Eosinophilic inflammation is an important feature in
the pathogenesis of chronic rhinosinositis (CRS) with
nasal polyps with NP. The eosinophilic accumulation
in the polyp stroma is basically caused by increased
transendothelial migration and increased survival time
in the tissue, where an increased concentration of interleukine
5 (IL-5) plays a major role. The
increased amount of IL-5 is predominantly released
from T-lymphocytes, independently of atopy, and the
highest concentration has been found in polyps from
patients with non-allergic asthma and acetylsalicylic
acid (ASA) intolerance. These are the sub-groups of
patients also known to exhibit the greatest accumulation
of eosinophils.
In the ASA intolerant patients, a lowered prostaglandin
E2 (PGE2) production has been observed. PGE2
has a significant anti-inflammatory
activity, including
inhibition of eosinophils. A possible intrinsic defect in
PGE2 production might, therefore, be responsible for a
further increase
of eosinophilic accumulation in ASA
intolerant patients.
