Purpose. Herpes simplex virus type 1 (HSV-1) infection of the human cornea resulted in severe necrotizing keratitis. Existing evidence suggested that the corneal infiltrates were composed of inflammatory cells. In this study, the capacity of HSV-1 infection to modulate the expression of cytokines, intercellular adhesion molecule-1 (ICAM-1), and adherence of leucocytes in human corneal keratocytes (HCKs)was investigated. Method. Cultured primary HCKs were infected with HSV-1 at indicated time and multiplicities of infection (MOI). The increase of membrane-bound intercellular adhesion molecule-1 (ICAM-1) was tested by whole-cell enzyme-linked immunosorbent assay(whole- cell ELISA) and immunocytochemistry. Upregulation of cytokines and ICAM-1 mRNA was analyzed by RT-PCR. Bichannel flow cytometry was use to detect membrane-bound ICAM-1 in HSV-1 infected cells simultaneously. Cytokines level of supernatant from HSV-1 infected cells was determined by ELISA. The time course of the HSV-1-induced increase in membrane-bound interleukin-8 (IL-8) was evaluated by whole-cell ELISA. Leukocytes adhesion assay was applied on the adherence of polymorphonuclear neutrophils (PMN) and peripheral blood monocytes (PBMC) to the HSV-1 infected HCKs. Results. Stimulation of tumor necrosis factor-α(TNF-α) resulted in the increase of membrane- bound ICAM-1 in HCKs with a time- and dose-related pattern, which was confirmed by immunocytochemistry and whole- cell ELISA. Compared to interleukin-6 (IL-6), interleukin-8 (IL-8) was more potent to up-regulate the membrane-bound ICAM-1 in HCKs. RT-PCR analysis revealed the upregulation of ICAM-1, IL-1β,IL-6, and IL-8 mRNA in HCKs after 6 hrs infected with HSV-1. No expression of IL-1α, TNF-αand INF-γwas found in HSV-1-infected and mock-stimulated HCKs. Flow cytometric analysis showed the increase of membrane-bound ICAM-1 in HSV-1 infected cells versus uninfected cells, which was MOI-related. The membrane-bound IL-8 of HCKs began to rise around 8 hours postinfection, and reached to the peak around 18 hours postinfection. The adhesion of PMN to HSV-1 infected HCKs increased more than that of PBMC around 18 hours postinfection. Conclusion. Increased expression of ICAM-1, IL-1β, IL-8, and IL-6 was induced in HSV-1 infected HCKs. With the multiplicities of infection employed, IL6, membrane-bound IL-8, and membrane-bound ICAM-1 were upregulated at mRNA and functional protein level in HSV-1 infected HCKs. In addition, the adhesion of PMN and PBMC on HSV-1 infected HCKs was enhanced. It is concluded that the interactions among ICAM-1, cytokines, and leukocytes represented part of the mechanism responsible for inflammation in herpes simplex keratitis.