Further investigations are required to characterize the specific pathways involved. In summary, here we demonstrated that LT suppresses macrophage phagocytosis through both MEK/MAPK dependent and independent pathways. Our results suggest that a two-step inhibition of macrophage phagocytosis by LT. The first stage involved a MEK-independent inhibition when the LT concentration was lower than the MEK/MAPK suppressive dosage. In this stage, LT suppresses macrophage phagocytosis and bacterial clearance in vivo to facilitate bacterial infection. Because anthrax can cause massive bacteremia, in the second stage, LT might progressively increase and eventually reach an MEK/MAPK suppressive dose, thereby leading to a p38 MAPK dependent inhibition. Our results suggest that LT is able to transmit a phagocytic suppressive signal through an MEK/ MAPK independent pathway, which could be beneficial for the survival of B. anthracis during early infectious stages. Physiological and pathological changes in cardiac workload can cause prominent alterations in gene expression. These adaptive genetic responses have been well described for cardiac hypertrophy and are characterized by an elevation of abundance of fetal genes, for example in b-myosin heavy chain. Remarkably, opposite changes in cardiac workload, although associated with distinct phenotypes, produce strikingly similar transcriptional changes. This BMS-354825 principle finding was confirmed by several groups demonstrating uni-directional changes in hypertrophy-associated mRNAs – including ANP, bMHC and a-skeletal actin – in hypertrophied and atrophied hearts. These observations suggested that respective changes, although characteristic for the remodeling process, may have a limited role in regulating the direction of cardiac plasticity. MicroRNAs have recently been identified as superordinate regulators of global gene networks acting mainly at the translational level. These small, endogenous, non-coding RNA molecules are capable of suppressing gene expression in a sequence-specific manner. Depending on the grade of complementarity with the target mRNA, miRNAs either repress translation or induce degradation of mRNA. Usually the interaction of a miRNA with its target mRNA is characterized by mismatches, which then leads to translation repression rather than a decrease in mRNA amount. Recent studies have documented an essential role for various miRNAs in modulating key components of the hypertrophic process in the heart. Moreover, miRNA expression profiling in pathologically hypertrophied or failing hearts in humans and mice suggests that miRNA expression changes may be typical for specific cardiac diseases.