Anti-inflammatory protein TNFα-stimulated gene-6 (TSG-6) reduces inflammatory response after brain injury in mice.


Journal

BMC immunology
ISSN: 1471-2172
Titre abrégé: BMC Immunol
Pays: England
ID NLM: 100966980

Informations de publication

Date de publication:
04 08 2021
Historique:
received: 21 04 2020
accepted: 09 07 2021
entrez: 5 8 2021
pubmed: 6 8 2021
medline: 29 1 2022
Statut: epublish

Résumé

Current research suggests that the glial scar surrounding penetrating brain injuries is instrumental in preserving the surrounding uninjured tissue by limiting the inflammatory response to the injury site. We recently showed that tumor necrosis factor (TNF)-stimulated gene-6 (TSG-6), a well-established anti-inflammatory molecule, is present within the glial scar. In the present study we investigated the role of TSG-6 within the glial scar using TSG-6 null and littermate control mice subjected to penetrating brain injuries. Our findings show that mice lacking TSG-6 present a more severe inflammatory response after injury, which was correlated with an enlarged area of astrogliosis beyond the injury site. Our data provides evidence that TSG-6 has an anti-inflammatory role within the glial scar.

Sections du résumé

BACKGROUND
Current research suggests that the glial scar surrounding penetrating brain injuries is instrumental in preserving the surrounding uninjured tissue by limiting the inflammatory response to the injury site. We recently showed that tumor necrosis factor (TNF)-stimulated gene-6 (TSG-6), a well-established anti-inflammatory molecule, is present within the glial scar. In the present study we investigated the role of TSG-6 within the glial scar using TSG-6 null and littermate control mice subjected to penetrating brain injuries.
RESULTS
Our findings show that mice lacking TSG-6 present a more severe inflammatory response after injury, which was correlated with an enlarged area of astrogliosis beyond the injury site.
CONCLUSION
Our data provides evidence that TSG-6 has an anti-inflammatory role within the glial scar.

Identifiants

pubmed: 34348643
doi: 10.1186/s12865-021-00443-7
pii: 10.1186/s12865-021-00443-7
pmc: PMC8336266
doi:

Substances chimiques

Cell Adhesion Molecules 0
Glycosaminoglycans 0
Tnfaip6 protein, mouse 0
Tumor Necrosis Factor-alpha 0

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

52

Subventions

Organisme : NEI NIH HHS
ID : P30 EY007551
Pays : United States
Organisme : NEI NIH HHS
ID : R01 EY029289
Pays : United States
Organisme : NIH HHS
ID : R01 EY029289
Pays : United States
Organisme : NIH HHS
ID : P30 EY07551
Pays : United States

Informations de copyright

© 2021. The Author(s).

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Auteurs

Kazadi Nadine Mutoji (KN)

College of Optometry, University of Houston, 4901 Calhoun Road, Houston, TX, 77204-2020, USA.

Mingxia Sun (M)

College of Optometry, University of Houston, 4901 Calhoun Road, Houston, TX, 77204-2020, USA.

Amanda Nash (A)

College of Optometry, University of Houston, 4901 Calhoun Road, Houston, TX, 77204-2020, USA.
Department of Bioengineering, Rice University, Houston, TX, 77030, USA.

Sudan Puri (S)

College of Optometry, University of Houston, 4901 Calhoun Road, Houston, TX, 77204-2020, USA.

Vincent Hascall (V)

Cleveland Clinic, Cleveland, OH, USA.

Vivien J Coulson-Thomas (VJ)

College of Optometry, University of Houston, 4901 Calhoun Road, Houston, TX, 77204-2020, USA. vcoulsonthomas@gmail.com.

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