The balancing act between colonisers and inflammation : T regulatory and TH17 cells in mucosal immunity during otitis media
journal contributionposted on 06.12.2017, 00:00 by Jessica Browne, Evan Matthews, Jennelle Kyd, Andrew Taylor-Robinson
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 media.