Download Pediatric gastrointestinal disease : pathophysiology, by W Allan Walker; et al PDF

By W Allan Walker; et al

This textbook comprises sections on improvement, pathophysiology, medical manifestations and administration, and knowledge had to diagnose and deal with sufferers. It additionally appears on the rules of treatment, therefore supplying info at the administration of gastrointestinal illness states, together with rehydration and nutrients, drugs, biopsychosocial and surgical help. This version contains the most recent advancements, reminiscent of gene remedy, hepatitis, AIDS, and transplantation

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Additional resources for Pediatric gastrointestinal disease : pathophysiology, diagnosis, management

Example text

227 The participation of the ECM in intestinal inflammation comprises two domains. 231 The second area of investigation is related to the quantitative and qualitative changes occurring in the intestine during inflammation. 235 Regardless of specificity, changes in ECM translate to an active process of tissue remodeling in the inflamed intestine resulting from the action of agents that both promote and hinder ECM deposition. For instance, TGF-β1 selectively augments collagen synthesis by intestinal smooth muscle cells,236 a response that contributes to intestinal fibrosis.

161,162 GROWTH FACTORS Intestinal inflammation has traditionally been considered as an excessively strong insult by activated immune cells and their products that ultimately results in a tissuedestructive process. An alternate and complementary view is that intestinal inflammation results from an inadequate IMMUNOREGULATORY AND EFFECTOR CYTOKINES CYTOKINE MAIN CELLULAR SOURCE MAIN TARGET CELL DOMINANT FUNCTION IFN-γ T cells, natural killer cells Most cells Induction of MHC class II antigens, monocyte activation, Th1 differentiation, and IL-4 suppression GM-CSF Phagocytes, B cells Hematopoietic cells Leukocyte differentiation IL-3 Multiple cells Hematopoietic cells Leukocyte differentiation IL-5 T cells, mast cells Eosinophils Mediation of allergic and parasitic diseases IL-9 Th2 cells T cells, mast cells Undefined IL-11 Hematopoietic stromal cells Multiple cells Stimulation of intestinal crypt cells IL-15 Most cells IL-2R–bearing cells T-cell expansion, epithelial cell differentiation GM-CSF = granulocyte-macrophage colony-stimulating factor; IFN = interferon; IL = interleukin; IL-2R = interleukin-2 receptor; MHC = major histocompatibility complex; Th = T helper.

In particular, evidence for the existence of classic cytotoxic T cells, which specifically recognize and destroy intestinal cell targets, is still missing. 34 The most recent type of T cells to attract considerable attention in intestinal inflammation is regulatory T cells (Treg). 35 The best defined types are T regulator 37 Chapter 3 • Inflammation 1 (Tr1) cells, which mediate suppression primarily through the release of immunosuppressive cytokines such as interleukin (IL)-10 and CD4+CD25+ cells, which seemingly exert suppression by direct cell contact, and T helper (Th) 3 cells, which produce large amounts of transforming growth factor (TGF)-β.

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