background:
- Platelets are key in hemostasis and immunity, responding to vascular damage signals.
- The antimicrobial peptide LL-37 has been found to activate platelets in processes linked to thrombosis and inflammation.
Purpose of the Study:
- To investigate the impact of LL-37 on the antimicrobial functions of human platelets.
- To determine if LL-37 enhances platelet-mediated microbial recognition and killing.
Main Methods:
- Human platelets were treated with LL-37.
- Analysis included surface receptor expression (e.g., TLRs, CD markers, integrins) via flow cytometry.
- Antimicrobial molecule secretion and platelet binding to microbes (E. coli, S. aureus, C. albicans) were assessed.
- Microbial growth inhibition assays were performed.
Main Results:
- LL-37 treatment increased expression of microbial-recognition receptors and antigen-presentation molecules on platelets.
- Platelets secreted antimicrobial proteins like BPI, azurocidin, HNP-1, and myeloperoxidase.
- LL-37-treated platelets showed enhanced binding to E. coli, S. aureus, and C. albicans.
- Platelet supernatant inhibited E. coli growth, indicating direct antimicrobial activity.
Conclusions:
- LL-37 significantly enhances the antimicrobial capabilities of human platelets.
- Platelets activated by LL-37 play a direct role in combating microbial infections through enhanced recognition, secretion, and inhibition of pathogen growth.
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