Interleukin-1${eta}$ $(IL-1{eta})$ is one of the key proinflammatory cytokines and it plays an important role for the antimycobacterial host defense mechanisms. In this study, we examined Mycobacterium tuberculosis (MTB)-stimulated induction of IL-1${eta}$ and evaluated the associated signal transduction pathways. In PMA-differentiated THP-1 cells, MTB infection increased mRNA expression of IL-$1{eta}$ in a dose-dependent manner. The expression of IL-1${eta}$ mRNA began to be induced at 1.5 h after infection, and induced expression of IL-1${eta}$ was retained for 48 h after MTB infection. The increase in expression of IL-1${eta}$ caused by MTB was reduced in cells treated with Ro-31-8425 (an inhibitor of PK$C{alpha}$, ${eta}I$, ${eta}II$, ${gamma}$, ${varepsilon}$) or PD98059 (an inhibitor of MEK1), meanwhile, pre-treatment with $Gddot{o}6976$ (an inhibitor of $Ca^{2+}$ dependent PK$C{alpha}$ and PK$C{eta}I$) or Rottlerin (an inhibitor of PK$C{delta}$) has no effect on MTB-induced expression of $IL-1{eta}$ mRNA. These results show that the expression of $IL-1{eta}$ mRNA caused by MTB may be mediated via MEK1 and PKC isoforms including PK$C{eta}II$, $PKC{gamma}$, or $PKC{varepsilon}$. Further studies are required to determine whether other PKC isoforms $(PKC {eta},;{ heta},;{varepsilon},;and;{lambda}/{iota})$, except $PKC{delta}$, $PKC{alpha}$, and $PKC{eta}I$, are also involved in $IL-1{eta}$ mRNA expression after mycobacterial infection.