Intestinal Permeability in Patients With Ankylosing Spondylitis and Their Healthy Relatives

Martínez‐González, Olga; Cantero-Hinojosa, J.; Paule-Sastre, P.; Gómez-Magán, J. C.; Salvatierra-Ríos, D.

doi:10.1093/rheumatology/33.7.644

Cited by 101 publications

(54 citation statements)

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“…The link between increased intestinal permeability and AS has been clearly established [50]. Using different markers of TJ permeability, two independent studies [51,52] found an increased intestinal permeability in both AS patients and their relatives. These changes precede the clinical manifestations of the disease, suggesting a pathogenic role of TJ dysfunction in AS.…”

Section: Ankylosing Spondylitismentioning

confidence: 99%

Leaky Gut and Autoimmune Diseases

Fasano

2011

Clinic Rev Allerg Immunol

282

179

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Autoimmune diseases are characterized by tissue damage and loss of function due to an immune response that is directed against specific organs. This review is focused on the role of impaired intestinal barrier function on autoimmune pathogenesis. Together with the gut-associated lymphoid tissue and the neuroendocrine network, the intestinal epithelial barrier, with its intercellular tight junctions, controls the equilibrium between tolerance and immunity to non-self antigens. Zonulin is the only physiologic modulator of intercellular tight junctions described so far that is involved in trafficking of macromolecules and, therefore, in tolerance/immune response balance. When the zonulin pathway is deregulated in genetically susceptible individuals, autoimmune disorders can occur. This new paradigm subverts traditional theories underlying the development of these diseases and suggests that these processes can be arrested if the interplay between genes and environmental triggers is prevented by re-establishing the zonulin-dependent intestinal barrier function. Both animal models and recent clinical evidence support this new paradigm and provide the rationale for innovative approaches to prevent and treat autoimmune diseases.

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Section: Ankylosing Spondylitismentioning

confidence: 99%

Leaky Gut and Autoimmune Diseases

Fasano

2011

Clinic Rev Allerg Immunol

282

179

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“…The increased prevalence of AS in young adult males may result from a higher starch intake and consequent increase in Klebsiella growth in the gut. 2 The site at which the triggering infection occurs is unclear, but the presence of histological signs of inflammation 86 and increased gut permeability 79 in patients with AS suggests an overt or occult enteric infection.…”

Section: Environmental Triggersmentioning

confidence: 99%

The pathogenesis of ankylosing spondylitis

Shamji

Bafaquh²,

Tsai³

2008

FOC

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✓ Ankylosing spondylitis (AS) is a chronic inflammatory disease that can cause significant functional complications by affecting the sacroiliac joints and axial skeleton. Despite a longstanding knowledge about the familial associations of this disease, particularly among patients positive for human leukocyte antigen (HLA)–B27, the fundamental pathogenetic mechanism by which this disease arises in genetically susceptible individuals remains ill defined. Furthermore, the molecular predilection for characteristic articular site involvement remains under ongoing investigation. Current theories about the HLA-B27 association range from the presentation of novel arthritogenic peptides, to abnormal autoimmune stimulation, to anomalous microbial tolerance. The immune effectors of this damage include CD4+, CD8+, and natural killer cells, with marked heterogeneity at different sites. Biomechanical stresses may trigger this disease by exposing the body to previously immune-sequestered autoantigens or by providing a route for bacterial seeding. Environmental triggers such as infection have not been definitively established but may represent a primary pathogenic step in a molecular-mimicry process. In this article, the authors review the current literature on the origin and pathophysiology of AS, focusing on genetic and molecular associations, consequent pathomechanisms, and associated triggers. An improved understanding of the sequence of molecular events that predispose and initiate the onset of this disease will allow for more specific and targeted therapy and better avoidance of the significant side effects of systemic immunomodulation.

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“…It may be of greater significance that 21-60% of first-degree relatives of patients with non-NSAIDtreated AS had increased intestinal permeability (53,54). These findings parallel the increased intestinal permeability found in 10-54% of first-degree relatives of patients with Crohn's disease (49,55,56).…”

Section: Effect Of Treatment On Spondylarthropathic Ileitismentioning

confidence: 99%