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The central adaptor molecule TRIF influences L. sigmodontis worm development.
Parasitol Res 2019; 118(2):539-549PR

Abstract

Worldwide approximately 68 million people are infected with lymphatic filariasis (Lf), provoked by Wuchereria bancrofti, Brugia malayi and Brugia timori. This disease can lead to massive swelling of the limbs (elephantiasis) and disfigurement of the male genitalia (hydrocele). Filarial induced immune regulation is characterised by dominant type 2 helper T cell and regulatory immune responses. In vitro studies have provided evidence that signalling via Toll-like receptor-mediated pathways is triggered by filarial associated factors. Nevertheless, until now, less is known about the role of the adapter molecule TRIF during in vivo infections. Here, we used the rodent-specific nematode Litomosoides sigmodontis to investigate the role of TLR signalling and the corresponding downstream adapter and regulatory molecules TRIF, MyD88, IRF1 and IRF3 during an ongoing infection in semi-susceptible C57BL/6 mice. Interestingly, lack of the central adapter molecule TRIF led to higher worm burden and reduced overall absolute cell numbers in the thoracic cavity (the site of infection) 30 days post-infection. In addition, frequencies of macrophages and lymphocytes in the TC were increased in infected TRIF-/- C57BL/6 mice, whereas frequencies of eosinophils, CD4+ and CD8+ T cells were reduced. Nevertheless, cytokine levels and regulatory T cell populations remained comparable between TRIF-deficient and wildtype C57BL/6 mice upon 30 days of L. sigmodontis infection. In summary, this study revealed a crucial role of the adapter molecule TRIF on worm recovery and immune cell recruitment into the site of infection 30 days upon L. sigmodontis infection in C57BL/6 mice.

Authors+Show Affiliations

Institute of Medical Microbiology, Immunology and Parasitology (IMMIP), University Hospital of Bonn, Sigmund Freud Str. 25, 53127, Bonn, Germany.Institute of Medical Microbiology, Immunology and Parasitology (IMMIP), University Hospital of Bonn, Sigmund Freud Str. 25, 53127, Bonn, Germany.Institute of Medical Microbiology, Immunology and Parasitology (IMMIP), University Hospital of Bonn, Sigmund Freud Str. 25, 53127, Bonn, Germany.Institute of Medical Microbiology, Immunology and Parasitology (IMMIP), University Hospital of Bonn, Sigmund Freud Str. 25, 53127, Bonn, Germany.Institute of Medical Microbiology, Immunology and Parasitology (IMMIP), University Hospital of Bonn, Sigmund Freud Str. 25, 53127, Bonn, Germany.LIMES, University of Bonn, Bonn, Germany.Research Foundation for Tropical Diseases and the Environment (REFOTDE), Buea, Cameroon. Parasite and Vector Research Unit (PAVRU), Department of Microbiology and Parasitology, University of Buea, Buea, Cameroon.Institute of Medical Microbiology, Immunology and Parasitology (IMMIP), University Hospital of Bonn, Sigmund Freud Str. 25, 53127, Bonn, Germany. German Centre for Infection Research (DZIF), partner site, Bonn-Cologne, Bonn, Germany.Institute of Medical Microbiology, Immunology and Parasitology (IMMIP), University Hospital of Bonn, Sigmund Freud Str. 25, 53127, Bonn, Germany. laura.layland@microbiology-bonn.de. German Centre for Infection Research (DZIF), partner site, Bonn-Cologne, Bonn, Germany. laura.layland@microbiology-bonn.de.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

30643971

Citation

Wiszniewsky, Anna, et al. "The Central Adaptor Molecule TRIF Influences L. Sigmodontis Worm Development." Parasitology Research, vol. 118, no. 2, 2019, pp. 539-549.
Wiszniewsky A, Ritter M, Krupp V, et al. The central adaptor molecule TRIF influences L. sigmodontis worm development. Parasitol Res. 2019;118(2):539-549.
Wiszniewsky, A., Ritter, M., Krupp, V., Schulz, S., Arndts, K., Weighardt, H., ... Layland, L. E. (2019). The central adaptor molecule TRIF influences L. sigmodontis worm development. Parasitology Research, 118(2), pp. 539-549. doi:10.1007/s00436-018-6159-1.
Wiszniewsky A, et al. The Central Adaptor Molecule TRIF Influences L. Sigmodontis Worm Development. Parasitol Res. 2019;118(2):539-549. PubMed PMID: 30643971.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The central adaptor molecule TRIF influences L. sigmodontis worm development. AU - Wiszniewsky,Anna, AU - Ritter,Manuel, AU - Krupp,Vanessa, AU - Schulz,Sandy, AU - Arndts,Kathrin, AU - Weighardt,Heike, AU - Wanji,Samuel, AU - Hoerauf,Achim, AU - Layland,Laura E, Y1 - 2019/01/15/ PY - 2018/08/13/received PY - 2018/11/14/accepted PY - 2019/1/16/pubmed PY - 2019/5/1/medline PY - 2019/1/16/entrez KW - Adapter molecule TRIF KW - Litomosoides sigmodontis KW - Lymphatic filariasis KW - Semi-susceptible C57BL/6 mice KW - TLR signalling KW - Worm burden SP - 539 EP - 549 JF - Parasitology research JO - Parasitol. Res. VL - 118 IS - 2 N2 - Worldwide approximately 68 million people are infected with lymphatic filariasis (Lf), provoked by Wuchereria bancrofti, Brugia malayi and Brugia timori. This disease can lead to massive swelling of the limbs (elephantiasis) and disfigurement of the male genitalia (hydrocele). Filarial induced immune regulation is characterised by dominant type 2 helper T cell and regulatory immune responses. In vitro studies have provided evidence that signalling via Toll-like receptor-mediated pathways is triggered by filarial associated factors. Nevertheless, until now, less is known about the role of the adapter molecule TRIF during in vivo infections. Here, we used the rodent-specific nematode Litomosoides sigmodontis to investigate the role of TLR signalling and the corresponding downstream adapter and regulatory molecules TRIF, MyD88, IRF1 and IRF3 during an ongoing infection in semi-susceptible C57BL/6 mice. Interestingly, lack of the central adapter molecule TRIF led to higher worm burden and reduced overall absolute cell numbers in the thoracic cavity (the site of infection) 30 days post-infection. In addition, frequencies of macrophages and lymphocytes in the TC were increased in infected TRIF-/- C57BL/6 mice, whereas frequencies of eosinophils, CD4+ and CD8+ T cells were reduced. Nevertheless, cytokine levels and regulatory T cell populations remained comparable between TRIF-deficient and wildtype C57BL/6 mice upon 30 days of L. sigmodontis infection. In summary, this study revealed a crucial role of the adapter molecule TRIF on worm recovery and immune cell recruitment into the site of infection 30 days upon L. sigmodontis infection in C57BL/6 mice. SN - 1432-1955 UR - https://www.unboundmedicine.com/medline/citation/30643971/The_central_adaptor_molecule_TRIF_influences_L._sigmodontis_worm_development L2 - https://dx.doi.org/10.1007/s00436-018-6159-1 DB - PRIME DP - Unbound Medicine ER -