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 s inusitis in children are not well understood To investigate this probl em, the nature and magnitude of the local cellular inflammatory respon se was evaluated in the sinus mucosa of 34 children (25 with chronic s inusitis and 9 with recurrent acute sinusitis), of which 27 are atopic and 7 are nonatopic. In addition, sinus mucosa from three patients wh o underwent sinus surgery for noninfectious sinus disease (two with an tral 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 c ells, T cells, macrophages, and MHC class II antigen presenting cells) in the epithelium, stroma, and periglandular compartments of the unci nate and ethmoid mucosal tissue layers. Eosinophils were assessed in t he 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 u ncinate or ethmoid mucosa. Of interest, the local accumulation of tiss ue eosinophils and/or their presence in nasal smears was not closely l inked to the presence of atopy. In three patients with noninfectious s inusitis, the majority of inflammatory cells had also accumulated in t he stroma; the mononuclear cell subset composition in those controls w as indistinguishable from the sinusitis population. No difference in t he number and distribution of any inflammatory cell subset was noted w ith respect to clinical classification, atopy or immunocompetency prof ile in our patient population. These observations indicate that the mu cosal 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 su ggest that local inflammatory mechanisms may not account for clinical differences in the pathophysiology of sinusitis.