Pulmonary eosinophilic inflammation

Walker BA (1996) Effects of adenosine on guinea pig pulmonary eosinophils. Inflammation 20(1) 11-21... 

Murine model of pulmonary eosinophilic inflammation airway inflammation augmentation of allergen-induced T cell proliferation, increased Th2 cytokine (IL-4 and IL-13) and IgE production local inflammatory response ameliorated with impaired recruitment of eosinophils and inferior levels of IL-5 vitamin D could sustain Th2 response, leading to increased prevalence of allergy, but promising beneficial effects in airway eosinophilia [127]... 

Key Words Allergy asthma lung pulmonary T cell mast cell eosinophil inflammation dendritic cell IgE B cell. 

Frequently, the EAR is followed by a late phase response 4-6 h later and it is caused by the pulmonary sequestration of eosinophils, neutrophils, mast cells, and T-lymphocytes. This leukocyte recruitment depends on mast cell-derived mediators such as TNFa and various chemokines, as well as on the expression of adhesion molecules on leukocytes (e.g. VLA-4, CD11/18) and vascular endothelial cells (e.g. VCAM-1, ICAM-1, E-selectin). Products of these leukocytes have several functions First, they cause the second phase of bron-choconstriction, mucus secretion, and airway swelling second, they cause tissue destruction third, they launch and entertain the chronic inflammation. 

Various studies have also examined animal models of pulmonary inflammation that are representative of primary eosinophil or neutrophil infiltration. Lung inflammation characterized by eosinophil influx has been used as a model of asthma and is not generally associated with lung fibrosis. After several episodes of repeated antigen challange, a subset of Ascaris -sensitive Cynomolgus monkeys developed a persistent eosinophilia and enhanced intercellular adhesion molecule-1 (ICAM-1) expression on pulmonary endothelial and epithelial cells when compared to control animals (Gundel etal., 1991, 1992). 

Animal models have helped define the significance of IL-5 and the eosinophil in the disease process. IL5 administered to mice results in an increase of eosinophils (458). Experiments with IL-5-deficient and IL-5-transgenic mice confirm a role for this cytokine in controlling eosinophilia(459,460). In IL-5 knockout mice, no eosinophils are produced in response to parasite infection or sensitization with ovalbumin, and there is minimal development of lung inflammation or tissue damage. When IL-5 expression is reconstituted in these mice, pulmonary eosinophilia, tissue destruction, and airflow limitation can be observed after allergen challenge (459). 

Chemokines have been found to be produced by an array of cells, including monocytes, alveolar macrophages, neutrophils, platelets, eosinophils, mast cells, T and B lymphocytes, NK cells, keratinocytes, mesangial cells, epithelial cells, hepatocytes, flbroblasts, smooth muscle cells, mesothelial cells, and endothelial cells. These cells can produce chemokines in response to a variety of factors, including viruses, bacterial products, IL-1, TNF, C5a, LTB4, and IFNs. The production of chemokines by both immune and nonimmune cells supports the contention that these cytokines may play a pivotal role in orchestrating chronic inflammation. We will focus our discussion on the role of the CXC and CC chemokine families in the context of pulmonary fibrosis. 

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