Chemical
mediators of inflammation (CMI) are important in host defense against
infection. The reduced capacity of host to induce the secretion of these mediators following
infection is one of the factors in host susceptibility to
infection.
Boron, which has been suggested for its role in
infection, is reported in this study to increase lymphocyte proliferation and the secretion of CMI by the
lipopolysaccharide (LPS)-stimulated peritoneal macrophages in BALB/c mice.
Boron was administered to mice orally as
borax at different doses for 10 consecutive days, followed by the stimulation of animals with
ovalbumin and isolation of splenocytes for proliferation assay. The lymphocyte subsets were determined by flow cytometry in spleen cell
suspension. The
mediators of inflammation, TNF-α,
IL-6, IL-1β and
nitric oxide (NO), were measured in culture supernatant of LPS-primed macrophages isolated from
borax treated mice. TNF and ILs were measured by ELISA. NO was determined by Griess test. The expression of
inducible nitric oxide synthase (iNOS) in macrophages was studied by confocal microscopy. Results showed a significant increase in T and B cell populations, as indicated by an increase in CD4 and CD19, but not CD8, cells.
Boron further stimulated the secretion of TNF-α,
IL-6, IL-1β, NO and the expression of iNOS by the LPS-primed macrophages. The effect was dose dependent and most significant at a dose level of 4.6 mg/kg b. wt. Taken together, the study concludes that
boron at physiological concentration induces lymphocyte proliferation and increases the synthesis and secretion of pro-inflammatory mediators by the LPS-primed macrophages, more specifically the M1 macrophages, possibly acting through
Toll-like receptor. The study implicates
boron as a regulator of the immune and inflammatory reactions and macrophage polarization, thus playing an important role in augmenting host defense against
infection, with possible role in
cancer and other diseases.