Recent studies suggest that interactions between leukocyte-associated integrins and the interstitial matrix may promote the migration and/or activation of extravasated leukocytes (e.g., T cells and monocytes) within the perivascular compartment ( 5, 6).
Members of the integrin family of molecules mediate cell adhesion to ECM proteins such as collagen, fibronectin, and laminin ( 4). Emigrated and residing cells must migrate along a chemotactic signal toward the site of infection/injury, identify the offending antigen, and undergo activation to perform their respective cell-specific functions. However, this initial adhesive event is followed by ano-ther critical step that occurs within the perivascular compartment and has yet to be fully explored. Leukocyte–endothelial cell interactions that result in recruitment of circulating cells into areas of inflammation are now recognized to represent an early and rate-limiting step in leukocyte-mediated tissue injury ( 3). This leukocyte accumulation is a cardinal histopathologic feature of acute and chronic inflammatory diseases of the gastrointestinal tract. Tissue obtained from patients with inflammatory bowel disease is characterized by a dense leukocyte infiltrate that may play an important role in the pathophysiology of inflammatory tissue injury ( 2). Human inflammatory bowel diseases (e.g., Crohn disease, ulcerative colitis) are associated with chronic, relapsing inflammation of the intestinal tract of unknown origin ( 1). Therapeutic strategies designed to disrupt such interactions may prove beneficial in treating intestinal inflammation. In summary, the data demonstrate that engagement of leukocyte-associated α 1β 1 receptors with ECM plays a pivotal role in mediating intestinal inflammation via promotion of monocyte movement and/or activation within the inflamed interstitium. In response to DSS, both α 1 deficiency and anti-α 1 mAb treatment significantly reduced monocyte accumulation and activation within the lamina propria. Importantly, we demonstrated that development and α 1-mediated inhibition of DSS-induced colitis occurred independently of lymphocytes ( Rag-2 –/– mice), and identified the monocyte as a key α 1β 1-expressing cell type involved in the development of colitis in this model. Blockade or loss of α 1β 1 was also associated with decreased mucosal inflammatory cell infiltrate and cytokine production. mAb’s directed against murine α 1 were found to significantly attenuate inflammation and injury in DSS-treated wild-type mice similar protection was seen in mice deficient for α 1β 1 integrin. We investigated the role of the collagen-binding integrin α 1β 1 in intestinal inflammation using the mouse model of colitis induced by dextran sodium sulfate (DSS). These are disabled by default, but you can enable them in Preferences > Markdown.Central to inflammatory responses are the integrin-mediated adhesive interactions of cells with their ECM-rich environment. Enable in Preferences > Markdown.Īs an added bonus, MacDown provides support for several obscure elements. Enable in Preferences > Rendering.ĭisabled by default. ElementĮnabled by default in Preferences > Markdown.ĭisabled by default. MacDown provides support for the following Markdown elements. You can enable and disable support for many syntax elements, a nice feature for people who simply don’t want or need all of the bells and whistles.
#MACDOWN INTEGRING FIGURE PDF#
Basic export options for HTML and PDF file format are provided. MacDown sports two panes - you type on the left and preview the formatted text on the right. MacDown provides excellent Markdown support.
#MACDOWN INTEGRING FIGURE FREE#
The application is free and open source, and it strikes a good balance between power and simplicity. MacDown is one of the best Markdown editors available for macOS.