In AR, mouth breathing was observed related to the nasal obstruction. Therefore, with the lower nasal filter function, increased allergen exposure develops. This process is resulted in hyperresponsivity of the airway. If additional chronic rhino-sinusitis and/or nasal polyposis were present, surgery help to improve nasal functions. In these patients, asthma control could be done better[15]. When nose blocked with a clip, response to cat-allergen was not detected in patients with cat allergy[16].

Inhale particles may be removed by the help of the mucociliary clearance. With this function and beat of the cilia, particles were carried toward the pharynx. In AR patients, secretions contain inflammatory mediators and cells[7,17]. When allergens inhaled, there was swelling of the nasal mucosa[18].

The trigeminal nevre is responsible for afferent sensory innervation of the nose. Efferent parasympathetic fibers are carried in the Vidian nevre. Vagal nevre supports afferent and efferent innervation of the lower airways[19]. Sneezing, coughing or bronchoconstriction occur with the help of reflex mechanisms. The receptors were present in the nose, trachea, larynx and respiratory tract. The are sensitive to the mechanical or chemical factors. Cold dry exposure of nasal mucosa can cause immediate bronchoconstriction in asthmatic patients[6,20,21].

Nasobronchial reflex is another mechanism for interaction between upper and lower airways. Receptors are localize in the nose, sinuses and pharynx. The signals were transferred to the medulla by trigeminal, facial and glossopharyngeal nerves[22]. In the medulla, connections with vagal nevre were performed and bronchoconstriction occur[23].

In infectious conditions of the nose and lungs, virus and bacteria may trigger the reflex system. Smoking, pollutant agents in the work places and environment may cause chronic inflammation[24]. Beta-blockers or aspirin, cold dry air exposure, and physical exercise may also trigger the AR and asthma[25].

Increase in the eosinophil count is detected in AR and asthma patients in the blood[26]. Nasal provocation, performed with methacholine, also increases the lower airway resistance. It may be said that systemic mediators may induce lower airway resistance[9]. In AR and asthma, inflammatory cells and progenitors may play a role[27-29].

Syptoms of rhinosinusitis are known as nasal congestion, discharge, purulence and postnasal drip; hyposmia, facial pressure, fever, halitosis, dental pain and headache. Chronic rhinosinusitis (CRS) may damage to the mucociliary clearance. CRS is an independent risk factor for asthma[2,3,30,31].

Rhinosinusitis and asthma were coexistently detected in 34%-50% of patients. In asthmatic patients, concomitant rhinosinusitis were present up to 84%[24].

In rhinosinusitis patients, there is the possibility of having asthma. When nasal disease was treated, asthma control maybe easier due to the reducing of bronchial hyperresponsiveness. Therefore, therapeutic approach to asthma and rhinosinusitis should be planned together[32].

Medical treatments or surgery for rhinosinusitis help the reduce of respiratory symptoms and impove the asthma. Cold air inhalation causes the decrease FEV1 in asthmatic patients[5].

In 19%-38% of AR patients, there are concomitant asthma. Moreover, 30%-80% of asthmatic patients also have AR. Rhinitis symptoms were reported in 98.9% of allergic asthmatics and in 78.4% of non-allergic asthmatics[35]. Bronchial hyperreactivity was observed in most of the AR patients[36]. In AR petients, 40% have involvement of the lower airways. Additionally, allergic asthma patients have concomitant rhinitis symptoms as a 80%[37,38].

The allergic response starts with the uptake of the antigen by antigen presenting cells, in particular dendritic cells[39,40]. Dendritic cells present the antigen to T lymphocytes in the regional lymph nodes[41,42]. B cells recognize antigen with surface immunoglobulin (sIg) receptors. The T cell receptor recognizes antigens and activation of the it stimulates the naive T helper cell, a ThO cell. It differentiates to either a Th1 or a Th2 subset[43,44].

Activation of Thl cell causes the release of IL-2 and lNF-y. Additionally IL-4, IL-5, IL-1O and IL-13 are also produced by Th2 cells. Th2 cytokines are also involved in IgE synthesis (IL-4)[45,46].

Nerve growth factor (NGF) and NGF receptors are expressed in the nasal mucosa[47]. In patients with AR and allergic asthma, serum levels[48-50]; and nasal and bronchial fluid levels of NGF increase[51-53].

Exposure to endotoxins reduces the risk of developing allergic rhinitis and asthma during the first years of life. Chlamydia pneumoniae infection has been suggested as a possible causative factor for asthma[54]. It was also reported as protective against the development of asthma in children[55]. In infancy, bacterial infection is associated with a reduced prevalence of atopic eczema, allergic rhinitis and asthma[56]. Viral respiratory infections stimulate nasal allergic inflammation in atopic patients; and virus-induced airway hyperresponsiveness develops[57].

The medical treatment of AR reduces the risk of asthma-related events in asthmatic patients[58]. Nasal corticosteroids stabilize bronchial hyperreactivity in allergic rhinitis patients with seasonal asthma[37,59]. The leukotriene receptor antagonists are less effective than antihistamines and nasal steroids in upper airway disease[60,61].

Allergen immunotherapy reduces asthma symptoms. This therapy also improves nasal disease[62,63]. By immunotherapy, progression of allergic rhinitis to bronchial asthma may be prevented. Specific immunotherapy with seasonal allergic rhinitis significantly reduced the asthma development risk[64,65].