An experimental model of keratoconjunctivitis sicca (KCS) was produced by removing the lacrimal gland and the gland of the third eyelid from the left eye of 6 cats. The right eye of each cat was left intact and used as a control. After 2 weeks, cats were euthanatized and the central portion of the upper eyelid from both eyes of each cat was excised. Histologic sections were stained with either hematoxylin and eosin or with a battery of biotinylated lectins including concanavalin A (conA), soybean agglutinin (SBA), wheat germ agglutinin (WGA), succinylated wheat germ agglutinin (S-WGA), Ulex europaeus agglutinin I (UEA), Dolichos biflorus agglutinin (DBA), Ricinus communis agglutinin (RCA), peanut agglutinin (PNA), and PNA pretreated with neuraminidase. Consistent differences in histologic features were not observed between conjunctivas with KCS and control conjunctivas. A variable degree of mononuclear cell infiltration of the substantia propria was observed in control conjunctivas and those with KCS. In both groups, conjunctival goblet cell density decreased and epithelial stratification increased as the degree of submucosal inflammatory cell infiltration increased. Lectin binding sites for DBA, WGA, S-WGA, UEA, PNA, and PNA pretreated with neuraminidase were detected on conjunctival goblet cells of conjunctivas with KCS and control conjunctivas. The mucus/glycocalyx layer of conjunctival epithelial cells in both groups of conjunctivas bound lectins RCA, WGA, UEA, and conA, but inconsistently bound S-WGA. In both groups, DBA principally bound to the mucus layer overlying normal epithelium, whereas PNA pretreated with neuraminidase consistently bound to the mucus layer of stratified epithelial surfaces free of goblet cells. Binding of SBA to goblet cells and the mucus/glycocalyx layer was variable.

Phorbol myristate acetate (PMA), which induces acute pulmonary injury in mammals, induced acute airsacculitis in turkeys after intra-airsac inoculation of 0.1 mg/kg. Grossly, air sacs contained multifocal to diffuse hemorrhage and edema at postinoculation hours (PIH) 3 and 6. Microscopically, there was multifocal congestion and small thrombocyte aggregates within small blood vessels by PIH 0.5, with a few vessels containing small numbers of marginating heterophils. By PIH 1.5, thrombocyte aggregates were larger and more numerous, and moderate numbers of heterophils were located perivascularly. Erythrocytes and proteinaceous fluid were in air sac interstitium. By PIH 3 and 6, hemorrhage and exudation of proteinaceous fluid had increased, in some instances severely distending the air sac. Ultrastructurally, changes resulting from PMA-induced injury were thrombocyte aggregation and degeneration, air sac epithelial cell vacuolation with separation of interdigitating cell processes, and endothelial cell vacuolar degeneration with loss of vascular integrity. Air sac lavage fluids had mildly increased total cell counts by PIH 1.5, but values returned to baseline by the end of the experiment, indicating lack of cell exudation into the air sac lumen. Circulating leukocyte changes included transient lymphopenia at PIH 3 and marked heterophilia at PIH 6. These results indicate that thrombocytes and/or heterophils are central to the pathogenesis of injury induced in air sacs by PMA and that the air sac responds differently to PMA than to pathogenic bacteria.