Inhibitory effects of Montelukast on mediator release by nasal epithelial cells from asthmatic subjects with or without allergic rhinitis

Abstract

Montelukast treatment for asthma symptoms reversibly suppresses nasal AEC release of pro-inflammatory mediators (i.e. IL-8 and RANTES) but only in those cells cultured from subjects with concomitant allergic rhinitis.

Epithelial folliculin enhances airway inflammation in aspirin‐exacerbated respiratory disease

“…Similarly, montelukast, a cysteinyl LT receptor‐1 antagonist, may elicit its effects by inhibiting the release of GM‐CSF and eosinophil survival . Montelukast was able to inhibit IL‐8 release from nasal epithelial cells in patients with asthma and allergic rhinitis . More importantly, convincing evidence showed that montelukast was able to reverse airway remodelling induced by eosinophils, which should be further elucidated by recovery of TJ and AJ proteins as shown in the present study.…”

“…41 Montelukast was able to inhibit IL-8 release from nasal epithelial cells in patients with asthma and allergic rhinitis. 42 More importantly, convincing evidence showed that montelukast was able to reverse airway remodelling induced by eosinophils, 26,35 which should be further elucidated by recovery of TJ and AJ proteins as shown in the present study. Taken together, dexamethasone and montelukast are involved in restoring epithelial activation and disintegrity induced by LTE 4 and eosinophils in AERD.…”

Primary airway epithelial cell culture and asthma in children-lessons learnt and yet to come

“…Fourth, cytokine release from nasal AECs and bronchial AECs can be inconsistently associated with diagnosed asthma, for example release of nasal (but not bronchial) AEC VEGF is increased in children with wheeze but the same individuals have reduced release of MMP‐9 from bronchial (but not nasal) AECs . A further (and theoretical) limitation in using nasal AECs as a surrogate for bronchial AECs is that the presence of allergic rhinitis may affect nasal AEC responses independent of lower respiratory disease; this has not been studied in children but a study in adults with asthma found no difference in mediator release between those with and without rhinitis . The nose is usually the first point of contact between the inhaled environment and the respiratory tract and it is plausible that nasal and bronchial responses will be marginally different, and in particular some nasal anti‐infective and pro‐inflammatory responses are likely to be up‐regulated, while others down‐regulated relative to bronchial AEC.…”

“…17 A further (and theoretical) limitation in using nasal AECs as a surrogate for bronchial AECs is that the presence of allergic rhinitis may affect nasal AEC responses independent of lower respiratory disease; this has not been studied in children but a study in adults with asthma found no difference in mediator release between those with and without rhinitis. 22 The nose is usually the first point of contact between the inhaled environment and the respiratory tract and it is plausible that nasal and bronchial responses will be marginally different, and in particular some nasal anti-infective and pro-inflammatory responses are likely to be up-regulated, while others down-regulated relative to bronchial AEC. Therefore while nasal AECs are attractive as a surrogate for bronchial AECs, and may be the only means to assess AEC function in some settings, bronchial AECs currently remain the gold standard for AEC studies.…”

Association of PCBs and allergies in children

“…The following sentences explain some of the reasons why the above-mentioned candidate markers were selected. IL-6 and IL-8 are pro-inflammatory cytokines, and many studies have detected increases in both IL-6 and IL-8 production in allergic patients [14,17,18]. In addition, it was recently reported that IL-10 has strong anti-inflammatory and immunosuppressive effects [19].…”