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Neuroimmune interactions: potential target for mitigating or treating intestinal radiation injury

Departments of Surgery and Pathology, University of Arkansas for Medical Sciences and Central Arkansas Veterans Healthcare System, Little Rock, AR 72205, USA

View larger version (17K): [in this window] [in a new window]   Figure 1. Sequence of events in the pathogenesis of intestinal radiation injury. In addition to breakdown of the epithelial barrier, the development of early and delayed manifestations is influenced by a large number of inflammatory mediators, cytokines and growth factors(right), many of which are released by cells of the immune system. In the special case of the bowel, injury is also significantly influenced by the contents of the intestinal lumen (left). These contents are normally separated from the intestinal stromal tissues by the mucosal barrier. After irradiation, breakdown of the mucosal barrier allows intraluminal factors to gain access to and affect the stromal tissue and thus exacerbate manifestations of intestinal injury.

View larger version (32K): [in this window] [in a new window]   Figure 2. Mechanisms by which mast cells may promote fibroblast proliferation and collagen deposition. FGF, fibroblast growth factor; IL-4, interleukin-4; PAR-2, proteinase-activated receptor 2; TGF-1, transforming growth factor 1; TNF, tumour necrosis factor ; tPA, tissue-type plasminogen activator; uPA, urokinase plasminogen activator.

View larger version (23K): [in this window] [in a new window]   Figure 3. Putative neuroimmune interactions involved in the intestinal radiation response. MMC, mucosal mast cells; CTMC, connective tissue mast cells; CGRP, calcitonin gene-related peptide.