Pulmonary immune cells in health and disease: the eosinophil leucocyte (Part I)

Abstract

P Pu ul lm mo on na ar ry y i im mm mu un ne e c ce el ll ls s i in n h he ea al lt th h a an nd d d di is se ea as se e: : t th he e e eo os si in no op ph hi il l l le eu uc co oc cy yt te e ( (P Pa ar rt t I I) ) ABSTRACT: Increasing evidence has accumulated to suggest that eosinophils play a key role in the pathogenesis of asthma and other pulmonary diseases by damaging infiltrated bronchial tissue and lung parenchyma. The first part of this review on eosinophils describes the cellular characteristics and properties of the cell, which help in understanding its role in disease. The article focuses on origin, maturation and differentiation of the eosinophil, its morphological and phenotypical properties, as well as its preformed and newly generated mediators of inflammation. The cause and putative significance of eosinophil heterogeneity in respect to function and density will also be discussed. In addition, the naturally occurring mediators through which eosinophils are activated and communicate with other inflammatory cells are outlined.The first part closes with new aspects of eosinophil recruitment from the circulation into perivascular tissue, including nonselective and putative selective adhesion mechanisms and chemotaxis.

C/EBP regulates the promoter of the eosinophil-derived neurotoxin/RNS2 gene in human eosinophilic cells

“…Parasite killing and tissue damage found in allergic lesions are both linked to production of toxic oxygen metabolites and to the release of eosinophil granule proteins by degranulation or exocytosis [2][3][4]. Eosinophil-derived cytotoxic proteins include major basic protein (MBP), eosinophil peroxidase (EPO), eosinophil cationic protein (ECP), and eosinophil-derived neurotoxin (EDN) [1,5].…”

Variations in Eosinophil Chemokine Responses: An Investigation of CCR1 and CCR3 Function, Expression in Atopy, and Identification of a Functional CCR1 Promoter

“…Eosinophils are able to contribute to the inflammatory response by release of mediators that induce bronchoconstriction, increased microvascular permeability, and mucus formation, and through the release of toxic granule contents that cause tissue damage in the lungs (1,2). Eosinophils may further contribute to the inflammatory response through their abilities to function as APC (3).…”

Eotaxin Expression by Epithelial Cells and Plasma Cells in Chronic Asthma

“…The presence of intraepithelial eosinophils is regarded as a distinctive histopathological feature of the disease (Bousquet et al, 1990), although the specific role of these inflammatory cells in the pathogenesis of the functional abnormalities associated with an acute attack remains poorly understood. Eosinophils release a variety of potentially toxic granule products (Kroegel et al, 1994;Weller, 1991), which have long been regarded as important in causing epithelial injury leading to airway hyperreactivity (AHR) (Coyle et al, 1994;Frigas et al, 1981). However, recent studies using a humanized antibody to interleukin-5 (IL-5), which inhibits accumulation of eosinophils, have provided persuasive evidence that AHR can develop in the absence of eosinophil recruitment (Leckie et al, 2000).…”