In vivo expression of CD69 on lung eosinophils in eosinophilic pneumonia: CD69 as a possible activation marker for eosinophils

Nishikawa, Kiyoshi; Morii, Takeshi; Ako, Hirofumi; Hamada, Kaoru; Saito, Shigeru; Narita, Nobuhiro

doi:10.1016/0091-6749(92)90068-d

Cited by 74 publications

(51 citation statements)

References 18 publications

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“…CD69 which is expressed on a number of cells has been described as a marker for eosinophil activation [1,2]. Several studies have reported elevated expression of this surface antigen on BAL eosinophils compared to peripheral blood eosinophils in diseases such as eosinophil pneumonia and asthma [1,5,6]. While CD69 expression on eosinophils in vitro can be induced by incubation with cytokines such as IL-3, IL-5, and GM-CSF [1], the factors leading to CD69 expression on eosinophils in vivo remain unclear.…”

Section: Discussionmentioning

confidence: 99%

Mucosal inflammation in severe glucocorticoid-dependent asthma

et al. 1999

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CD69 surface expression on human lung eosinophils after segmental allergen provocation. P. Julius, W. Luttmann, B. Knoechel, C. Kroegel, H. Matthys, J.C. Virchow Jr. #ERS Journals Ltd 1999. ABSTRACT: CD69 expression on eosinophils is observed in asthma and has been proposed as a marker of eosinophil activation. The role of allergens in the in vivo regulation of CD69 expression on eosinophils, however, remains incompletely understood. It was therefore investigated whether CD69 expression on eosinophils can be induced by allergen provocation in vivo.Ten allergic asthmatics were studied by segmental allergen provocation. Two segments of the right and left lung were challenged with allergen or saline. CD69 expression was determined by flow cytometry and concentrations of interleukins were analysed by enzyme-linked immunosorbent assay in bronchoalveolar lavage (BAL) fluid.Expression of CD69 on BAL eosinophils in the segments lavaged 10 min following saline instillation (28.38.8 specific mean fluorescence (SMF)) was not significantly different to segments lavaged 10 min after allergen (80.221.8 SMF) and segments lavaged 18 h after saline challenge (87.223.3 SMF). However, CD69 expression on eosinophils increased significantly 18 h after allergen challenge (128.621.9 SMF, p<0.03) which was accompanied by elevated granulocyte-macrophage colony-stimulating factor (GM-CSF) concentrations (114.942.9 pg . mL -1 , p<0.05). CD69 expression on eosinophils and GM-CSF concentrations correlated 18 h following allergen provocation (r=0.7, p<0.025).These results suggest that in allergic asthma there is an allergen dependent, endobronchial upregulation of eosinophil activation as assessed by CD69 expression on eosinophils.

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Section: Discussionmentioning

confidence: 99%

Mucosal inflammation in severe glucocorticoid-dependent asthma

et al. 1999

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“…The lower percentage of CD69 + eosinophils is suggestive of a minor contribution of early activation events during this process. Nishikawa et al (1992) demonstrated that lung eosinophils obtained from the bronchoalveolar lavage fluid of patients with eosinophilic pneumonia expressed significant levels of CD69, whereas peripheral blood eosinophils did not express CD69. In our study we have found that CD69 was not expressed on peripheral blood eosinophils from patients with chronic S. mansoni infection.…”

Section: Cd62l Is Increased During Human Schistosoma Mansoni Infection -mentioning

confidence: 99%

High expression of co-stimulatory and adhesion molecules are observed on eosinophils during human Schistosoma mansoni infection

Silveira-Lemos

Teixeira-Carvalho

Martins‐Filho

et al. 2006

Mem. Inst. Oswaldo Cruz

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Herein we have focused attention on major phenotypic features of peripheral blood eosinophils from chronic Schistosoma mansoni-infected patients. For this purpose, detailed immunophenotypic profiles of a range of cell surface markers were performed, including activation markers (CD23/CD69/CD25/HLA-DR), co-stimulatory molecules (CD28/CD80/CD86), chemokine receptors (CXCR1/CXCR2/CCR3/CCR5) besides L-selectin-CD62L and adhesion molecules (CD18/CD54). Our major findings pointed out increased frequency of CD23 + -cells, besides decreased percentages of CD69 + -eosinophils, suggesting a chronic activation status with low frequency of early activated eosinophils in chronic S. mansoni-infected patients (INT) in comparison to non-infected individuals (NI). Moreover, a dichotomic expression of beta-chemokine receptors was observed during human schistosomiasis mansoni with higher CCR5 and lower levels of CCR3 observed between groups. Enhanced expression of co-stimulatory receptors (CD28/CD86) and adhesion molecules (CD54/CD18), besides striking lower frequency of L-selectin + were reported for eosinophils from INT group as compared to NI. Interestingly, the frequency of CD62L + -eosinophils and a range of cell activation related molecules pointed out an opposite pattern of association in NI and INT, where only INT patients that display lower frequency of CD62L + -eosinophils (first CD62L tertile) kept the unusual relationship between the expression of L-selectin and the CD23 activation marker. These findings suggest that distinct dynamic of activation markers expressed by eosinophils may occur during chronic S. mansoni infection.Key words: schistosomiasis -eosinophils -activation markers -L-selectin Eosinophils have been shown to play a major role in the immune response to helminthic infections (Butterworth et al. 1979, Hamann et al. 1987. In this context, transendothelial migration is essential for eosinophil recruitment from blood vessels into inflammatory tissues. At the inflammatory site, further interaction with invading parasites occurs via adherence with subsequent larval damage mediated by release of eosinophil toxic granular effector molecules, proinflammatory lipids, and cytokines (Greene et al. 1981, Medina-De la Garza et al. 1990, Strote et al. 1990, Brattig et al. 1991, Wildenburg et al. 1994. The prerequisite for adherence of effector eosinophils to parasite's larval stages is their sequential activation and chemotactic attraction that favor the eosinophils tethering. The migration of mature activated eosinophils from circulatory pools into the inflammatory foci depends on specific upregulation of adhesion molecules and chemokine receptors, which direct transmigration through a positive chemotactic gradient. This phenomenon seems to represent the key element for eosinophils recruitment that lead to accumulation of these proinflammatory cells that surround the parasite in its microenvironment (Pearlman 1997, Tachimoto et al. 2000.The profile of cell surface molecules expression on mature eosinophils resembles...

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“…In addition to immunoglobulin receptors, a number of adhesion molecules have been detected on eosinophils, including the β 1 -integrin very late activation antigen (VLA) (CD29, CDw49), the β 2 -integrins CD11a, CD11b (CR3), CD11c and their common β-chain CD18, the immunoglobulin superfamily (intercellular adhesion molecule-1 (ICAM)-1, CD16, CD31, CD32, CD58), as well as selectins, the major histocompatibilty antigen HLA-DR, CD4, CD69 and interleukin-2R (IL-2R) [19,[35][36][37][38][39][40][41][42][43][44]. Some of these surface antigens are expressed only on activated eosinophils (see below).…”

Section: Adhesionmoleculesmentioning

confidence: 99%

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

Kroegel¹,

Virchow²,

Luttmann³

et al. 1994

Eur Respir J

129

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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.

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In vivo expression of CD69 on lung eosinophils in eosinophilic pneumonia: CD69 as a possible activation marker for eosinophils

Cited by 74 publications

References 18 publications

Mucosal inflammation in severe glucocorticoid-dependent asthma

Mucosal inflammation in severe glucocorticoid-dependent asthma

High expression of co-stimulatory and adhesion molecules are observed on eosinophils during human Schistosoma mansoni infection

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

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