transforming-growth-factor-beta and Esophagitis

The clinical and pathologic features of eosinophilic esophagitis (EE) include extensive tissue remodeling. Increasing evidence supports a key role for the eosinophil in multiple aspects of the esophageal remodeling and fibrosis seen in this allergic disease. This article reviews the clinical implications of esophageal remodeling and fibrosis in EE and discusses the possible pathogenic mechanisms inducing and regulating these responses. The focus is specifically on eosinophil and cytokine interactions with the esophageal epithelium, vascular endothelium, resident fibroblasts, and smooth muscle. Current and potential therapeutic interventions are discussed that may impact the development or resolution of chronic esophageal remodeling and fibrosis in EE.

Topics: Animals; Cell Communication; Cell Movement; Cell Survival; Chemotactic Factors, Eosinophil; Endothelial Cells; Eosinophilia; Eosinophils; Esophagitis; Fibroblasts; Fibrosis; Humans; Hypersensitivity; Inflammation; Intestinal Mucosa; Nerve Growth Factors; Transforming Growth Factor beta

Although the esophagus is a common site of opportunistic infection in AIDS patients, little is known about the impact of HIV as well as opportunistic infection in the esophageal mucosa. Our aim is to analyze the esophageal immune profile in HIV+ patients with different immunological status with and without the opportunistic Candida infection.. Immunohistochemistry to CD4. Esophageal CD4

Topics: Adult; Candidiasis; CD4-Positive T-Lymphocytes; CD8-Positive T-Lymphocytes; Esophageal Mucosa; Esophagitis; Female; HIV Infections; Humans; Interleukin-17; Interleukin-6; Male; Middle Aged; Opportunistic Infections; Transforming Growth Factor beta

Periostin is an extracellular matrix protein that has been primarily studied in the context of the heart, where it has been shown to promote cardiac repair and remodeling. In this study, we focused on the role of periostin in an allergic eosinophilic inflammatory disease (eosinophilic esophagitis (EE)) known to involve extensive tissue remodeling. Periostin was indeed markedly overexpressed (35-fold) in the esophagus of EE patients, particularly in the papillae, compared with control individuals. Periostin expression was downstream from transforming growth factor-beta and interleukin-13, as these cytokines were elevated in EE esophageal samples and markedly induced periostin production by primary esophageal fibroblasts (107- and 295-fold, respectively, at 10 ng ml(-1)). A functional role for periostin in eliciting esophageal eosinophilia was demonstrated, as periostin-null mice had a specific defect in allergen-induced eosinophil recruitment to the lungs and esophagus (66 and 72% decrease, respectively). Mechanistic analyses revealed that periostin increased (5.8-fold) eosinophil adhesion to fibronectin. As such, these findings extend the involvement of periostin to esophagitis and uncover a novel role for periostin in directly regulating leukocyte (eosinophil) accumulation in T helper type 2-associated mucosal inflammation in both mice and humans.

Topics: Animals; Asthma; Cell Adhesion; Cell Adhesion Molecules; Dermatitis, Atopic; Eosinophils; Esophagitis; Esophagus; Fibroblasts; Humans; Hypersensitivity; Interleukin-13; Lung; Mice; Mice, Knockout; Pulmonary Eosinophilia; Rhinitis; Transforming Growth Factor beta