Monocytes That Have Ingested<i>Yersinia enterocolitica</i>Serotype O:3 Acquire Enhanced Capacity To Bind to Nonstimulated Vascular Endothelial Cells via P-Selectin

Wuorela, Maarit; Tohka, Sami; Granfors, Kaisa; Jalkanen, Sirpa

doi:10.1128/iai.67.2.726-732.1999

Cited by 12 publications

(2 citation statements)

References 43 publications

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“…If the triggering antigen is present in the synovium, and it has activated the synovial microvasculature, the preactivated gut‐originated cells would then be able to immigrate into the synovial tissue and trigger the inflammatory circle. For instance, on contact with endothelial cells, monocytes fed with bacteria can trigger P‐selectin expression (88). P‐selectin appears to play a very central role in allowing endothelial adherence of gut‐originated monocytic cells (89, 90), which can take the triggering antigen with them into the synovial tissue.…”

Section: Recirculation Routes and Extra‐intestinal Manifestations Of mentioning

confidence: 99%

Lymphocyte homing to the gut: attraction, adhesion, and commitment

Salmi

Jalkanen

2005

Immunological Reviews

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100

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Lymphocytes continuously migrate from the blood into the intestine. Naive lymphocytes leave the blood through high endothelial venules in Peyer's patches. During the multistep extravasation cascade, they sequentially roll on, firmly adhere to, and transmigrate through the endothelial layer using multiple adhesion molecules and chemotactic signals. In the organized lymphoid tissues of the gut, lymphocytes can become activated, if they meet their cognate antigens transported to Peyer's patches through the gut epithelium. During activation and proliferation, the lymphocytes become imprinted by the local dendritic cells, so that after returning to systemic circulation via the efferent lymphatic vasculature, they preferentially home to lamina propria of the gut to execute their effector functions. In inflammation, the recirculation routes of lymphocytes are altered, and these may explain the pathogenesis of certain extra-intestinal manifestations of gut infections and inflammatory bowel diseases. The increased knowledge on the mechanisms that regulate lymphocyte homing and imprinting has clear applicability in designing more effective vaccination regimens. A detailed understanding of the mucosal homing has recently led to the development of the first successful anti-adhesive therapeutics in human.

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Section: Recirculation Routes and Extra‐intestinal Manifestations Of mentioning

confidence: 99%

Lymphocyte homing to the gut: attraction, adhesion, and commitment

Salmi

Jalkanen

2005

Immunological Reviews

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100

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“…Além disso, os fagócitos que englobam as bactérias podem se disseminar através da circulação sanguínea para o fígado e o baço. Uma vez presente nas placas de Peyer, linfonodos mesentéricos, baço ou fígado, Y. enterocolitica leva à formação de micro abscessos no espaço extracelular (WUORELA et al, 1999), podendo causar a destruição das placas de Peyer (BOTTONE, 2015). Dentro dessas lesões, as bactérias formam micro colônias e mostram-se resistentes à fagocitose por macrófagos e neutrófilos (OELLERICH et al, 2007).…”

Section: Y Introduçãounclassified

FATORES DE PATOGENICIDADE DE Yersinia enterocolitica

Silva¹,

Silveira²,

Timm³

2022

SAH

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Yersinia enterocolitica é um patógeno causador de Doenças Transmitidas por Alimentos (DTA) envolvido em casos de toxi-infecções alimentares em humanos. Os sinais clínicos relacionados a yersiniose resultam em gastroenterite aguda, que cursa com febre, dor abdominal e diarreia. Y. enterocolitica apresenta seis diferentes biotipos (1A, 1B, 2, 3, 4 e 5). O biotipo 1B é considerado altamente patogênico, enquanto os biotipos 2 e 5 possuem patogenicidade baixa a moderada. Y. enterocolitica também pode ser classificada sorologicamente em mais de 70 sorotipos. Para ocorrer a infecção por essa bactéria é necessária a presença do gene ail, bem como do gene inv. O gene ail está relacionado à adesão e invasão de células do hospedeiro, já o gene inv é o principal gene envolvido na invasão dessas células. O presente estudo teve como objetivo realizar uma revisão de literatura a fim de sintetizar o conhecimento disponível a respeito dos fatores de patogenicidade de Y. enterocolitica, tendo em vista a importância deste gênero bacteriano na saúde pública.

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Immunologische Störung durch intestinale Dysbiose und Stress als wesentliche Grundlage der reaktiven Arthritis

He,

Qian

2024

Z Rheumatol

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Reactive arthritis (ReA) is defined as arthritis resulting from infections in other body parts, such as the gastrointestinal and urogenital tracts. The primary clinical manifestations involve acute-onset and self-limiting asymmetric large joint inflammation in the lower limbs. Although bacterial or chlamydia infections have long been recognized as playing a pivotal role in its pathogenesis, recent studies suggest that antibiotic treatment may perpetuate rather than eradicate chlamydia within the host, indicating an involvement of other mechanisms in Reactive arthritis. Reactive arthritis is currently believed to be associated with infection, genetic marker (HLA-B27), and immunologic derangement. As an autoimmune disease, increasing attention has been given to understanding the role of the immune system in Reactive arthritis. This review focuses on elucidating how the immune system mediates reactive arthritis and explores the roles of intestinal dysbiosis-induced immune disorders and stress-related factors in autoimmune diseases, providing novel insights into understanding reactive arthritis.

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Monocytes That Have IngestedYersinia enterocoliticaSerotype O:3 Acquire Enhanced Capacity To Bind to Nonstimulated Vascular Endothelial Cells via P-Selectin

Cited by 12 publications

References 43 publications

Lymphocyte homing to the gut: attraction, adhesion, and commitment

Lymphocyte homing to the gut: attraction, adhesion, and commitment

FATORES DE PATOGENICIDADE DE Yersinia enterocolitica

Immunologische Störung durch intestinale Dysbiose und Stress als wesentliche Grundlage der reaktiven Arthritis

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