Laboratory Evidence and biomarkers linking allergic inflammation
to increased risk of middle ear inflammation.
Several authors have tried to show an association between allergy and
middle ear inflammation by animal studies as well as experimental human
models. The phenotype more frequently involved in these studies was OME
as reported in table 1. The inflammatory substrate observed in atopic
OME patients seems to be similar to that of the late phase of allergic
response in AR and asthma patients.Several
authors15-17have demonstrated a higher percentage of
TH-2 mediators, (eosinophils, T-lymphocytes, IL-4 and IL-5), as well as
a hyper-expression of major basic protein and eosinophilic cationic
protein in the middle ear fluid, adenoid tissue, and middle ear mucosa
in atopic versus non-atopic children with OME. Several other cytokines
as tumor necrosis factor alfa, IL-1b, IL-13, IL-6, and IL-8 are elevated
in middle ear fluid in children with OME.18 Smirnova
et al. have demonstrated that these cytokines might play a role as
molecular regulators of middle ear inflammation switching the acute
phase of inflammation to the chronic
stage.19Furthermore, histologic studies have
demonstrated that there is an increased level of IL-4, IL-5, and
eosinophils not only in middle ear fluid but also at both ends of the ET
suggesting again the possibility of activating an allergic mechanism in
sensitized children.20Accordingly, some authors
observed a significantly lower rate of neutrophils and IFN-gamma
(predominant in TH-1 inflammatory response) in atopic vs non-atopic
OME.16
Previous authors have demonstrated that allergic inflammation in the ear
of children with OME is similar to that of other target organs
confirming the hypothesis that ear is part of unified
airway.21, 22In addition, animal models demonstrated
that middle ear effusion can be preventedby inhibiting allergy
cytokines.22
Experimental evidence showed that trans-tympanic histamine challenge
compromise muco-ciliary clearance and ventilating function of ET in rat
models.23In particular, Hardy et
al.24 demonstrated that late-phase allergy leads to
significant ET dysfunction and subsequent formation of effusion by
impairing the ventilatory and clearance function of the ET. Furthermore,
Pollok et al.25 demonstrated that the late-phase
allergic inflammatory response and middle ear effusion may be prevented
by pre-treatment with soluble interleukin (IL)-4 receptors (sIL-4R) and
more modestly with IL-5 antibodies (IL-5Ab).
The most relevant articles included in the qualitative analyses are
summarized in table 1. The majority of articles supports the link
between allergy and otitis media with effusion.