Chemokines in inflammatory bowel disease

Papadakis, Konstantinos A.

doi:10.1007/s11882-004-0048-7

Cited by 79 publications

(56 citation statements)

References 68 publications

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“…It has previously been reported that not only is chemokine expression up-regulated during active colitis, but that chemokines are involved in disease initiation and progression (38). In our own microarray studies presented here, it is clear that IEC greatly upregulate expression of a number of chemokine genes, including CCL7 and CXCL5.…”

Section: Discussionsupporting

confidence: 57%

Intestinal Epithelial Cell Up-Regulation of LY6 Molecules during Colitis Results in Enhanced Chemokine Secretion

Flanagan¹,

Modrušan²,

Cornelius³

et al. 2008

The Journal of Immunology

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In the healthy colon, intestinal epithelial cells (IEC) form a physical barrier separating the myriad of gut Ags from the cells of the immune system. Simultaneously, IEC use several mechanisms to actively maintain immunologic tolerance to nonpathogenic Ags, including commensal bacteria. However, during inflammatory bowel disease (IBD), the line of defense provided by IEC is breached, resulting in uncontrolled immune responses. As IEC are a principal mediator of immune responses in the gut, we were interested in discerning the gene expression pattern of IEC during development and progression of IBD. Laser capture microdissection and microarray analysis were combined to identify the LY6 superfamily as strongly up-regulated genes in inflamed IEC of the colon in two models of murine colitis. Surface expression of LY6A and LY6C on IEC is induced by several cytokines present within the colitic gut, including IL-22 and IFN-γ. Furthermore, cross-linking of LY6C results in production of a number of chemokines which are known to be involved in the immunopathogenesis of IBD. Increased chemokine production was cholesterol dependent, suggesting a role for lipid raft structures in the mechanism. As such, LY6 molecules represent novel targets to down-regulate chemokine expression in the colon and limit subsequent inflammation associated with IBD.

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Section: Discussionsupporting

confidence: 57%

Intestinal Epithelial Cell Up-Regulation of LY6 Molecules during Colitis Results in Enhanced Chemokine Secretion

Flanagan¹,

Modrušan²,

Cornelius³

et al. 2008

The Journal of Immunology

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“…It is possible that these cells were recruited from the peripheral blood by chemokines such as MIP3␣/CCL20, released from nonimmune tissue cells, similar to the observations made with models of inflammatory bowel disease (24) or pulmonary inflammation (22,25). DCs migrated to the target eye before the host B or T cells, reaching a peak on day 4 and declining slightly on day 7.…”

Section: Discussionmentioning

confidence: 64%

Active Participation of Antigen-Nonspecific Lymphoid Cells in Immune-Mediated Inflammation

Chen¹,

Fujimoto²,

Vistica³

et al. 2006

The Journal of Immunology

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The pathogenic process of tissue-specific autoimmune disease depends to a large extent on recruitment of Ag-nonspecific cells into the target tissue. Little is known, however, about the recruitment process and the features that characterize the recruited cells. In this study, we analyzed the recruitment of Ag-nonspecific lymphoid cells into an inflammatory site by using an experimental system in which TCR-transgenic Th1 cells are adoptively transferred to induce ocular inflammation in recipient mice that express the target Ag in their eyes. A sharp increase in number of all host cell populations was observed in the recipient spleen, reaching a peak on day 4 postcell transfer and declining thereafter. A large portion of the host’s spleen CD4 cells underwent phenotypic changes that facilitate their migration into the target organ, the eye. These changes included increased expression of the chemokine receptor CXCR3, and the adhesion molecule CD49d, as well as a decline in expression of CD62L. The host lymphocytes migrated into the recipient mouse eye more slowly than the donor cells, but became the great majority of the infiltrating cells at the peak of inflammation on day 7 postcell injection. Interestingly, the mass migration of host T cells was preceded by an influx of host dendritic cells, that reached their peak on day 4 postcell injection. The eye-infiltrating host CD4 lymphocytes underwent additional changes, acquiring a profile of activated lymphocytes, i.e., up-regulation of CD25 and CD69. Our results thus provide new information about the active participation of Ag-nonspecific lymphoid cells in immune-mediated inflammation.

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“…Substance P is known to activate resident macrophages to release proinflammatory cytokines, such as TNF-␣, which may then recruit the surrounding circular muscle cells to amplify the secretion of specific inflammatory mediators. Thus neuronal reflexes and increased circulating levels of proinflammatory cytokines (24) may induce a fullblown inflammation-like response in the muscularis externa, without the infiltration and activation of lymphocytes seen in patients with ulcerative colitis (32). The circular smooth muscle contractility in these patients is suppressed without any apparent presence and activation of immune cells in the muscle layers (45).…”

Section: Discussionmentioning

confidence: 99%

Transcriptional regulation of inflammatory mediators secreted by human colonic circular smooth muscle cells

Shi¹,

Sarna²

2005

American Journal of Physiology-Gastrointestinal and Liver Physi

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Chemokines in inflammatory bowel disease

Cited by 79 publications

References 68 publications

Intestinal Epithelial Cell Up-Regulation of LY6 Molecules during Colitis Results in Enhanced Chemokine Secretion

Intestinal Epithelial Cell Up-Regulation of LY6 Molecules during Colitis Results in Enhanced Chemokine Secretion

Active Participation of Antigen-Nonspecific Lymphoid Cells in Immune-Mediated Inflammation

Transcriptional regulation of inflammatory mediators secreted by human colonic circular smooth muscle cells

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