TLR2 Signaling in Skin Nonhematopoietic Cells Induces Early Neutrophil Recruitment in Response to Leishmania major Infection.
Animals
Bone Marrow Transplantation
Cell Communication
/ immunology
Chemokine CXCL1
/ immunology
Disease Models, Animal
Humans
Keratinocytes
/ immunology
Leishmania major
/ immunology
Leishmaniasis, Cutaneous
/ immunology
Mice
Mice, Knockout
Neutrophil Infiltration
Neutrophils
/ immunology
Parasite Load
Signal Transduction
/ genetics
Skin
/ cytology
Toll-Like Receptor 2
/ genetics
Transplantation Chimera
Journal
The Journal of investigative dermatology
ISSN: 1523-1747
Titre abrégé: J Invest Dermatol
Pays: United States
ID NLM: 0426720
Informations de publication
Date de publication:
06 2019
06 2019
Historique:
received:
06
07
2018
revised:
14
11
2018
accepted:
05
12
2018
pubmed:
31
12
2018
medline:
10
5
2020
entrez:
31
12
2018
Statut:
ppublish
Résumé
Neutrophils are rapidly recruited to the mammalian skin in response to infection with the cutaneous Leishmania pathogen. The parasites use neutrophils to establish the disease; however, the signals driving early neutrophil recruitment are poorly known. Here, we identified the functional importance of TLR2 signaling in this process. Using bone marrow chimeras and immunohistology, we identified the TLR2-expressing cells involved in this early neutrophil recruitment to be of nonhematopoietic origin. Keratinocytes are damaged and briefly in contact with the parasites during infection. We show that TLR2 triggering by Leishmania major is required for their secretion of neutrophil-attracting chemokines. Furthermore, TLR2 triggering by L. major phosphoglycans is critical for neutrophil recruitment to negatively affect disease development, as shown by better control of lesion size and parasite load in Tlr2
Identifiants
pubmed: 30594488
pii: S0022-202X(18)01302-7
doi: 10.1016/j.jid.2018.12.012
pmc: PMC8024985
mid: NIHMS1685362
pii:
doi:
Substances chimiques
Chemokine CXCL1
0
Cxcl1 protein, mouse
0
Tlr2 protein, mouse
0
Toll-Like Receptor 2
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
1318-1328Subventions
Organisme : World Health Organization
ID : 001
Pays : International
Organisme : Medical Research Council
ID : MR/K019384/1
Pays : United Kingdom
Organisme : NIAID NIH HHS
ID : R01 AI031078
Pays : United States
Informations de copyright
Copyright © 2018 The Authors. Published by Elsevier Inc. All rights reserved.
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