Enhanced inhibition of nasal epithelial cell repair by innate stimulation in patients with allergic rhinitis
Anna Lewandowska-Polak, Małgorzata Brauncajs, Marzanna Jarzębska, Agnieszka Olszewska-Ziąber, Joanna Makowska, Marek L. Kowalski
Introduction. Impaired repair of airway epithelium may lead to persistence
of inflammation and remodelling. Regeneration of injured
epithelium is a complex phenomenon and the role of toll-like receptors
(TLRs) and respiratory virus products in this process have not been established.
Aim of the study. In this study we aimed to test if wound repair in
nasal epithelial cells is modulated by microbial products and if this
process was different in patients with allergic rhinitis and in healthy
Materials and methods. Injured human nasal epithelial cells (hNECs)
monolayers were incubated with the toll-like receptors agonists: poly
(I:C) and lipopolisacharide (LPS); allergen Der p1, and supernatants
from virus-infected epithelial cells. Regeneration of injured epithelium
was assessed by measuring changes in the area of epithelial damage.
Results. Addition of either poly (I:C) or LPS induced a dose dependant
inhibition of wound repair in hNECs monolayers. Supernatants
from RV1b-infected cells decreased epithelial cell regeneration after
mechanical injury only in allergic patients. At baseline conditions the
dynamics of epithelial repair was similar in allergic and non-allergic
epithelium. However, inhibitory effects of innate stimuli on epithelial
repair was stronger in patients with allergic rhinitis as compared to
Conclusions. This study showed that microbial products may affect
regeneration of the nasal epithelium, and allergic patients are more
susceptible to suppression of epithelial regeneration.
Keywords: nasal epithelium, wound repair, TLRs; poly (I:C), LPS
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