Vol 50, No 4 (2012)
Original paper
Published online: 2012-12-23
Production of cytokines by mononuclear cells of hypertrophic adenoids in children with otitis media with effusion
DOI: 10.5603/FHC.2012.0082
Folia Histochem Cytobiol 2012;50(4):586-589.
Abstract
Hypertrophic adenoids with otitis media with effusion is a common infectious disease and present
a serious otological problem in children. Cytokines, potent inflammatory mediators, play important role in the
initiation of immunological response in otitis media. Adenoids excised due to hypertrophy with or without chronic
otitis media with effusion were used to isolate mononuclear cells. Secretion of cytokines by non-stimulated and
PHA-stimulated cells was determined by specific ELISAs. We found a significant increase in the production of
IL-5 and TNF-a secreted by adenoidal cells of children with otitis media with effusion compared to group with
hypertrophic adenoids. No differences were found in the secretion of IL-8, IL-6, and IL-10 between these two
groups of patients. Our results suggest a difference between the immunological responses in the course of hypertrophic
adenoids with otitis media as compared to hypertrophic adenoids.
a serious otological problem in children. Cytokines, potent inflammatory mediators, play important role in the
initiation of immunological response in otitis media. Adenoids excised due to hypertrophy with or without chronic
otitis media with effusion were used to isolate mononuclear cells. Secretion of cytokines by non-stimulated and
PHA-stimulated cells was determined by specific ELISAs. We found a significant increase in the production of
IL-5 and TNF-a secreted by adenoidal cells of children with otitis media with effusion compared to group with
hypertrophic adenoids. No differences were found in the secretion of IL-8, IL-6, and IL-10 between these two
groups of patients. Our results suggest a difference between the immunological responses in the course of hypertrophic
adenoids with otitis media as compared to hypertrophic adenoids.
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