Macrophage migration inhibitory factor of Thelazia callipaeda induces M2-like macrophage polarization through TLR4-mediated activation of the PI3K-Akt pathway.


Journal

FASEB journal : official publication of the Federation of American Societies for Experimental Biology
ISSN: 1530-6860
Titre abrégé: FASEB J
Pays: United States
ID NLM: 8804484

Informations de publication

Date de publication:
09 2021
Historique:
revised: 06 08 2021
received: 21 04 2021
accepted: 09 08 2021
entrez: 20 8 2021
pubmed: 21 8 2021
medline: 10 9 2021
Statut: ppublish

Résumé

Macrophage migration inhibitory factor (MIF), an immunoregulatory cytokine plays an important role in inflammation and the immune response, and has been described as having a potential role in immune evasion by parasites. Thelazia callipaeda, a vector-borne zoonotic eye worm with a broad host range, has been documented as an agent of ocular infection of thelaziosis. The ability of T. callipaeda to persist in an immunologically competent host has led to the suggestion that it has evolved specific measures to counter immune defenses. To date, whether the immune evasion of T. callipaeda is related to MIF and the possible related signaling pathway and molecular mechanism have remained unclear. In the present study, we examined the effect of T. callipaeda MIF (T. cp-MIF) on macrophages. We analyzed the antigenic epitopes of the candidate T. cp-MIF and found that it exhibited an ideal antigenic index. Morphology, Flow cytometry, and cytokine analysis showed that T. cp-MIF induced the dynamic polarization of THP-1 macrophages from the M1-like phenotype to the M2-like phenotype. The chemotaxis assay revealed an inhibitory effect of T. cp-MIF on THP-1 macrophages. Western blotting suggested that, compared to the control, THP-1 macrophages exposed to T. cp-MIF had higher TLR4 protein expression and the phosphatidylinositol 3'-kinase (PI3K) -Akt pathway activation. In conclusion, T. cp-MIF induces M2-like macrophage polarization through TLR4-mediated activation of the PI3K-Akt pathway, which might provide a basis for future research on how it affects the immune system of the host.

Identifiants

pubmed: 34416031
doi: 10.1096/fj.202100676R
doi:

Substances chimiques

Epitopes 0
Macrophage Migration-Inhibitory Factors 0
TLR4 protein, human 0
Toll-Like Receptor 4 0
AKT1 protein, human EC 2.7.11.1
Proto-Oncogene Proteins c-akt EC 2.7.11.1

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

e21866

Informations de copyright

© 2021 Federation of American Societies for Experimental Biology.

Références

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Auteurs

Juan Cai (J)

Department of Parasitology, Zunyi Medical University, Zunyi, China.

Lin Huang (L)

Qiannan Medical College for Nationalities, Duyun, China.

Hongri Tang (H)

Department of Parasitology, Zunyi Medical University, Zunyi, China.

Hongling Xu (H)

Department of Parasitology, Zunyi Medical University, Zunyi, China.

Lingjun Wang (L)

Department of Parasitology, Zunyi Medical University, Zunyi, China.

Minghui Zheng (M)

Department of Parasitology, Zunyi Medical University, Zunyi, China.

Hongsong Yu (H)

Department of Immunology, Special Key Laboratory of Ocular Diseases of Guizhou Province, Zunyi Medical University, Zunyi, China.

Hui Liu (H)

Department of Parasitology, Zunyi Medical University, Zunyi, China.

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