Ojanen, M.J.T., Uusi-Mäkelä, M.I.E., Harjula, S.E. et al. Intelectin 3 is dispensable for resistance against a mycobacterial infection in zebrafish (Danio rerio). Sci Rep 9, 995 (2019). https://doi.org/10.1038/s41598-018-37678-1
Intelectin 3 is dispensable for resistance against a mycobacterial infection in zebrafish (Danio rerio)
|Author:||Ojanen, Markus J. T.1,2; Uusi-Mäkelä, Meri I. E.1; Harjula, Sanna-Kaisa E.1;|
1Laboratory of Experimental Immunology, BioMediTech Institute and Faculty of Medicine and Life Sciences, University of Tampere, Tampere, Finland
2Laboratory of Immunoregulation, BioMediTech Institute and Faculty of Medicine and Life Sciences, University of Tampere, Tampere, Finland
3Laboratory of Protein Dynamics, BioMediTech Institute and Faculty of Medicine and Life Sciences, University of Tampere, Tampere, Finland
4Department of Dermatology, Tampere University Hospital, Tampere, Finland
5Department of Pediatrics, Tampere University Hospital, Tampere, Finland
6Department of Children and Adolescents, Oulu University Hospital, Oulu, Finland
7PEDEGO Research Unit and Medical Research Center Oulu, University of Oulu, Oulu, Finland
|Online Access:||PDF Full Text (PDF, 3.7 MB)|
|Persistent link:|| http://urn.fi/urn:nbn:fi-fe2020042722589
|Publish Date:|| 2020-04-27
Tuberculosis is a multifactorial bacterial disease, which can be modeled in the zebrafish (Danio rerio). Abdominal cavity infection with Mycobacterium marinum, a close relative of Mycobacterium tuberculosis, leads to a granulomatous disease in adult zebrafish, which replicates the different phases of human tuberculosis, including primary infection, latency and spontaneous reactivation. Here, we have carried out a transcriptional analysis of zebrafish challenged with low-dose of M. marinum, and identified intelectin 3 (itln3) among the highly up-regulated genes. In order to clarify the in vivo significance of Itln3 in immunity, we created nonsense itln3 mutant zebrafish by CRISPR/Cas9 mutagenesis and analyzed the outcome of M. marinum infection in both zebrafish embryos and adult fish. The lack of functional itln3 did not affect survival or the mycobacterial burden in the zebrafish. Furthermore, embryonic survival was not affected when another mycobacterial challenge responsive intelectin, itln1, was silenced using morpholinos either in the WT or itln3 mutant fish. In addition, M. marinum infection in dexamethasone-treated adult zebrafish, which have lowered lymphocyte counts, resulted in similar bacterial burden in both WT fish and homozygous itln3 mutants. Collectively, although itln3 expression is induced upon M. marinum infection in zebrafish, it is dispensable for protective mycobacterial immune response.
|Type of Publication:||
A1 Journal article – refereed
|Field of Science:||
This study was financially supported by the Academy of Finland (M.R., 277495, M.P. 295814 and 286477), the Sigrid Juselius Foundation (M.R.), the Jane and Aatos Erkko Foundation (M.R.), the Competitive State Research Financing of the Expert Responsibility Area of Tampere University Hospital (M.R., M.P. 9U047 and 9V049), the Competitive State Research Financing of the Expert Responsibility area of Oulu University Hospital (M.R.), the Tampere Tuberculosis Foundation (M.O., M.R., S.-K.H., M.P.), the City of Tampere Science Foundation (S.-K.H), the Väinö and Laina Kivi Foundation (M.O., S.-K.H.), the Finnish Cultural Foundation, the Central Fund (S.-K.H.), the Finnish Concordia Fund (S.-K.H.), the Orion Research Foundation sr (S.-K.H), the Maud Kuistila Memorial Foundation (M.O.), the University of Tampere Doctoral Programme in Biomedicine and Biotechnology (M.O.), the Cancer Society of Finland (M.P.) and Tays tukisäätiö (Tays Support Foundation) (M.P.). We thank the Tampere Zebrafish Core Facility, partly funded by Biocenter Finland, for maintaining and providing the zebrafish. The use of the facilities and expertise of the Protein Technologies core facility of the University of Tampere, a member of Biocenter Finland, is also gratefully acknowledged.
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