Nocardia seriolae cell wall lipids : An effective protective mechanism in resistance and virulence
© 2023 John Wiley & Sons Ltd.
| Publié dans: | Journal of fish diseases. - 1998. - 46(2023), 4 vom: 17. Apr., Seite 405-416 |
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| Auteur principal: | |
| Autres auteurs: | , , , |
| Format: | Article en ligne |
| Langue: | English |
| Publié: |
2023
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| Accès à la collection: | Journal of fish diseases |
| Sujets: | Journal Article Nocardia seriolae cell wall-associated lipids delipidation resistance virulence Lipids |
| Résumé: | © 2023 John Wiley & Sons Ltd. Piscine nocardiosis, caused by Nocardia seriolae, is a refractory granulomatous disease in South-East Asian aquaculture. This study investigates the virulence of nocardial lipids essential for pathogenesis among Actinomycetes. Petroleum ether (PE) was used to selectively delipidate two groups of N. seriolae, namely, live cell (LC) and killed cell (KC); resulting in delipidated live cell (DLC) and delipidated killed cell (DKC), respectively. Changes post-delipidation on genus characteristics, such as loss in acid-fast nature and resistance to lysozyme were observed. Transmission electron microscopy revealed notable changes in the lipid layer. Additionally, Lates calcarifer, Asian seabass intraperitoneally injected with LC and DLC had mortality rates of 90% and 50%, respectively, with the latter exhibiting a delay in mortality. Reverse-transcription quantitative PCR (RT-qPCR) analysis of host cytokines from the spleen and head kidney showed delipidation contributed to the induction of an immune response with increased transcriptional levels of interferon-γ (ifn-γ). Histopathological samples collected on day 7 post-inoculation displayed a varied granulomatous response between the treatment groups and scored for pathological changes. These findings affirm that the virulence of the lipids remains independent of the living state of the cell, significantly altering the immune and granulomatous responses in L. calcarifer to N. seriolae |
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| Description: | Date Completed 10.03.2023 Date Revised 10.03.2023 published: Print-Electronic Citation Status MEDLINE |
| ISSN: | 1365-2761 |
| DOI: | 10.1111/jfd.13753 |