Inflammatory response cells participating

Bronchial epithelial cells participate in inflammation by releasing eicosanoids, peptidases, matrix proteins, cytokines, and nitric oxide. Epithelial shedding results in heightened airway responsiveness, altered permeability of the airway mucosa, depletion of epithelial-derived relaxant factors, and loss of enzymes responsible for degrading inflammatory neuropeptides. 

Some of these are involved in haematopoiesis (e.g. IL-1, -3, -5, -6 GM-, M-, G-CSF) their role is described in Chapter 2. Others (e.g. IL-1, -6, -8 TNF a- GM-, M-, G-CSF) are implicated in inflammation either directly (e.g. pure IL-1 can cause some symptoms of inflammation) or indirectly, via their ability to activate immune cells that participate in the inflammatory response (e.g. lymphocytes, neutrophils and macrophages) some of these effects are described in Chapters 2 and 3. Such cytokines as IL-4, interferon-a and IL-10 may be involved in immunosuppression others, such as IL-1, IL-6, TNF a and TGF j3, are involved in tissue remodelling. 

Considerable evidence has emerged to suggest that histamine participates in the immune regulation of the inflammatory response in several diseases. Histamine interferes with the peripheral tolerance induced during SIT in several pathways. Histamine induces the production of IL-10 by DCs [184]. In addition, histamine induces IL-10 production by Th2 cells [188]. Furthermore, histamine enhances the suppressive activity of... 

Mechanisms of Complement Activation. Complement is a major mediator of the inflammatory response. Complement recruits and enlists the participation of humoral and cellular effector systems, induces histamine release from mast cells and directs migration of leukocytes (chemotaxis), in addition to producing phagocytosis and the release of lysosomal constituents from phagocytes. 

The ability of PMNs to elaborate O and its reactive progeny and the capacity of these progeny to react with many components of cells attracted the interest of investigators of the molecular basis of the inflammatory response. One way in which PMNs may participate is by acting as the source of the molecules such as OH which may destroy tissue. The inhibition of the inflammatory effects of Carrageenan by superoxide dismutase might represent such an effect. 

Episodes of airway obstruction or bronchoconstriction may be induced in asthmatics by exposure to stimuli to which they are sensitized, such as inhalation of a specific pollen or house dust mite, or exposure to an occupational stimulus, e.g., red cedar dust [47]. Binding of antigen (e.g., pollen) to specific receptors (antibodies) on the surface of an inflammatory cell (e.g., mast cell) results in the elaboration of prestored mediators, such as histamine, and in the synthesis of newly formed mediators, such as arachidonic acid metabolites (e.g., prostaglandins and leukotrienes). Cellular sources of the various mediators are shown in Table 3. Cytokines and chemokines are proteins that participate in pulmonary immune and inflammatory responses. While important, these have not been subjected to discussion in this chapter because these fields are changing very... 

Fig. 11. Airway epithelial cells as sources of cytokines and chemokines in the airways. Airway epithelial cells express and release a variety of cytokines/chemokines, adhesion molecules, and lipid mediators, and thereby participate in the regulation of inflammatory responses in the airways.

Coumarin derivatives are known to possess antiinflammatory and antimetastatic properties. The mode of action of coumarins is mainly attributed to their direct action on cells participating in the inflammatory process [58]. The influence of coumarins on the complement system, which is involved in the different stages of inflammatory response, has not been thoroughly investigated. 

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