Contribution of Lewis X Carbohydrate Structure to Neuropathogenic Murine Coronaviral Spread
Although Lewis X (Lex), a carbohydrate structure, is involved in innate immunity through cell-to-cell and pathogen recognition, its expression has not been observed in mouse monocytes/macrophages (Mo/Mas). The Mo/Mas that infiltrate the meninges after infection with the neuropathogenic murine corona...
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| Published in | Japanese Journal of Infectious Diseases Vol. 69; no. 5; pp. 405 - 413 |
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| Main Authors | , , , |
| Format | Journal Article |
| Language | English |
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Japan
National Institute of Infectious Diseases, Japanese Journal of Infectious Diseases Editorial Committee
2016
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| Abstract | Although Lewis X (Lex), a carbohydrate structure, is involved in innate immunity through cell-to-cell and pathogen recognition, its expression has not been observed in mouse monocytes/macrophages (Mo/Mas). The Mo/Mas that infiltrate the meninges after infection with the neuropathogenic murine coronavirus strain srr7 are an initial target of infection. Furthermore, higher inflammatory responses were observed in gene-manipulated mice lacking α1,3-fucosyltransferase 9, which determines the expression of the Lex structure, than in wild type mice after infection. We investigated Lex expression using CD11b-positive peritoneal exudate cells (PECs) and found that Lex is inducible in Mo/Mas after infection with srr7, especially in the syncytial cells during the late phase of infection. The number of syncytial cells was reduced after treatment of the infected PECs with anti-Lex antibody, during the late phase of infection. In addition, the antibody treatment induced a marked reduction in the number of the infected cells at 24 hours post inoculation, without changing the infected cell numbers during the initial phase of infection. These data indicate that the Lex structure could play a role in syncytial formation and cell-to-cell infection during the late phase of infection. |
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| AbstractList | Although Lewis X (Le(x)), a carbohydrate structure, is involved in innate immunity through cell-to-cell and pathogen recognition, its expression has not been observed in mouse monocytes/macrophages (Mo/Mas). The Mo/Mas that infiltrate the meninges after infection with the neuropathogenic murine coronavirus strain srr7 are an initial target of infection. Furthermore, higher inflammatory responses were observed in gene-manipulated mice lacking α1,3-fucosyltransferase 9, which determines the expression of the Le(x) structure, than in wild type mice after infection. We investigated Le(x) expression using CD11b-positive peritoneal exudate cells (PECs) and found that Le(x) is inducible in Mo/Mas after infection with srr7, especially in the syncytial cells during the late phase of infection. The number of syncytial cells was reduced after treatment of the infected PECs with anti-Le(x) antibody, during the late phase of infection. In addition, the antibody treatment induced a marked reduction in the number of the infected cells at 24 hours post inoculation, without changing the infected cell numbers during the initial phase of infection. These data indicate that the Le(x) structure could play a role in syncytial formation and cell-to-cell infection during the late phase of infection.Although Lewis X (Le(x)), a carbohydrate structure, is involved in innate immunity through cell-to-cell and pathogen recognition, its expression has not been observed in mouse monocytes/macrophages (Mo/Mas). The Mo/Mas that infiltrate the meninges after infection with the neuropathogenic murine coronavirus strain srr7 are an initial target of infection. Furthermore, higher inflammatory responses were observed in gene-manipulated mice lacking α1,3-fucosyltransferase 9, which determines the expression of the Le(x) structure, than in wild type mice after infection. We investigated Le(x) expression using CD11b-positive peritoneal exudate cells (PECs) and found that Le(x) is inducible in Mo/Mas after infection with srr7, especially in the syncytial cells during the late phase of infection. The number of syncytial cells was reduced after treatment of the infected PECs with anti-Le(x) antibody, during the late phase of infection. In addition, the antibody treatment induced a marked reduction in the number of the infected cells at 24 hours post inoculation, without changing the infected cell numbers during the initial phase of infection. These data indicate that the Le(x) structure could play a role in syncytial formation and cell-to-cell infection during the late phase of infection. Although Lewis X (Le super(x)), a carbohydrate structure, is involved in innate immunity through cell-to-cell and pathogen recognition, its expression has not been observed in mouse monocytes/macrophages (Mo/Mas). The Mo/Mas that infiltrate the meninges after infection with the neuropathogenic murine coronavirus strain srr7 are an initial target of infection. Furthermore, higher inflammatory responses were observed in gene-manipulated mice lacking alpha 1,3-fucosyltransferase 9, which determines the expression of the Le super(x) structure, than in wild type mice after infection. We investigated Le super(x) expression using CD11b-positive peritoneal exudate cells (PECs) and found that Le super(x) is inducible in Mo/Mas after infection with srr7, especially in the syncytial cells during the late phase of infection. The number of syncytial cells was reduced after treatment of the infected PECs with anti-Le super(x) antibody, during the late phase of infection. In addition, the antibody treatment induced a marked reduction in the number of the infected cells at 24 hours post inoculation, without changing the infected cell numbers during the initial phase of infection. These data indicate that the Le super(x) structure could play a role in syncytial formation and cell-to-cell infection during the late phase of infection. Although Lewis X (Le(x)), a carbohydrate structure, is involved in innate immunity through cell-to-cell and pathogen recognition, its expression has not been observed in mouse monocytes/macrophages (Mo/Mas). The Mo/Mas that infiltrate the meninges after infection with the neuropathogenic murine coronavirus strain srr7 are an initial target of infection. Furthermore, higher inflammatory responses were observed in gene-manipulated mice lacking α1,3-fucosyltransferase 9, which determines the expression of the Le(x) structure, than in wild type mice after infection. We investigated Le(x) expression using CD11b-positive peritoneal exudate cells (PECs) and found that Le(x) is inducible in Mo/Mas after infection with srr7, especially in the syncytial cells during the late phase of infection. The number of syncytial cells was reduced after treatment of the infected PECs with anti-Le(x) antibody, during the late phase of infection. In addition, the antibody treatment induced a marked reduction in the number of the infected cells at 24 hours post inoculation, without changing the infected cell numbers during the initial phase of infection. These data indicate that the Le(x) structure could play a role in syncytial formation and cell-to-cell infection during the late phase of infection. Although Lewis X (Lex), a carbohydrate structure, is involved in innate immunity through cell-to-cell and pathogen recognition, its expression has not been observed in mouse monocytes/macrophages (Mo/Mas). The Mo/Mas that infiltrate the meninges after infection with the neuropathogenic murine coronavirus strain srr7 are an initial target of infection. Furthermore, higher inflammatory responses were observed in gene-manipulated mice lacking α1,3-fucosyltransferase 9, which determines the expression of the Lex structure, than in wild type mice after infection. We investigated Lex expression using CD11b-positive peritoneal exudate cells (PECs) and found that Lex is inducible in Mo/Mas after infection with srr7, especially in the syncytial cells during the late phase of infection. The number of syncytial cells was reduced after treatment of the infected PECs with anti-Lex antibody, during the late phase of infection. In addition, the antibody treatment induced a marked reduction in the number of the infected cells at 24 hours post inoculation, without changing the infected cell numbers during the initial phase of infection. These data indicate that the Lex structure could play a role in syncytial formation and cell-to-cell infection during the late phase of infection. |
| Author | Togayachi, Akira Watanabe, Rihito Narimatsu, Hisashi Kakizaki, Masatoshi |
| Author_xml | – sequence: 1 fullname: Kakizaki, Masatoshi organization: Department of Bioinformatics, Graduate School of Engineering, Soka University – sequence: 2 fullname: Togayachi, Akira organization: Glycoscience and Glycotechnology Research Group, Biotechnology Research Institute for Drug Discovery, National Institute of Advanced Industrial Science and Technology (AIST) – sequence: 3 fullname: Narimatsu, Hisashi organization: Glycoscience and Glycotechnology Research Group, Biotechnology Research Institute for Drug Discovery, National Institute of Advanced Industrial Science and Technology (AIST) – sequence: 4 fullname: Watanabe, Rihito organization: Department of Bioinformatics, Graduate School of Engineering, Soka University |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/26902214$$D View this record in MEDLINE/PubMed |
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| CitedBy_id | crossref_primary_10_1111_neup_12374 crossref_primary_10_3389_fimmu_2020_568565 crossref_primary_10_1111_neup_12386 crossref_primary_10_1111_neup_12302 |
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| References_xml | – reference: 17. Taguchi F, Yamada A, Fujiwara K. Resistance to highly virulent mouse hepatitis virus acquired by mice after lowvirulence infection: enhanced antiviral activity of macrophages. Infect Immun. 1980;29:42-9. – reference: 7. Glass WG, Chen BP, Liu MT, et al. Mouse hepatitis virus infection of the central nervous system: chemokine-mediated regulation of host defense and disease. Viral Immunol. 2002;15:261-72. – reference: 28. Schindler H, Lutz MB, Rollinghoff M, et al. The production of IFN-γ by IL-12/IL-18-activated macrophages requires STAT4 signaling and is inhibited by IL-4. J Immunol. 2001;166:3075-82. – reference: 40. Kashiwazaki H, Taguchi F, Ikehara Y, et al. Characterization of splenic cells during the early phase of infection with neuropathogenic mouse hepatitis virus. Jpn J Infect Dis. 2011;64:256-9. – reference: 29. Nakagaki K, Nakagaki K, Taguchi F. Receptor-independent spread of a highly neurotropic murine coronavirus JHMV strain from initially infected microglial cells in mixed neural cultures. J Virol. 2005;79:6102-10. – reference: 30. Ribechini E, Greifenberg V, Sandwick S, et al. Subsets expansion and activation of myeloid-derives suppressor cells. Med Microbiol Immunol. 2010;199:273-81. – reference: 22. Nishihara S, Iwasaki H, Nakajima K, et a1. 3-Fucosyltransferase IX (Fut9) determines Lewis X expression in brain. Glycobiology. 2003;13:445-55. – reference: 34. van Kooyk Y, Rabinovich GA. Protein-glycan interactions in the control of innate and adaptive immune responses. Nat Immunol. 2008;9:593-601. – reference: 38. Gracia-Vallejo JJ, Ilarregui JM, Kalay H, et al. CNS myelin induces regulatory functions of DC-SIGN-expressing, antigen-presenting cells via cognate interaction with MOG. J Exp Med. 2014;211:1465-83. – reference: 31. Dijkman R, Jebbink MF, Deijs M, et al. Replication-dependent downregulation of cellular angiotensin-converting enzyme 2 protein expression by human coronavirus NL63. J Gen Virol. 2012;93:1924-9. – reference: 14. Andersson T, Schwarcz R, Love A, et al. Measles virus-induced hippocampal neurodegeneration in the mouse: a novel. Neurosci Lett. 1993;154:109-12. – reference: 39. Kawauchi Y, Takagi H, Hanafusa K, et al. SIGNR1-mediated phagocytosis, but not SIGNR1-mediated endocytosis or cell adhesion, suppresses LPS-induced secretion of IL-6 from murine macrophages. Cytokine. 2015;71:45-53. – reference: 26. Schleicher U, Hesse A, Bogdan C. Minute numbers of contaminant CD8 + T cells or CD11b + CD11c + NK cells are the source of IFN-γ in IL-12/IL-18-stimulated mouse macrophage populations. Blood. 2005;105:1319-28. – reference: 19. Cook AD, Braine EL,Hamilton JA. The phenotype of inflammatory macrophages is stimulus dependent: implications for the nature of the inflammatory response. J immunol. 2003;17:4816-23. – reference: 42. 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| Snippet | Although Lewis X (Lex), a carbohydrate structure, is involved in innate immunity through cell-to-cell and pathogen recognition, its expression has not been... Although Lewis X (Le(x)), a carbohydrate structure, is involved in innate immunity through cell-to-cell and pathogen recognition, its expression has not been... Although Lewis X (Le super(x)), a carbohydrate structure, is involved in innate immunity through cell-to-cell and pathogen recognition, its expression has not... |
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| SubjectTerms | Animals bystander effect Cells, Cultured Coronaviridae Coronavirus - growth & development Coronavirus - physiology Fut9 JHM Lewis X Antigen - metabolism Macrophages - chemistry Macrophages - immunology Macrophages - virology Mice, Inbred BALB C Monocytes - chemistry Monocytes - immunology Monocytes - virology thioglycollate Virus Internalization |
| Title | Contribution of Lewis X Carbohydrate Structure to Neuropathogenic Murine Coronaviral Spread |
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