Helminth Products Potently Modulate Experimental Autoimmune Encephalomyelitis by Downregulating Neuroinflammation and Promoting a Suppressive Microenvironment
A negative correlation between the geographical distribution of autoimmune diseases and helminth infections has been largely associated in the last few years with a possible role for such type of parasites in the regulation of inflammatory diseases, suggesting new pathways for drug development. Howe...
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| Format: | Article |
| Language: | English |
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Wiley
2017-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2017/8494572 |
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| author | Alberto N. Peón Yadira Ledesma-Soto Jonadab E. Olguín Marcel Bautista-Donis Edda Sciutto Luis I. Terrazas |
| author_facet | Alberto N. Peón Yadira Ledesma-Soto Jonadab E. Olguín Marcel Bautista-Donis Edda Sciutto Luis I. Terrazas |
| author_sort | Alberto N. Peón |
| collection | DOAJ |
| description | A negative correlation between the geographical distribution of autoimmune diseases and helminth infections has been largely associated in the last few years with a possible role for such type of parasites in the regulation of inflammatory diseases, suggesting new pathways for drug development. However, few helminth-derived immunomodulators have been tested in experimental autoimmune encephalomyelitis (EAE), an animal model of the human disease multiple sclerosis (MS). The immunomodulatory activities of Taenia crassiceps excreted/secreted products (TcES) that may suppress EAE development were sought for. Interestingly, it was discovered that TcES was able to suppress EAE development with more potency than dexamethasone; moreover, TcES treatment was still effective even when inoculated at later stages after the onset of EAE. Importantly, the TcES treatment was able to induce a range of Th2-type cytokines, while suppressing Th1 and Th17 responses. Both the polyclonal and the antigen-specific proliferative responses of lymphocytes were also inhibited in EAE-ill mice receiving TcES in association with a potent recruitment of suppressor cell populations. Peritoneal inoculation of TcES was able to direct the normal inflammatory cell traffic to the site of injection, thus modulating CNS infiltration, which may work along with Th2 immune polarization and lymphocyte activation impairment to downregulate EAE development. |
| format | Article |
| id | doaj-art-0da504e3369c4287ba29d695e97b9250 |
| institution | Kabale University |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2017-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-0da504e3369c4287ba29d695e97b92502025-02-03T01:10:21ZengWileyMediators of Inflammation0962-93511466-18612017-01-01201710.1155/2017/84945728494572Helminth Products Potently Modulate Experimental Autoimmune Encephalomyelitis by Downregulating Neuroinflammation and Promoting a Suppressive MicroenvironmentAlberto N. Peón0Yadira Ledesma-Soto1Jonadab E. Olguín2Marcel Bautista-Donis3Edda Sciutto4Luis I. Terrazas5Unidad de Biomedicina, Facultad de Estudios Superiores Iztacala (FES-I), Universidad Nacional Autónoma de Mexico (UNAM), MEX, MexicoUnidad de Biomedicina, Facultad de Estudios Superiores Iztacala (FES-I), Universidad Nacional Autónoma de Mexico (UNAM), MEX, MexicoUnidad de Biomedicina, Facultad de Estudios Superiores Iztacala (FES-I), Universidad Nacional Autónoma de Mexico (UNAM), MEX, MexicoDepartamento de Inmunología, Instituto de Investigaciones Biomédicas, UNAM, Mexico City, MexicoDepartamento de Inmunología, Instituto de Investigaciones Biomédicas, UNAM, Mexico City, MexicoUnidad de Biomedicina, Facultad de Estudios Superiores Iztacala (FES-I), Universidad Nacional Autónoma de Mexico (UNAM), MEX, MexicoA negative correlation between the geographical distribution of autoimmune diseases and helminth infections has been largely associated in the last few years with a possible role for such type of parasites in the regulation of inflammatory diseases, suggesting new pathways for drug development. However, few helminth-derived immunomodulators have been tested in experimental autoimmune encephalomyelitis (EAE), an animal model of the human disease multiple sclerosis (MS). The immunomodulatory activities of Taenia crassiceps excreted/secreted products (TcES) that may suppress EAE development were sought for. Interestingly, it was discovered that TcES was able to suppress EAE development with more potency than dexamethasone; moreover, TcES treatment was still effective even when inoculated at later stages after the onset of EAE. Importantly, the TcES treatment was able to induce a range of Th2-type cytokines, while suppressing Th1 and Th17 responses. Both the polyclonal and the antigen-specific proliferative responses of lymphocytes were also inhibited in EAE-ill mice receiving TcES in association with a potent recruitment of suppressor cell populations. Peritoneal inoculation of TcES was able to direct the normal inflammatory cell traffic to the site of injection, thus modulating CNS infiltration, which may work along with Th2 immune polarization and lymphocyte activation impairment to downregulate EAE development.http://dx.doi.org/10.1155/2017/8494572 |
| spellingShingle | Alberto N. Peón Yadira Ledesma-Soto Jonadab E. Olguín Marcel Bautista-Donis Edda Sciutto Luis I. Terrazas Helminth Products Potently Modulate Experimental Autoimmune Encephalomyelitis by Downregulating Neuroinflammation and Promoting a Suppressive Microenvironment Mediators of Inflammation |
| title | Helminth Products Potently Modulate Experimental Autoimmune Encephalomyelitis by Downregulating Neuroinflammation and Promoting a Suppressive Microenvironment |
| title_full | Helminth Products Potently Modulate Experimental Autoimmune Encephalomyelitis by Downregulating Neuroinflammation and Promoting a Suppressive Microenvironment |
| title_fullStr | Helminth Products Potently Modulate Experimental Autoimmune Encephalomyelitis by Downregulating Neuroinflammation and Promoting a Suppressive Microenvironment |
| title_full_unstemmed | Helminth Products Potently Modulate Experimental Autoimmune Encephalomyelitis by Downregulating Neuroinflammation and Promoting a Suppressive Microenvironment |
| title_short | Helminth Products Potently Modulate Experimental Autoimmune Encephalomyelitis by Downregulating Neuroinflammation and Promoting a Suppressive Microenvironment |
| title_sort | helminth products potently modulate experimental autoimmune encephalomyelitis by downregulating neuroinflammation and promoting a suppressive microenvironment |
| url | http://dx.doi.org/10.1155/2017/8494572 |
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