Abstract
The pathophysiology of processes that underlie the onset and progression of reactive nasal inflammatory conditions is very complex. These include a heterogeneous group of disorders, ranging from seasonal allergic rhinitis to nonallergic, persisting, refractory forms of chronic rhinosinusitis (CRS). About 400 million people worldwide are affected by allergic rhinitis and another 200 million are thought to be affected by nonallergic forms of nasal inflammation including CRS.
Highlights
The pathophysiology of processes that underlie the onset and progression of reactive nasal inflammatory conditions is very complex. These include a heterogeneous group of disorders, ranging from seasonal allergic rhinitis to nonallergic, persisting, refractory forms of chronic rhinosinusitis (CRS)
About 400 million people worldwide are affected by allergic rhinitis and another 200 million are thought to be affected by nonallergic forms of nasal inflammation including CRS [1,2]
While the inflammatory responses underlying allergic rhinitis are triggered by exposure to molecules with intrinsic allergenic properties, which promote type 2 T helper cell- (Th2-) biased, IgE-dependent immune responses, triggers of nonallergic rhinitis or CRS are nonspecific and largely unknown [5,6]
Summary
The pathophysiology of processes that underlie the onset and progression of reactive nasal inflammatory conditions is very complex. About 400 million people worldwide are affected by allergic rhinitis and another 200 million are thought to be affected by nonallergic forms of nasal inflammation including CRS [1,2].
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