Evaluation of the TLR3 involvement during Schistosoma japonicum-induced pathology.

Amelioration Liver Schistosoma japonicum TLR3

Journal

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

Informations de publication

Date de publication:
03 Jan 2024
Historique:
received: 15 03 2023
accepted: 13 11 2023
medline: 4 1 2024
pubmed: 4 1 2024
entrez: 3 1 2024
Statut: epublish

Résumé

Despite the functions of TLRs in the parasitic infections have been extensively reported, few studies have addressed the role of TLR3 in the immune response to Schistosoma japonicum infections. The aim of this study was to investigate the properties of TLR3 in the liver of C57BL/6 mice infected by S. japonicum. The production of TLR3 Flow cytometry results showed that the expression of TLR3 increased significantly after S. japonicum infection (P < 0.05). Hepatic myeloid and lymphoid cells could express TLR3, and the percentages of TLR3-expressing MDSC, macrophages and neutrophils were increased after infection. Knocking out TLR3 ameliorated the damage and decreased infiltration of inflammatory cells in infected C57BL/6 mouse livers.,The number of WBC was significantly reduced in TLR3 KO-infected mice compared to WT-infected mice (P < 0.01), but the levels of RBC, platelet and HGB were significantly increased in KO infected mice. Moreover, the relative titers of anti-SEA IgG and anti-SEA IgM in the serum of infected KO mice were statistically decreased compared with the infected WT mice. We also compared the activation-associated molecules expression between S.japonicum-infected WT and TLR3 KO mice. Taken together, our data indicated that TLR3 played potential roles in the context of S. japonicum infection and it may accelerate the progression of S. japonicum-associated liver pathology.

Sections du résumé

BACKGROUND BACKGROUND
Despite the functions of TLRs in the parasitic infections have been extensively reported, few studies have addressed the role of TLR3 in the immune response to Schistosoma japonicum infections. The aim of this study was to investigate the properties of TLR3 in the liver of C57BL/6 mice infected by S. japonicum.
METHODS METHODS
The production of TLR3
RESULTS RESULTS
Flow cytometry results showed that the expression of TLR3 increased significantly after S. japonicum infection (P < 0.05). Hepatic myeloid and lymphoid cells could express TLR3, and the percentages of TLR3-expressing MDSC, macrophages and neutrophils were increased after infection. Knocking out TLR3 ameliorated the damage and decreased infiltration of inflammatory cells in infected C57BL/6 mouse livers.,The number of WBC was significantly reduced in TLR3 KO-infected mice compared to WT-infected mice (P < 0.01), but the levels of RBC, platelet and HGB were significantly increased in KO infected mice. Moreover, the relative titers of anti-SEA IgG and anti-SEA IgM in the serum of infected KO mice were statistically decreased compared with the infected WT mice. We also compared the activation-associated molecules expression between S.japonicum-infected WT and TLR3 KO mice.
CONCLUSIONS CONCLUSIONS
Taken together, our data indicated that TLR3 played potential roles in the context of S. japonicum infection and it may accelerate the progression of S. japonicum-associated liver pathology.

Identifiants

pubmed: 38172683
doi: 10.1186/s12865-023-00586-9
pii: 10.1186/s12865-023-00586-9
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

2

Informations de copyright

© 2023. The Author(s).

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Auteurs

Hongyan Xie (H)

Department of Laboratory Medicine, The Sixth Affiliated Hospital of Guangzhou Medical University, Qingyuan People's Hospital, Qingyuan, 511518, China.
China Sino-French Hoffmann Institute, Department of basic Medical Science, Guangzhou Medical University, Guangzhou, 511436, China.

Dianhui Chen (D)

Department of Infectious Diseases, The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, 510150, China.

Yuanfa Feng (Y)

China Sino-French Hoffmann Institute, Department of basic Medical Science, Guangzhou Medical University, Guangzhou, 511436, China.

Feng Mo (F)

Department of Infectious Diseases, The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, 510150, China.

Lin Liu (L)

China Sino-French Hoffmann Institute, Department of basic Medical Science, Guangzhou Medical University, Guangzhou, 511436, China.

Junmin Xing (J)

China Sino-French Hoffmann Institute, Department of basic Medical Science, Guangzhou Medical University, Guangzhou, 511436, China.

Wei Xiao (W)

China Sino-French Hoffmann Institute, Department of basic Medical Science, Guangzhou Medical University, Guangzhou, 511436, China.

Yumei Gong (Y)

China Sino-French Hoffmann Institute, Department of basic Medical Science, Guangzhou Medical University, Guangzhou, 511436, China.

Shanni Tang (S)

Department of Infectious Diseases, The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, 510150, China.

Zhengrong Tan (Z)

China Sino-French Hoffmann Institute, Department of basic Medical Science, Guangzhou Medical University, Guangzhou, 511436, China.

Guikuan Liang (G)

China Sino-French Hoffmann Institute, Department of basic Medical Science, Guangzhou Medical University, Guangzhou, 511436, China.

Shan Zhao (S)

Department of Laboratory Medicine, The Sixth Affiliated Hospital of Guangzhou Medical University, Qingyuan People's Hospital, Qingyuan, 511518, China. zhaoshan@gzhmu.edu.cn.
China Sino-French Hoffmann Institute, Department of basic Medical Science, Guangzhou Medical University, Guangzhou, 511436, China. zhaoshan@gzhmu.edu.cn.

Weiguo Yin (W)

Department of Laboratory Medicine, The Sixth Affiliated Hospital of Guangzhou Medical University, Qingyuan People's Hospital, Qingyuan, 511518, China. hyyinweiguo@hotmail.com.

Jun Huang (J)

Department of Laboratory Medicine, The Sixth Affiliated Hospital of Guangzhou Medical University, Qingyuan People's Hospital, Qingyuan, 511518, China. hj165@sina.com.
China Sino-French Hoffmann Institute, Department of basic Medical Science, Guangzhou Medical University, Guangzhou, 511436, China. hj165@sina.com.
State Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangzhou, China. hj165@sina.com.

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