Allergen-specific challenge induces intercellular adhesion molecule 1 (ICAM-1 or CD54) on nasal epithelial cells in allergic subjects. Relationships with early and late inflammatory phenomena.

Abstract

Intercellular adhesion molecule 1 (ICAM-1 or CD54) expression on epithelial cells (EC) has been demonstrated to play a role in the local molecular events of inflammation following allergen-specific conjunctival challenge. In the light of these observations, we evaluated the possible expression of ICAM-1 on nasal EC after allergen-specific challenge. Three groups of subjects were studied: (1) 14 symptomless patients sensitized to mites, (2) 15 symptomless patients sensitized to pollen, and (3) 10 healthy volunteers as controls. The study was performed during winter. At baseline we found that both pollinosic and healthy subjects did not express CD54 on epithelial cells, whereas mite-sensitive patients showed a mild expression (possibly caused by a persistent natural allergen exposure). In addition, clinical and cellular responses were induced by lower allergen dosages in mite-sensitive patients compared with pollen-sensitive patients. CD54 was detectable in all the allergic patients but not in the control subjects 30 min after challenge. At 6 h all patients showed a marked inflammatory infiltration and CD54 persistence on EC: such an infiltration was more relevant in patients developing clinical late-phase reaction (LPR). Finally, 24 h after challenge EC CD54 expression persisted, as well as a cellular infiltrate mainly caused by eosinophils (the latter being more pronounced in mite-sensitive individuals). CD54 should be regarded as an early and sensitive marker of inflammation in both LPR-positive and LPR-negative patients. A cellular inflammatory infiltrate was detectable in both LPR-positive and LPR-negative subjects, although relevant differences in eosinophil counts were observed between the two groups. The study emphasizes the importance of the different events of inflammation in allergy.

Altered MicroRNA Expression of Nasal Mucosa in Long-Term Asthma and Allergic Rhinitis

“…This is in agreement with previous studies in which no increase in the number of inflammatory cells, markers of eosinophilic activation, or cell surface adhesion molecules in seasonal AR were observed in the absence of environmental allergen exposure [14][15][16] . On the other hand, in HDM-sensitized AR patients, inflammation in nasal mucosa has been detected in symptomfree subjects [17] .…”

“…In the absence of allergen exposure, no increase in numbers of inflammatory cells, markers of eosinophilic activation, or cell surface adhesion molecule expression have been detected in seasonal AR [14][15][16] . In addition, in patients with indoor allergy, nasal eosinophilia is not a permanent feature [3] .…”

Bronchial Hyperreactivity and Spirometric Impairment in Patients with Perennial Allergic Rhinitis

“…We have to bear in mind that we chose the model of perennial allergy. The exposure to perennial allergen is characterized by a persistent nasal inflammation as previously described by ourselves [24]. This concept is consistent with a consequent bronchial inflammation [25].…”

Recurrent Respiratory Syncytial Virus Infections in Allergen-Sensitized Mice Lead to Persistent Airway Inflammation and Hyperresponsiveness

“…Our results show that allergen sensitization and/or RSV infection up-regulate the expression of several molecules, either additively or synergistically, which leads to the persistence of inflammation and, consequently, airway hyperreactivity. Thus, RSV infection increases ICAM-1 expression on nasal epithelial cells (41) and MIP-1␣ in the lung tissue, which may enhance allergic inflammation by augmenting lymphocyte recruitment. Primary infection also induces IFN-␥, which has been reported to increase the survival of eosinophils and thus enhance inflammation in the lung (42).…”