Lipoteichoic acid isolated from Lactobacillus plantarum K8 (pLTA) alleviates
lipopolysaccharide (LPS)-induced excessive
inflammation through inhibition of TNF-α and
interleukin (IL)-6. In addition, pLTA increases the survival rate of mice in a
septic shock model. In the current study, we have found that pLTA contributes to homeostasis through regulation of pro- and anti-inflammatory
cytokine production. In detail, pLTA decreased the production of
IL-10 by phorbol-12-myristate-13-acetate (PMA)-differentiated THP-1 cells stimulated with
prostaglandin E2 (PGE-2) and LPS. However, TNF-α production which was inhibited by
PGE-2+LPS increased by pLTA treatment. The regulatory effects of
IL-10 and TNF-α induced by PGE-2 and LPS in PMA-differentiated THP-1 cells were mediated by pLTA, but not by other LTAs isolated from either Staphylococcus aureus (aLTA) or L. sakei (sLTA). Further studies revealed that pLTA-mediated
IL-10 inhibition and TNF-α induction in
PGE-2+LPS-stimulated PMA-differentiated THP-1 cells were mediated by dephosphorylation of p38 and phosphorylation of
c-Jun N-terminal kinase (JNK), respectively. Reduction of pLTA-mediated
IL-10 inhibited the
metastasis of
breast cancer cells (MDA-MB-231), which was induced by
IL-10 or
conditioned media prepared from
PGE-2+LPS-stimulated PMA-differentiated THP-1 cells. Taken together, our data suggest that pLTA contributes to inflammatory homeostasis through induction of repressed pro-inflammatory
cytokines as well as inhibition of excessive anti-inflammatory
cytokines.