Human polymorphonuclear leukocytes(PMN) are the most numerous host cell in periodontal pockets and their presumed role is to form a protective barrier between the bacteria and periodontal tissues. Microbial component LPS activates macrophages to produce $IL-1{eta}$, $MIP-1{alpha}$, $-1{eta}$, $TNF-{alpha}$ and IL-6, etc. These cytokines have autocrine function to the macrophages, and paracrine function to other cell such as PMN and affect them to produce some biological functions. In the present study, human PMN were tested for the expression of $IL-1{eta}$ and $MIP-1{alpha}$ mRNA. Also we performed the receptor binding assay and in vitro assay for the antimicrobial action of HL-60 cell to determine whether HL-60 can replace the peripheral PMN in analyzing the biological functions. PMN were stimulated with $IL-1{eta}$, TPA, $MIP-1{alpha}$, LPS, IL-2 and total cytoplasmic RNA were extracted for the northern blot analysis. In order to determine the induction kinetics of $IL-1{eta}$ or $MIP-1{alpha}$ mRNA expression, cells were stimulated for 0,1,2,3 hours. We found peak expression of $IL-1{eta}$ mRNA after 1hr of induction with $IL-1{eta}$, LPS and after 2hr of induction with TPA. $MIP-l{alpha}$ also induced but a scarce $IL-l{eta}$ message from PMN. In contrast to the $IL-l{eta}$ mRNA expression, $MIP-1{alpha}$ were not induced from PMN in any culture conditions. Receptors for $MIP-1{alpha}$ were identified on dibutyryl cyclic AMP(dbcAMP)-treated HL-60 as well as peripheral PMN. dbcAMP treatment significantly enhanced antimicrobial action of undifferentiated HL-60 cell. MIP-1 further increased enhancing effect of dbcAMP. $IL-1{eta}$, to a lesser extent, also increased dbcAMP-induced enhancing effect of antimicrobial action of HL-60 cell.