The present investigation was undertaken to study if
curcumin, which is recognized for its potential as an
antineoplastic and immunopotentiating agent, can also influence the process of myelopoiesis in a
tumor-bearing host. Administration of
curcumin to
tumor-bearing host augmented count of bone marrow cell (BMC) accompanied by an up-regulated BMC survival and a declined induction of apoptosis.
Curcumin administration modulated expression of cell survival regulatory molecules: Bcl2, p53,
caspase-activated DNase (CAD) and p53-upregulated modulator of apoptosis (PUMA) along with enhanced expression of genes of receptors for
M-CSF and
GM-CSF in BMC. The BMC harvested from
curcumin-administered hosts showed an up-regulated colony forming ability with predominant differentiation into bone marrow-derived macrophages (BMDM), responsive for activation to tumoricidal state. The number of F4/80 positive bone marrow resident macrophages (BMM), showing an augmented expression of
M-CSF, was also augmented in the bone marrow of
curcumin-administered host. In vitro reconstitution experiments indicated that only BMM of
curcumin-administered hosts, but not in vitro
curcumin-exposed BMM, augmented BMC survival. It suggests that
curcumin-dependent modulation of BMM is of indirect nature. Such prosurvival action of
curcumin is associated with altered T(H1)/T(H2)
cytokine balance in serum. Augmented level of serum-borne IFN-γ was found to mediate modulation of BMM to produce enhanced amount of
monokines (IL-1, IL-6, TNF-α), which are suggested to augment the BMC survival. Taken together the present investigation indicates that
curcumin can potentiate myelopoiesis in a
tumor-bearing host, which may have implications in its therapeutic utility.