Factors contributing to nasal allergic late phase eosinophilia.

OBJECTIVE: This study focused on factors contributing to eosinophilia after intranasal allergen challenge. METHODS: Nasal secretions of 13 allergic individuals were gained over a period of 8 hours after nasal allergen challenge. Early and late phase reactions were determined by acoustic rhinometry and changes of volume and total protein in nasal secretions. Eosinophilia was demonstrated by nasal eosinophilic cationic protein. Interleukin (IL)-5; the chemokines IL-8, monocyte chemotactic protein (MCP)-1 and MCP-3, and eotaxin; soluble vascular cell adhesion molecule 1 (sVCAM-1); and the leukotriene C4 (LTC4) were analyzed by enzyme-linked immunosorbent assay for their suggested impacts on tissue eosinophilia. RESULTS: By means of rhinometry, we observed in 69% an alternating type of late phase response, followed by a bilateral (15%) or unilateral (8%) type. A biphasic kinetic could be demonstrated by changes in nasal volume and total protein of nasal secretions, reflecting the early and late phase responses. A typical late phase kinetic was observed for IL-5, MCP-1, eotaxin, sVCAM-1, and LTC4. Interleukin 8 was characteristic for early phase reaction but increased in late phase as well. We could not detect any MCP-3 in our samples. CONCLUSIONS: Our data point to a relevant role of the T(H)2 cytokine IL-5; of the chemokines IL-8, MCP-1, and eotaxin; of the adhesion molecule sVCAM-1; and of the leukotriene LTC4 for the allergic late phase eosinophilia.

An approach of immunoneurological aspects in nasal allergic late phase.

This examination is an approach of the allergic early phase reaction (EPR) and late-phase reaction (LPR) via quality of life (QoL), acoustic rhinometry, and eosinophilic cationic protein (ECP), interleukin (IL)-5, and leukotriene C4 (LTC4). Results are discussed under consideration of a possible neurological participation in the occurrence and persistence of the allergic inflammatory process. Thirteen patients suffering from seasonal allergic rhinitis were challenged intranasally by their specific allergen. In a time window of 8 hours after provocation, patients completed QoL questionnaires, and underwent acoustic rhinometry. Nasal secretions were analyzed for total protein, ECP, IL-5, and LTC4 The need to sneeze and a runny nose were the strongest symptoms during the EPR and LPR. Restriction of overall QoL persisted much longer than any other symptom. Evaluation of acoustic rhinometry revealed an EPR in 100% and a LPR in 92%. The EPR was marked by increases in volume of nasal secretions, total protein, and elevations in LTC4. Allergic LPR was marked by increases in nasal secretions, total protein, ECP, IL-5, and LTC4. Both the need to sneeze as strongest and announcing symptom of the allergic LPR and the persisting restriction in overall QoL seem to propose a possible neurological participation in the development of the allergic late-phase inflammation and consequent hyperresponsiveness of the nasal mucosa. In addition, the persistence and enhancement of the nasal cycle during the allergic LPR can be interpreted in favor of a hypothetical activation of the autonomous nervous system. LTC4 enters this discussion as a promising link at the immunoneurological interface.