Inflammation of the middle ear, otitis media, is a significant cause of pain and reduced auditory acuity in
children. Recurrent episodes may delay development of speech, learning and social behaviour. Streptococcus pneumoniae,
non-typeable Haemophilus influenzae and Moraxella catarrhalis are most often implicated. These bacteria colonise the
nasopharynx asymptomatically but host tolerance of high nasopharyngeal load contributes to onset of inflammation.
Immunosuppression is evident in susceptible children which may contribute to tolerance and therefore to progression to
chronic disease. While the causative factors involved in the immunosuppressive response are not known, evidence from
other mucosal sites suggests that T regulatory (Treg) lymphocytes, a subset of T helper (TH) lymphocytes, contribute to
regulation of immunosuppression to commensal bacteria and promote advancement of infection. The major function of
Treg lymphocytes is induction of immune tolerance via immunosuppression in the periphery to foreign and self antigen.
They have been identified in adenoids and tonsils and are known to have a positive association with pneumococcus
nasopharyngeal colonisation. Interestingly, the pro-inflammatory TH17 lymphocyte response to S. pneumoniae is reduced
in pneumococcal-positive children. Furthermore, inadequate T lymphocyte proliferation to non-typeable H. influenzae is
evident in otitis media-prone children. A weak T lymphocyte repertoire in young children may explain high
nasopharyngeal bacterial carriage observed in this population. However, TH17 and TH1 lymphocyte responses may be
subdued due to Treg lymphocyte suppression. The immune factors that regulate nasopharyngeal colonisation are not well
understood and further research is required to elucidate the immunological mechanism that underlies development of otitis
Keywords: Commensal, immunity, mucosal, nasopharynx, otitis media, T regulatory lymphocytes.
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