Defining a role for platelets in allergic inflammation

TY - JOUR

T1 - Defining a role for platelets in allergic inflammation

AU - Pitchford, S C

PY - 2007/11

Y1 - 2007/11

N2 - There is now considerable evidence suggesting a role for platelets as inflammatory cells. These actions are distinct from their classically known actions performed during thrombosis and haemostasis, and include the expression of adhesion molecules and contact-dependent activation of leucocytes, the release of a plethora of inflammatory mediators, activation in cells of the adaptive immune response and the ability to migrate and undergo chemotaxis. Chronic asthma is a disease characterized by a mixed inflammatory cell pulmonary infiltrate, AHR (airways hyper-responsiveness) and tissue remodelling. Clinical data from patients suffering from asthma, allergic rhinitis and allergic dermatitis reveal changes in platelet behaviour and function during or after allergen exposure. Furthermore, mouse models of allergic inflammation demonstrate a role for intact platelets in eosinophil and lymphocyte recruitment to the lungs, a mechanism that is P-selectin (platelet selectin)-dependent. Models of chronic inflammation also reveal the participation of platelets in tissue remodelling events whereby platelet depletion was found to be more effective in suppressing airway remodelling processes than the administration of a glucocorticosteroid. This process of destruction and repair to the architecture of airway tissue is therefore perhaps enhanced by platelet activation. Recent evidence demonstrates that platelets can undergo chemotaxis and indicates an ability to migrate through inflamed tissue, where they localize to specific tissue sites. Indeed, platelets have been shown to become activated and recruited to various body compartments in direct response to allergen via IgE and this is suggestive of a link between the innate and adaptive immune responses. Thus these actions may lead to pathophysiological events that alter disease progression, since platelet depletion suppresses AHR in allergic rabbits. Further investigations into the role of platelets in inflammation may be beneficial in the search for future therapeutic targets in the treatment of asthma and allergy.

AB - There is now considerable evidence suggesting a role for platelets as inflammatory cells. These actions are distinct from their classically known actions performed during thrombosis and haemostasis, and include the expression of adhesion molecules and contact-dependent activation of leucocytes, the release of a plethora of inflammatory mediators, activation in cells of the adaptive immune response and the ability to migrate and undergo chemotaxis. Chronic asthma is a disease characterized by a mixed inflammatory cell pulmonary infiltrate, AHR (airways hyper-responsiveness) and tissue remodelling. Clinical data from patients suffering from asthma, allergic rhinitis and allergic dermatitis reveal changes in platelet behaviour and function during or after allergen exposure. Furthermore, mouse models of allergic inflammation demonstrate a role for intact platelets in eosinophil and lymphocyte recruitment to the lungs, a mechanism that is P-selectin (platelet selectin)-dependent. Models of chronic inflammation also reveal the participation of platelets in tissue remodelling events whereby platelet depletion was found to be more effective in suppressing airway remodelling processes than the administration of a glucocorticosteroid. This process of destruction and repair to the architecture of airway tissue is therefore perhaps enhanced by platelet activation. Recent evidence demonstrates that platelets can undergo chemotaxis and indicates an ability to migrate through inflamed tissue, where they localize to specific tissue sites. Indeed, platelets have been shown to become activated and recruited to various body compartments in direct response to allergen via IgE and this is suggestive of a link between the innate and adaptive immune responses. Thus these actions may lead to pathophysiological events that alter disease progression, since platelet depletion suppresses AHR in allergic rabbits. Further investigations into the role of platelets in inflammation may be beneficial in the search for future therapeutic targets in the treatment of asthma and allergy.

KW - Blood Platelets

KW - Chemotaxis

KW - Humans

KW - Hypersensitivity

KW - Immunoglobulin E

KW - Inflammation

KW - Platelet Activation

U2 - 10.1042/BST0351104

DO - 10.1042/BST0351104

M3 - Article

C2 - 17956289

SN - 0300-5127

VL - 35

SP - 1104

EP - 1108

JO - Biochemical Society Transactions

JF - Biochemical Society Transactions

IS - 5

M1 - N/A

ER -