In vitro regulation of neutrophil migration by beta 2 integrins (LFA-1 and Mac-1) in patients with otitis media.

Beta 2 integrins are located on the surface of neutrophils and have important roles in cell migration to an inflammatory site. We investigated the inhibitory effect of antibodies to the beta 2 integrin family for neutrophil migration into middle ear effusion (MEE) during acute otitis media in children and chronic otitis media with effusion in both children and adults. Neutrophil migration to MEE samples was assessed in vitro in a 48-well Boyden chamber. The migration index value and the activity of chemoattractants in MEE was found to be proportional to the number of infiltrated cells. Migration of activated neutrophils into MEE was significantly inhibited by blocking surface-expressed cell adhesion molecules (CAM) with anti-CD11b (Mac-1 alpha) and anti-CD18 (common beta 2 subunit) antibodies (P < 0.001) but not with anti-CD11a (LFA-1 alpha) antibody. These inhibitory effects of anti-CAM antibodies were found in all types of MEE in all age groups studied. A new therapeutic approach to inflammation has been considered recently that utilizes inhibition of neutrophil migration with a blocking antibody to CAM. Our in vitro data support a possible therapeutic effect of anti-CAM antibody, indicating that administration of anti-CD11b and CD18 antibodies may be useful for treating human otitis media.