Acute laryngotracheitis in the rat induced by Sendai virus: The influx of six different types of immunocompetent cells into the laryngeal mucosa differs strongly between the subglottic and the glottic compartment

Objectives: Acute laryngotracheitis is a disease in which mainly the subglo ttic area is infected, whereas adjacent parts of the larynx, especially the narrow glottic fold, remain unaffected. The reason for the difference betw een these two directly adjacent regions is unknown. Therefore, in the prese nt study the influx of dendritic cells, neutrophils, T and B lymphocytes, n atural killer cells, and macrophages into the mucosa of different laryngeal compartments was investigated after Sendai virus infection in the rat. The aims were to study both the influx of immunocompetent cells and the adhesi on of the pathogen and to correlate them to the different reactions of the laryngeal areas during pseudocroup. Methods. Acute laryngotracheitis was in duced by intranasal application of Sendai virus in brown Norway rats. This virus is exclusively pneumotropic in rodents and belongs to the parainfluen za virus type 1, the main pathogen of acute laryngotracheitis in children. The numbers of dendritic cells, neutrophils, T and B lymphocytes, natural k iller cells, and macrophages were determined in the supraglottic, glottic, subglottic, and tracheal mucosa on days 2, 5, 7, and 14 after virus applica tion. Furthermore, the nucleoprotein of the virus and major histocompatibil ity complex (MHC) Class II expression were detected immunohistologically on the laryngeal epithelium. Results. All cell subsets entered the laryngeal mucosa during inflammation. The highest influx was detected among dendritic cells subglottically. This was accompanied by a strong virus adhesion and MHC Class II expression on the subglottic epithelium. In contrast, only a f ew immunocompetent cells entered the adjacent glottic mucosa, and on the gl ottic epithelium staining for virus nucleoprotein and MHC Class II expressi on was weak. Conclusions. The inflammatory response of the laryngeal mucosa shows great regional differences in this animal model during experimental viral infection. The response was characterized by a strong subglottic and a weak glottic reaction. A possible reason for this difference might be reg ion-specific viral adhesion on the epithelium of the laryngeal areas, as we ll as differences in MHC Class II expression. Thus, these data agree with t he clinical observation during acute laryngotracheitis and may explain why the subglottic part of the larynx is affected preferentially during pseudoc roup. The molecular mechanisms mediating the different reactions await clar ification.