Macrophage inflammatory protein-1alpha and C-C chemokine receptor-1 in allergen-induced skin late-phase reactions: relationship to macrophages, neutrophils, basophils, eosinophils and T lymphocytes.
BACKGROUND
Macrophage inflammatory protein (MIP)-1alpha binds to C-C chemokine receptor (CCR)-1 with high affinity. CCR-1 is expressed on neutrophils, eosinophils, monocytes, T lymphocytes and basophils; cells characteristic of atopic allergic inflammation. In vitro, MIP-1alpha is chemotactic for monocytes, T cells and basophils and is also a potent histamine-releasing factor for basophils and mast cells. Although increased levels of MIP-1alpha were shown in atopic allergic disorders, the kinetics of expression of these CC chemokines in vivo is largely unknown.


OBJECTIVE
To investigate the kinetics of expression of MIP-1alpha and receptor CCR-1 and the relationships between the expression and infiltration of inflammatory cells in allergen-induced cutaneous late-phase reactions in atopic subjects.


METHODS
Cryostat sections, obtained from skin biopsies from 10 human atopic subjects at 6, 24, 48, 72 h and 7 days after allergen challenge, were processed for immunohistochemistry and in situ hybridization using 35S-labelled riboprobes.


RESULTS
The peak expression of allergen-induced mRNA for MIP-1alpha and CCR-1 was 6 h. This was maintained at 24 h, and gradually returned to base line at 7 days. At 6 h, the number of cells expressing MIP-1alpha mRNA significantly correlated with elastase+ neutrophils and BB-1+ basophils. At 24 h, the MIP-1alpha mRNA+ cells significantly correlated with CD68+ macrophages. There were significant inverse correlations between the numbers of MIP-1alpha mRNA cells and the numbers of Tryptase+ mast cells at 6 and 24 h after allergen challenge.


CONCLUSIONS
Allergen-induced cutaneous late-phase reactions in humans were associated with increased expression of MIP-1alpha and CCR-1. This may be relevant to the infiltration of neutrophils, eosinophils, basophils and macrophages.
Ying
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Department of Allergy and Clinical Immunology, Faculty of Medicine, Imperial College, Royal Brompton Campus, National Heart & Lung Institute, Dovehouse Street, London, UK.
Meng
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Barata
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Kay
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D001491:Basophils / Q000187:drug effects / Q000276:immunology; D054405:Chemokine CCL3; D054407:Chemokine CCL4; D019742:Chemokines, CC / Q000276:immunology* / Q000378:metabolism*; D017449:Dermatitis, Allergic Contact / Q000378:metabolism*; D004804:Eosinophils / Q000187:drug effects / Q000276:immunology; D006801:Humans; D008131:London; D019402:Macrophage Inflammatory Proteins / Q000276:immunology* / Q000378:metabolism*; D008264:Macrophages / Q000187:drug effects / Q000276:immunology; D020556:Neutrophil Infiltration / Q000187:drug effects / Q000276:immunology; D009504:Neutrophils / Q000187:drug effects / Q000276:immunology; D012333:RNA, Messenger / Q000187:drug effects / Q000276:immunology / Q000378:metabolism; D019707:Receptors, Chemokine / Q000187:drug effects* / Q000276:immunology*; D013601:T-Lymphocytes / Q000187:drug effects / Q000276:immunology; D013997:Time Factors
D054405:Chemokine CCL3; D054407:Chemokine CCL4; D019742:Chemokines, CC; D019402:Macrophage Inflammatory Proteins; D012333:RNA, Messenger; D019707:Receptors, Chemokine