Fibrin is a critical regulator of neutrophil effector function at the oral mucosal barrier-Reference-Cited by-同舟云学术

Fibrin is a critical regulator of neutrophil effector function at the oral mucosal barrier

Published:2021-12-24 Issue:6575 Volume:374 Page:
ISSN:0036-8075
Container-title:Science
language:en
Short-container-title:Science

Author:

Silva Lakmali M.¹²^ORCID,Doyle Andrew D.³^ORCID,Greenwell-Wild Teresa²,Dutzan Nicolas²⁴^ORCID,Tran Collin L.¹^ORCID,Abusleme Loreto²⁵^ORCID,Juang Lih Jiin⁶,Leung Jerry⁶,Chun Elizabeth M.¹,Lum Andrew G.²,Agler Cary S.⁷^ORCID,Zuazo Carlos E.²,Sibree Megan¹^ORCID,Jani Priyam⁸^ORCID,Kram Vardit⁸,Martin Daniel⁹^ORCID,Moss Kevin⁷,Lionakis Michail S.¹⁰^ORCID,Castellino Francis J.¹¹^ORCID,Kastrup Christian J.⁶¹²¹³,Flick Matthew J.¹⁴^ORCID,Divaris Kimon¹⁵¹⁶^ORCID,Bugge Thomas H.¹^ORCID,Moutsopoulos Niki M.²^ORCID

Affiliation:

1. Proteases and Tissue Remodeling Section, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD, USA.

2. Oral Immunity and Inflammation Section, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD, USA.

3. NIDCR Imaging Core, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD, USA.

4. Department of Conservative Dentistry, Faculty of Dentistry, University of Chile, Santiago, Chile.

5. Department of Pathology and Oral Medicine, Faculty of Dentistry, University of Chile, Santiago, Chile.

6. Michael Smith Laboratories and Department of Biochemistry and Molecular Biology, The University of British Columbia, Vancouver, BC, Canada.

7. Division of Oral and Craniofacial Health Sciences, Adams School of Dentistry, University of North Carolina, Chapel Hill, NC, USA.

8. Molecular Biology of Bones and Teeth Section, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD, USA.

9. NIDCR Genomics and Computational Biology Core, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD, USA.

10. Fungal Pathogenesis Section, Laboratory of Clinical Immunology and Microbiology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.

11. WM Keck Center for Transgene Research, University of Notre Dame, Notre Dame, IN, USA.

12. Blood Research Institute, Versiti, Milwaukee, WI, USA.

13. Departments of Surgery, Biochemistry, Biomedical Engineering, and Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, WI, USA.

14. Department of Pathology and Laboratory Medicine, University of North Carolina, Chapel Hill, NC, USA.

15. Division of Pediatric and Public Health, Adams School of Dentistry, University of North Carolina, Chapel Hill, NC, USA.

16. Department of Epidemiology, Gillings School of Global Public Health, University of North Carolina, Chapel Hill, NC, USA.

Abstract

Fibrin gums up the works Plasmin is an abundant plasma protease that cleaves and deactivates the clot-associated protein fibrin. Human deficiencies in plasmin and its inactive proenzyme form, plasminogen (PLG), cause severe inflammation in mucosal tissues such as the mouth and eyes. Silva et al . report that, like humans, mice lacking plasminogen accumulate extravascular fibrin and develop an oral pathology that phenocopies human ligneous periodontitis (see the Perspective by Vicanolo and Hidalgo). The excess fibrin activates neutrophils through the αMβ2 (Mac-1) integrin receptor, which triggers the production of reactive oxygen species and neutrophil extracellular traps. Additionally, certain human polymorphisms in the PLG gene were found to be associated with increased likelihood of developing periodontitis, suggesting that fibrin–neutrophil interactions may be an attractive target for future treatments of this prevalent disease. —STS

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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