1,721,189 research outputs found
Role of subclinical gut inflammation in the pathogenesis of spondyloarthritis
Full text linkSubclinical 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
Gut inflammation in spondyloarthritis
No full textSpondyloarthritis (SpA) is a group of related diseases sharing common etiopathogenic mechanisms and clinical manifestations supported by a complex genetic predisposition. Gut inflammation is present in patients with SpA including patients showing clinically evident intestinal inflammation in the form of Crohn's disease or ulcerative colitis and patients who despite the absence of signs and symptoms of intestinal inflammation display a subclinical gut inflammation. Emerging evidence suggests that subclinical gut inflammation in patients with SpA, apparently driven by intestinal dysbiosis, is not the consequence of the systemic inflammatory process but rather an important pathophysiological event actively participating in the pathogenesis of the disease. The dysregulation of intestinal epithelial barrier possibly modulated by intestinal dysbiosis and especially in HLA-B27 + patients modulates local and systemic inflammation possibly representing the occult mechanism of the disease. This review aims to summarise current data on the role of the gastrointestinal involvement and intestinal microbiota in the pathogenesis of systemic rheumatic disease
Histopathology of the gut in rheumatic diseases
Full text linkThe gastrointestinal tract regulates the trafficking of macromolecules between the environment and the host through an epithelial barrier mechanism and is an important part of the immune system controlling the equilibrium between tolerance and immunity to non-self-antigens. Various evidence indicates that intestinal inflammation occurs in patients with rheumatic diseases. In many rheumatic diseases intestinal inflammation appears to be linked to dysbiosis and possibly represents the common denominator in the pathogenesis of different rheumatic diseases. The continuative interaction between dysbiosis and the intestinal immune system may lead to the aberrant activation of immune cells that can re-circulate from the gut to the sites of extraintestinal inflammation as observed in patients with ankylosing spondylitis. The exact contribution of genetic factors in the development of intestinal inflammation in rheumatic diseases needs to be clarified
Pathogenesis of polymyalgia rheumatica
Full text linkPolymyalgia rheumatica (PMR) is a chronic, inflammatory disorder of unknown cause, almost exclusively occurring in people aged over 50 and often associated with giant cell arteritis. The evidence that PMR occurs almost exclusively in individuals aged over 50 may indicate that age-related immune alterations in genetically predisposed subjects contribute to development of the disease. Several infectious agents have been investigated as possible triggers of PMR even though the results are inconclusive. Activation of the innate and adaptive immune systems has been proved in PMR patients as demonstrated by the activation of dendritic cells and monocytes/macrophages and the altered balance between Th17 and Treg cells. Disturbed B cell distribution and function have been also demonstrated in PMR patients suggesting a pathogenesis more complex than previously imagined. In this review we will discuss the recent findings regarding the pathogenesis of PMR
Gut-derived CD8+ tissue-resident memory T cells are expanded in the peripheral blood and synovia of SpA patients
Full text linkInterstitial Lung Disease in Elderly Rheumatoid Arthritis Patients
Full text linkThe increase in life expectancy together with better care of rheumatoid arthritis (RA) has led to higher proportions of elderly individuals with RA. This has challenged the treatment of the disease in older aged patients, usually characterized by comorbid conditions and polypharmacy. Overall, the lung involvement in RA is present in up to 80% of patients, depending on the assessment tools used, and interstitial abnormalities are among the most common; when present, interstitial lung disease (ILD) worsens the prognosis of RA, and is the second most common cause of mortality. The aged lung undergoes functional and structural changes termed immunosenescence and inflammaging, which facilitate the occurrence of fibrosis of the lung. Therefore, ILD tends to occur more frequently in older patients with RA. The age at onset of RA distinguishes patients as having young-onset RA (YORA, < 60 years) or late-onset RA (LORA, > 60 years); the latter are characterized by more severe features of the disease and higher rates of lung involvement. The most frequent RA-related ILD radiological pattern is usual interstitial pneumonia (UIP); this includes peripheral and basal predominant reticulation and honeycombing with or without associated traction bronchiectasis. Patients with the UIP pattern are usually older and have more rapid decline in lung function and a worse prognosis. Treatment with corticosteroids in elderly patients carries the risk of adverse effects, such as osteoporosis, infections, diabetes, peptic ulcers, and cataract. The use of disease-modifying antirheumatic drugs (DMARDs) is generally well-tolerated by the elderly. The current narrative review aims at elucidating the association between ILD and RA in older individuals
Going Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
The role of the gastrointestinal tract in the pathogenesis of rheumatic diseases
Full text linkDysregulation of the intestinal epithelial barrier in genetically
susceptible individuals may lead to both intestinal and extraintestinal
autoimmune disorders. There is emerging literature on
the role of microbiota changes in the pathogenesis of systemic
rheumatic diseases such as rheumatoid arthritis, spondyloarthropathies,
and connective tissue diseases. Although the role of
the gastrointestinal tract in the pathogenesis of spondyloartropathies
is well defined and many studies underline the importance
of gastrointestinal inflammation in modulating local and
systemic inflammation, the data are inconclusive regarding the
effect of dysbiosis on rheumatoid arthritis and connective tissue
diseases. This review aims to summarize current data on the role
of the gastrointestinal involvement and intestinal microbiota in
the pathogenesis of systemic rheumatic disease
Cell Immunity in Inflammatory Vasculitis
No full textThe vasculitides are a highly heterogeneous group of disorders characterized by the presence of inflammatory leukocytes in the vessel walls and reactive inflammation. Giant cell arteritis (GCA) and Takayasu’s arteritis (TA) are the two primary large-vessel vasculitides. Two distinct cellular pathways have been identified in GCA: Th17 polarization and IL-17 secretion and generation of Th1 cells which secrete IFN-γ. These two pathways may play different roles in the pathogenesis of vasculitides. The antineutrophil cytoplasmic antibody (ANCA)-associated vasculitides (AAVs) are small vessel vasculitis associated with antibodies directly to myeloperoxidase (MPO-ANCA) such as eosinophilic granulomatosis with polyangiitis (EGPA) and microscopic polyangiitis (MPA) or with antibodies directly to proteinase 3 (PR3-ANCA) such as granulomatosis with polyangiitis (GPA). Both in vitro and in vivo experimental data have shown that MPO-ANCA can induce necrotizing smallvessel vasculitis; however the presence of granulomatous lesions suggests the involvement of cell-mediated immune responses. Behçet syndrome (BS) is a chronic relapsing vasculitis of arteries and veins with unclear etiology. Exogenous and endogenous antigens, innate immune cells such as dendritic, NK, neutrophils and adaptive-immune cells are involved
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