Dictionary of Allergies .. Adhesion molecules in asthma and allergic diseases

The role of adhesion molecules in asthma has been studied in experimental models and in human lung biopsies. The studies of animal models of granulocyte mediated inflammatory lung diseases have shown that a single cell adhesion glycoprotein, ICAM-1, seems to contribute to the pathogenesis of antigen-induced airways hyperresponsiveness and pulmonary oxygen toxicity. ICAM-1 confers these effects through its upregulated expression on vascular endothelium, directing granulocyte margination and managing granulocyte diapedesis as well as its expression on airways and alveolar epithelium governing granulocyte retention, activation and mediated tissue injury. In late phase reaction ELAM-1 was found to play a dominating role. These findings suggest that the dominating molecule will vary based on the condition components and injury associated with the underlying inflammatory processes[1].

Mucosal inflammation is the feature of both bronchial asthma and allergic rhinitis with evident of tissue eosinophilia, mast cells, eosinophils and T-lymphocytes activation. The initial phase of cell recruitment is the margination and adhesion of leucocytes to the endothelium, prior to their transendothelial migration under a directed chemotactic stimulus. This adhesion occurs through specific ligand-receptor couplets involving leucocyte-endothelial adhesion molecules. One of these cell adhesion molecules is ICAM-1, an important early marker of immune activation and response. Its ligand, leukocyte function-associated antigen one (LFA-1) is expressed on neutrophils, eosinophils and T-cells. ICAM-1 was found to be expressed on epithelial and endothelial cells in rhinitis patients and in bronchial biopsies obtained from asthmatics also after allergen challenge. Circulating forms of these adhesion molecules have been identified in the peripheral blood, bronchoalveolar lavage (BAL) fluid and nasal lavage in patients with asthma and rhinitis. Systemic and local up-regulation of sICAM-1 suggests a function role for this soluble form of ICAM in the allergic inflammation[2].

(See Asthma, molecular mechanisms involved in asthmatic airway inflammation).

References

1. Wegner, C.D.: Role of endothelial epithelial and leukocyte adhesion molecules in asthma and other lung disease, in Adhesion molecules. Haskard O.O., Helwell, P.G., Gearing, A. (eds) IBC, London 1991.
2. Grzelewska-Rzymowska I, Pietrzkowicz M. Role of intra cellular adhesion molecule-1 (ICAM-1) and its soluble form (sICAM) in chronic airway inflammation.  Pol Merkur Lekarski. 2004 Feb;16(92):179-82.