Immunohistochemical analysis of mononuclear inflammatory cells in nasal and sinus epithelium in children with sinusitis

The etiology and pathophysiology of both recurrent acute and chronic sinusitis in children are not well understood To investigate this problem, the nature and magnitude of the local cellular inflammatory response was evaluated in the sinus mucosa of 34 children (25 with chronic sinusitis and 9 with recurrent acute sinusitis), of which 27 are atopic and 7 are nonatopic. In addition, sinus mucosa from three patients who underwent sinus surgery for noninfectious sinus disease (two with antral choanal polyp and one with facial pain syndrome) was studied for comparison and ''controls.'' Immunohistochemical methods were used to identify phenotypically distinct mononuclear cells subpopulations (B cells, T cells, macrophages, and MHC class II antigen presenting cells) in the epithelium, stroma, and periglandular compartments of the uncinate and ethmoid mucosal tissue layers. Eosinophils were assessed in the same sinus mucosal tissue compartments and in nasal secretions. For all patients, most of the inflammatory cells were found in the stroma. MHC class II positive cells and T cells were found in the epithelium of greater than 50%, and in the stroma of almost 100% of either the uncinate or ethmoid mucosa. Of interest, the local accumulation of tissue eosinophils and/or their presence in nasal smears was not closely linked to the presence of atopy. In three patients with noninfectious sinusitis, the majority of inflammatory cells had also accumulated in the stroma; the mononuclear cell subset composition in those controls was indistinguishable from the sinusitis population. No difference in the number and distribution of any inflammatory cell subset was noted with respect to clinical classification, atopy or immunocompetency profile in our patient population. These observations indicate that the mucosal surfaces studied were likely to have been immunocompetent. Taken together, the uniformly modest local inflammation and the similarity of cell subpopulations in patients with different clinical profiles suggest that local inflammatory mechanisms may not account for clinical differences in the pathophysiology of sinusitis.