Role of Dectin-1 in immune response of macrophages induced by Fonsecaea monophora wild strain and melanin-deficient mutant strain
ABSTRACTChromoblastomycosis is a chronic granulomatous subcutaneous fungal disease caused mainly by Fonsecaea monophora in southern China. Melanin is an important virulence factor in wild strain (Mel+), and the strains lack of the polyketide synthase gene is a melanin-deficient mutant strain (Mel-)....
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Taylor & Francis Group
2024-01-01
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Series: | Mycology |
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Online Access: | https://www.tandfonline.com/doi/10.1080/21501203.2023.2249010 |
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author | Jiaojiao Zhong Jing Zhang Jianchi Ma Wenying Cai Xiqing Li Junmin Zhang |
author_facet | Jiaojiao Zhong Jing Zhang Jianchi Ma Wenying Cai Xiqing Li Junmin Zhang |
author_sort | Jiaojiao Zhong |
collection | DOAJ |
description | ABSTRACTChromoblastomycosis is a chronic granulomatous subcutaneous fungal disease caused mainly by Fonsecaea monophora in southern China. Melanin is an important virulence factor in wild strain (Mel+), and the strains lack of the polyketide synthase gene is a melanin-deficient mutant strain (Mel-). We investigated the effect of melanin in F. monophora on Dectin-1 receptor-mediated immune responses in macrophages. Conidia and tiny hyphae of Mel+ and Mel- were co-cultured with THP-1 macrophages expressing normal or low levels of Dectin-1. Compare the killing rate, phagocytosis rate, and expression levels of the inflammatory cytokines tumour necrosis factor-α, interleukin-1β, interleukin-6, and nitric oxide in each group. The results showed that the killing rate, phagocytosis rate, and pro-inflammatory factor levels of Mel+ infected macrophages with normal expression of Dectin-1 were lower than those of Mel-. And the knockdown of Dectin-1 inhibited the phagocytic rate, killing rate, and proinflammatory factor expression in macrophages infected with Mel+ and Mel-. And there was no significant difference in the above indexes between Mel+ and Mel- groups in Dectin-1 knockdown macrophages. In summary, the study reveals that melanin of F. monophora inhibits the immune response effect of the host by hindering its binding to Dectin-1 on the surface of macrophage, which may lead to persistent fungal infections. |
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issn | 2150-1203 2150-1211 |
language | English |
last_indexed | 2024-04-24T18:41:00Z |
publishDate | 2024-01-01 |
publisher | Taylor & Francis Group |
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series | Mycology |
spelling | doaj.art-69fe157512c44e128afbc3df0e63654e2024-03-27T12:44:51ZengTaylor & Francis GroupMycology2150-12032150-12112024-01-01151455610.1080/21501203.2023.2249010Role of Dectin-1 in immune response of macrophages induced by Fonsecaea monophora wild strain and melanin-deficient mutant strainJiaojiao Zhong0Jing Zhang1Jianchi Ma2Wenying Cai3Xiqing Li4Junmin Zhang5Department of Dermatology, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, ChinaDepartment of Dermatology, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, ChinaDepartment of Dermatology, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, ChinaDepartment of Dermatology, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, ChinaDepartment of Dermatology, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, ChinaDepartment of Dermatology, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, ChinaABSTRACTChromoblastomycosis is a chronic granulomatous subcutaneous fungal disease caused mainly by Fonsecaea monophora in southern China. Melanin is an important virulence factor in wild strain (Mel+), and the strains lack of the polyketide synthase gene is a melanin-deficient mutant strain (Mel-). We investigated the effect of melanin in F. monophora on Dectin-1 receptor-mediated immune responses in macrophages. Conidia and tiny hyphae of Mel+ and Mel- were co-cultured with THP-1 macrophages expressing normal or low levels of Dectin-1. Compare the killing rate, phagocytosis rate, and expression levels of the inflammatory cytokines tumour necrosis factor-α, interleukin-1β, interleukin-6, and nitric oxide in each group. The results showed that the killing rate, phagocytosis rate, and pro-inflammatory factor levels of Mel+ infected macrophages with normal expression of Dectin-1 were lower than those of Mel-. And the knockdown of Dectin-1 inhibited the phagocytic rate, killing rate, and proinflammatory factor expression in macrophages infected with Mel+ and Mel-. And there was no significant difference in the above indexes between Mel+ and Mel- groups in Dectin-1 knockdown macrophages. In summary, the study reveals that melanin of F. monophora inhibits the immune response effect of the host by hindering its binding to Dectin-1 on the surface of macrophage, which may lead to persistent fungal infections.https://www.tandfonline.com/doi/10.1080/21501203.2023.2249010Fonsecaea monophoramelaninDectin-1macrophagephagocytosiscytokine |
spellingShingle | Jiaojiao Zhong Jing Zhang Jianchi Ma Wenying Cai Xiqing Li Junmin Zhang Role of Dectin-1 in immune response of macrophages induced by Fonsecaea monophora wild strain and melanin-deficient mutant strain Mycology Fonsecaea monophora melanin Dectin-1 macrophage phagocytosis cytokine |
title | Role of Dectin-1 in immune response of macrophages induced by Fonsecaea monophora wild strain and melanin-deficient mutant strain |
title_full | Role of Dectin-1 in immune response of macrophages induced by Fonsecaea monophora wild strain and melanin-deficient mutant strain |
title_fullStr | Role of Dectin-1 in immune response of macrophages induced by Fonsecaea monophora wild strain and melanin-deficient mutant strain |
title_full_unstemmed | Role of Dectin-1 in immune response of macrophages induced by Fonsecaea monophora wild strain and melanin-deficient mutant strain |
title_short | Role of Dectin-1 in immune response of macrophages induced by Fonsecaea monophora wild strain and melanin-deficient mutant strain |
title_sort | role of dectin 1 in immune response of macrophages induced by fonsecaea monophora wild strain and melanin deficient mutant strain |
topic | Fonsecaea monophora melanin Dectin-1 macrophage phagocytosis cytokine |
url | https://www.tandfonline.com/doi/10.1080/21501203.2023.2249010 |
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