[Rhino-bronchial syndrome]. / Sindrome rino-bronchiale.

A close anatomical and functional relationship between superior and inferior airways is well documented. A typical example is offered by the close relationship between allergic rhinitis and asthma whose close connection is documented by epidemiological and pathological data. The mechanisms which can explain this phenomenon are not fully known but naso-bronchial reflexes, mouth-breathing due to nasal obstruction and aspiration of nasal secretions seem all to be important. Moreover it has been recently proved that the treatment of rhinitis can improve the concomitant asthma thus confirming their relationship. Another less frequent association is between sinusitis and asthma. Such a connection seems to be frequent in patients suffering of atopic rhinitis but also in patients presenting a nasal obstruction of different nature such as deviations of the nasal septum, adenoid hypertrophy etc. Also in this case a correct medical or surgical treatment of sinusitis can improve asthma symptomathology. Finally a classic example of involvement of superior and inferior airways is represented by the syndrome of ASA intolerance. These patients in fact initially complain of rhinitis which afterwards is complicated by the onset of nasal polyposis and asthma which can prove clinically very severe. Nowadays, anyway, there is no evidence that the treatment of rhinitis or polypectomy can improve the clinical course of asthma. In conclusion, diseases of superior and inferior airways must be considered in strict connection and need the same global treatment.

[Cytokines and asthma]. / Citochine ed asma.

Asthma is a chronic inflammatory lung disease in which eosinophils are one of the most important involved cells. These cells accumulate in the lung because of cytokines, which are able to regulate cellular responses. The role of cytokines is well known in allergic asthma: IL4, IL5, IL3, GMCSF are the principally cytokine involved. IL4 regulate IgE synthesis while IL5, (and IL3) cause the activation and accumulation of eosinophils. In non allergic asthma, whilst only IL5 seemed to be important recent data, shows that also IL4 plays an important role. Therefore nowadays no relevant difference seems to exist between allergic and non allergic asthma; instead the primer is different: the allergen in allergic asthma and often an unknown factor in the non allergic asthma. Recently other cytokines have been proved to play a role in the pathogenesis of asthma. IL8 is chemotactic not only for neutrophils but also for eosinophils and might cause chronic inflammation in severe asthma. IL13 works like IL4, while RANTES seems to be a more important chemotactic agent than IL5. Finally IL10, which immunoregulates T lymphocyte responses, may reduce asthma inflammation. In conclusion cytokine made us to learn more about the pathogenesis of asthma even if we do not yet know when and how asthma inflammation develops.