IL-17RA receptor signaling contributes to lung inflammation and parasite burden during Toxocara canis infection in mice
IL-17 is a cytokine produced by innate and acquired immunity cells that have an action against fungi and bacteria. However, its action in helminth infections is unclear, including in Toxocara canis infection. Toxocariasis is a neglected zoonosis representing a significant public health problem with...
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| Format: | Article |
| Language: | English |
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Frontiers Media S.A.
2022-06-01
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| Series: | Frontiers in Immunology |
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| Online Access: | https://www.frontiersin.org/articles/10.3389/fimmu.2022.864632/full |
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| author | Thaís Leal-Silva Thaís Leal-Silva Camila de Almeida Lopes Flaviane Vieira-Santos Fabrício Marcus Silva Oliveira Lucas Kraemer Luiza de Lima Silva Padrão Luiza de Lima Silva Padrão Chiara Cássia Oliveira Amorim Jorge Lucas Nascimento Souza Remo Castro Russo Ricardo Toshio Fujiwara Ricardo Toshio Fujiwara Luisa Mourão Dias Magalhães Lilian Lacerda Bueno Lilian Lacerda Bueno |
| author_facet | Thaís Leal-Silva Thaís Leal-Silva Camila de Almeida Lopes Flaviane Vieira-Santos Fabrício Marcus Silva Oliveira Lucas Kraemer Luiza de Lima Silva Padrão Luiza de Lima Silva Padrão Chiara Cássia Oliveira Amorim Jorge Lucas Nascimento Souza Remo Castro Russo Ricardo Toshio Fujiwara Ricardo Toshio Fujiwara Luisa Mourão Dias Magalhães Lilian Lacerda Bueno Lilian Lacerda Bueno |
| author_sort | Thaís Leal-Silva |
| collection | DOAJ |
| description | IL-17 is a cytokine produced by innate and acquired immunity cells that have an action against fungi and bacteria. However, its action in helminth infections is unclear, including in Toxocara canis infection. Toxocariasis is a neglected zoonosis representing a significant public health problem with an estimated seroprevalence of 19% worldwide. In the present study, we describe the immunopathological action of IL-17RA in acute T. canis infection. C57BL/6j (WT) and IL-17RA receptor knockout (IL-17RA-/-) mice were infected with 1000 T. canis eggs. Mice were evaluated 3 days post-infection for parasite load and white blood cell count. Lung tissue was harvested for histopathology and cytokine expression. In addition, we performed multiparametric flow cytometry in the BAL and peripheral blood, evaluating phenotypic and functional changes in myeloid and lymphoid populations. We showed that IL-17RA is essential to control larvae load in the lung; however, IL-17RA contributed to pulmonary inflammation, inducing inflammatory nodular aggregates formation and presented higher pulmonary IL-6 levels. The absence of IL-17RA was associated with a higher frequency of neutrophils as a source of IL-4 in BAL, while in the presence of IL-17RA, mice display a higher frequency of alveolar macrophages expressing the same cytokine. Taken together, this study indicates that neutrophils may be an important source of IL-4 in the lungs during T. canis infection. Furthermore, IL-17/IL-17RA axis is important to control parasite load, however, its presence triggers lung inflammation that can lead to tissue damage. |
| first_indexed | 2024-12-12T07:24:23Z |
| format | Article |
| id | doaj.art-0427566506e94df4b66dd89f4022d212 |
| institution | Directory Open Access Journal |
| issn | 1664-3224 |
| language | English |
| last_indexed | 2024-12-12T07:24:23Z |
| publishDate | 2022-06-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Immunology |
| spelling | doaj.art-0427566506e94df4b66dd89f4022d2122022-12-22T00:33:11ZengFrontiers Media S.A.Frontiers in Immunology1664-32242022-06-011310.3389/fimmu.2022.864632864632IL-17RA receptor signaling contributes to lung inflammation and parasite burden during Toxocara canis infection in miceThaís Leal-Silva0Thaís Leal-Silva1Camila de Almeida Lopes2Flaviane Vieira-Santos3Fabrício Marcus Silva Oliveira4Lucas Kraemer5Luiza de Lima Silva Padrão6Luiza de Lima Silva Padrão7Chiara Cássia Oliveira Amorim8Jorge Lucas Nascimento Souza9Remo Castro Russo10Ricardo Toshio Fujiwara11Ricardo Toshio Fujiwara12Luisa Mourão Dias Magalhães13Lilian Lacerda Bueno14Lilian Lacerda Bueno15Laboratory of Immunology and Genomics of Parasites, Department of Parasitology, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, BrazilFaculdade de Medicina, Federal University of Minas Gerais, Belo Horizonte, BrazilLaboratory of Immunology and Genomics of Parasites, Department of Parasitology, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, BrazilLaboratory of Immunology and Genomics of Parasites, Department of Parasitology, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, BrazilLaboratory of Immunology and Genomics of Parasites, Department of Parasitology, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, BrazilLaboratory of Immunology and Genomics of Parasites, Department of Parasitology, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, BrazilLaboratory of Immunology and Genomics of Parasites, Department of Parasitology, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, BrazilFaculdade de Medicina, Federal University of Minas Gerais, Belo Horizonte, BrazilLaboratory of Immunology and Genomics of Parasites, Department of Parasitology, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, BrazilLaboratory of Immunology and Genomics of Parasites, Department of Parasitology, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, BrazilLaboratory of Pulmonary Immunology and Mechanics, Department of Physiology and Biophysics, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, BrazilLaboratory of Immunology and Genomics of Parasites, Department of Parasitology, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, BrazilFaculdade de Medicina, Federal University of Minas Gerais, Belo Horizonte, BrazilLaboratory of Immunology and Genomics of Parasites, Department of Parasitology, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, BrazilLaboratory of Immunology and Genomics of Parasites, Department of Parasitology, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, BrazilFaculdade de Medicina, Federal University of Minas Gerais, Belo Horizonte, BrazilIL-17 is a cytokine produced by innate and acquired immunity cells that have an action against fungi and bacteria. However, its action in helminth infections is unclear, including in Toxocara canis infection. Toxocariasis is a neglected zoonosis representing a significant public health problem with an estimated seroprevalence of 19% worldwide. In the present study, we describe the immunopathological action of IL-17RA in acute T. canis infection. C57BL/6j (WT) and IL-17RA receptor knockout (IL-17RA-/-) mice were infected with 1000 T. canis eggs. Mice were evaluated 3 days post-infection for parasite load and white blood cell count. Lung tissue was harvested for histopathology and cytokine expression. In addition, we performed multiparametric flow cytometry in the BAL and peripheral blood, evaluating phenotypic and functional changes in myeloid and lymphoid populations. We showed that IL-17RA is essential to control larvae load in the lung; however, IL-17RA contributed to pulmonary inflammation, inducing inflammatory nodular aggregates formation and presented higher pulmonary IL-6 levels. The absence of IL-17RA was associated with a higher frequency of neutrophils as a source of IL-4 in BAL, while in the presence of IL-17RA, mice display a higher frequency of alveolar macrophages expressing the same cytokine. Taken together, this study indicates that neutrophils may be an important source of IL-4 in the lungs during T. canis infection. Furthermore, IL-17/IL-17RA axis is important to control parasite load, however, its presence triggers lung inflammation that can lead to tissue damage.https://www.frontiersin.org/articles/10.3389/fimmu.2022.864632/fullIL-17RAtoxocariasiscytokineshelminthinflammationneutrophil |
| spellingShingle | Thaís Leal-Silva Thaís Leal-Silva Camila de Almeida Lopes Flaviane Vieira-Santos Fabrício Marcus Silva Oliveira Lucas Kraemer Luiza de Lima Silva Padrão Luiza de Lima Silva Padrão Chiara Cássia Oliveira Amorim Jorge Lucas Nascimento Souza Remo Castro Russo Ricardo Toshio Fujiwara Ricardo Toshio Fujiwara Luisa Mourão Dias Magalhães Lilian Lacerda Bueno Lilian Lacerda Bueno IL-17RA receptor signaling contributes to lung inflammation and parasite burden during Toxocara canis infection in mice Frontiers in Immunology IL-17RA toxocariasis cytokines helminth inflammation neutrophil |
| title | IL-17RA receptor signaling contributes to lung inflammation and parasite burden during Toxocara canis infection in mice |
| title_full | IL-17RA receptor signaling contributes to lung inflammation and parasite burden during Toxocara canis infection in mice |
| title_fullStr | IL-17RA receptor signaling contributes to lung inflammation and parasite burden during Toxocara canis infection in mice |
| title_full_unstemmed | IL-17RA receptor signaling contributes to lung inflammation and parasite burden during Toxocara canis infection in mice |
| title_short | IL-17RA receptor signaling contributes to lung inflammation and parasite burden during Toxocara canis infection in mice |
| title_sort | il 17ra receptor signaling contributes to lung inflammation and parasite burden during toxocara canis infection in mice |
| topic | IL-17RA toxocariasis cytokines helminth inflammation neutrophil |
| url | https://www.frontiersin.org/articles/10.3389/fimmu.2022.864632/full |
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