ADENOIDAL IMMUNITY IN CHILDREN: IS THERE A CORRELATION WITH PASSIVE SMOKE, ATOPY AND “LOW DOSE MEDICINE COMPOUND”?

The palatine tonsils and adenoids are the major components of the "Waldeyer's ring," a group of tissues that plays an important role in the mucosal immune system of the pharynx. Strategically positioned at the entrance of both the gastrointestinal and the respiratory tracts, the tonsils and adenoid represent the first defense line against antigens entering the body through the mouth or nose. These environmental and microbic antigens can lead to chronic state of inflammation, potentially responsible of adenoid hypertrophy, often requiring surgical removal. A characteristic feature of chronic inflammatory reactions is their persistence and predilection for certain sites. This work was proposed to study, for the first time, the possible effects of passive smoke, atopy and low-dose compound medicine on the immune adenoidal cellular response to in vitro antigen stimulation in a cohort of children with adenoid hypertrophy. In particular, in the first part of this research, we have evaluated the adenoidal humoral response (T-dependent and T-independent in vitro immunoglobulin production) in exposed/not exposed to passive tobacco smoke children and in atopic/not atopic children and we also have investigated the presence and the immunomodulatory role of B regulatory cells in adenoidal tissue. In the second part, we have observed the immune adenoidal cellular response after in vitro stimulation with a low-dose medicine compound, called citomix. Finally, we have highlighted a different cellular response to this low-dose medicine compound comparising citomix effect in atopic/not atopic and exposed/non exposed patients. Our results suggested that passive exposure to tobacco smoke and/or atopy do not seem to affect directly B cell function and cellular antigen- presentation ability in the adenoidal tissue. We have postulated that the variations in the cytokines and immunoglobulins production could be due to a persistent activation of antibody-producing cells in our patients, suggesting that B cells are more sensitive to external antigens when atopic or exposed to smoke. On the other side, the low-dose medicine compound determines a predictable increased in vitro immunoglobulin production, too. Anyway, we have to stress the reciprocal influence of the local and systemical inflammatory status of the children enrolled: that’s why the effect of citomix in exposed/not exposed and atopic/not atopic patients are a bit different from what was expected. Similarly, our analysis has been performed on local immune tissue, surgically removed because of chronic inflammation: this fact probably explains why we have found an increased production of inflammatory cytokines in not atopic and not exposed children also at the baseline, without citomix stimulation.