Role of Subclinical Gut Inflammation in the Pathogenesis of Spondyloarthritis
Subclinical gut inflammation occurring in patients affected by spondyloarthritis (SpA) is correlated with the severity of spine inflammation. Several evidences indicate that dysbiosis occurs in SpA, and that may modulate intestinal permeability and intestinal immune responses. The presence of intest...
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| Format: | Article |
| Language: | English |
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Frontiers Media S.A.
2018-05-01
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| Series: | Frontiers in Medicine |
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| Online Access: | http://journal.frontiersin.org/article/10.3389/fmed.2018.00063/full |
| _version_ | 1818858559757090816 |
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| author | Aroldo Rizzo Giuliana Guggino Angelo Ferrante Francesco Ciccia |
| author_facet | Aroldo Rizzo Giuliana Guggino Angelo Ferrante Francesco Ciccia |
| author_sort | Aroldo Rizzo |
| collection | DOAJ |
| description | Subclinical gut inflammation occurring in patients affected by spondyloarthritis (SpA) is correlated with the severity of spine inflammation. Several evidences indicate that dysbiosis occurs in SpA, and that may modulate intestinal permeability and intestinal immune responses. The presence of intestinal dysbiosis is accompanied in SpA patients with the presence of zonulin-dependent alterations of gut-epithelial and gut-vascular barriers. The leakage of epithelial and endothelial surface layers is followed by the translocation of bacterial products, such as lipopolysaccharide and intestinal fatty acid binding protein, in the systemic circulation. These bacterial products may downregulate the expression of CD14 on circulating monocytes leading to an “anergic” phenotype. In the gut, IL-23 may induce the expansion of innate immune cells such as mucosal-associated invariant T cells, γδ T cells, and innate lymphoid cells of group 3 that through the interaction with MAdCAM1 may recirculate form the gut to the sites of SpA active inflammation. On the basis of these findings, gut inflammation observed in SpA patient seems to be not only an epiphenomenon of the on going systemic inflammatory process but may also represent the base camp in which inflammatory cells are activated and from whom they shuttle. |
| first_indexed | 2024-12-19T08:58:13Z |
| format | Article |
| id | doaj.art-b9b364d4066a4a61ac5321ff44fee0a3 |
| institution | Directory Open Access Journal |
| issn | 2296-858X |
| language | English |
| last_indexed | 2024-12-19T08:58:13Z |
| publishDate | 2018-05-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Medicine |
| spelling | doaj.art-b9b364d4066a4a61ac5321ff44fee0a32022-12-21T20:28:33ZengFrontiers Media S.A.Frontiers in Medicine2296-858X2018-05-01510.3389/fmed.2018.00063323617Role of Subclinical Gut Inflammation in the Pathogenesis of SpondyloarthritisAroldo Rizzo0Giuliana Guggino1Angelo Ferrante2Francesco Ciccia3Dipartimento Biomedico di Medicina Interna e Specialistica, Università degli studi di Palermo, Palermo, ItalyUnità Operativa di Anatomia Patologica, Azienda Ospedaliera Ospedali Riuniti Villa Sofia Cervello, Palermo, ItalyUnità Operativa di Anatomia Patologica, Azienda Ospedaliera Ospedali Riuniti Villa Sofia Cervello, Palermo, ItalyUnità Operativa di Anatomia Patologica, Azienda Ospedaliera Ospedali Riuniti Villa Sofia Cervello, Palermo, ItalySubclinical gut inflammation occurring in patients affected by spondyloarthritis (SpA) is correlated with the severity of spine inflammation. Several evidences indicate that dysbiosis occurs in SpA, and that may modulate intestinal permeability and intestinal immune responses. The presence of intestinal dysbiosis is accompanied in SpA patients with the presence of zonulin-dependent alterations of gut-epithelial and gut-vascular barriers. The leakage of epithelial and endothelial surface layers is followed by the translocation of bacterial products, such as lipopolysaccharide and intestinal fatty acid binding protein, in the systemic circulation. These bacterial products may downregulate the expression of CD14 on circulating monocytes leading to an “anergic” phenotype. In the gut, IL-23 may induce the expansion of innate immune cells such as mucosal-associated invariant T cells, γδ T cells, and innate lymphoid cells of group 3 that through the interaction with MAdCAM1 may recirculate form the gut to the sites of SpA active inflammation. On the basis of these findings, gut inflammation observed in SpA patient seems to be not only an epiphenomenon of the on going systemic inflammatory process but may also represent the base camp in which inflammatory cells are activated and from whom they shuttle.http://journal.frontiersin.org/article/10.3389/fmed.2018.00063/fullspondylitisgut microbiomeinflammation mediatorsinnate immune responseenthesitis-related arthritis |
| spellingShingle | Aroldo Rizzo Giuliana Guggino Angelo Ferrante Francesco Ciccia Role of Subclinical Gut Inflammation in the Pathogenesis of Spondyloarthritis Frontiers in Medicine spondylitis gut microbiome inflammation mediators innate immune response enthesitis-related arthritis |
| title | Role of Subclinical Gut Inflammation in the Pathogenesis of Spondyloarthritis |
| title_full | Role of Subclinical Gut Inflammation in the Pathogenesis of Spondyloarthritis |
| title_fullStr | Role of Subclinical Gut Inflammation in the Pathogenesis of Spondyloarthritis |
| title_full_unstemmed | Role of Subclinical Gut Inflammation in the Pathogenesis of Spondyloarthritis |
| title_short | Role of Subclinical Gut Inflammation in the Pathogenesis of Spondyloarthritis |
| title_sort | role of subclinical gut inflammation in the pathogenesis of spondyloarthritis |
| topic | spondylitis gut microbiome inflammation mediators innate immune response enthesitis-related arthritis |
| url | http://journal.frontiersin.org/article/10.3389/fmed.2018.00063/full |
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