Since increased NOX2 has been associated with cardiac fibrosis in other diseases, it may play a similar role in LPS-induced cardiac fibrosis. The earliest mediators changes were an increase in IL-6 and NOX2, and a decrease in miR-29c. LPS dose-dependently activates isolated adult cardiac fibroblasts to increase IL-6 within 48 hours. IL-6 can convert cardiac fibroblasts to myofibroblasts with collagen deposition. In the current study, LPS decreased miR-29c and increased NOX2 in isolated adult mouse cardiac fibroblasts. Collectively, the results suggest that miR-29c and NOX2 may mediate LPS-induced cardiac fibrosis, with the cardiac fibroblast a key target for LPS. Additional studies are required to determine the role of each mediator, and how they may interact to induce cardiac fibrosis. Novel therapies that target miR-29c and/or NOX2 may be required to attenuate LPSinduced fibrosis. The development of new therapies to target miRs and NOX have emerged as an active area of investigation. The clinical significance of this study is that exposure to subclinical LPS is common with the potential adverse effect of inducing cardiac fibrosis. Cardiac fibrosis decreases cardiac compliance and contributes to heart failure with preserved ejection fraction. Although HFpEF is similar to heart failure with reduced ejection fraction in terms of incidence and mortality, in contrast, no therapies have been found to be effective for treating HFpEF. If subclinical LPS contributes to HFpEF, this may provide novel targets to ameliorate this burgeoning problem. Ever since the American surgeon Coley described streptococcal infection as a potential cure of cancer, other bacteria have been explored and were shown to infiltrate, replicate and accumulate in tumors. For some Rivastigmine (tartrate) extracellular bacteria, such as genetically modified obligate anaerobe Clostridium novyi, an anti-tumor effect was observed. Other extracellular bacteria such as Escherichia coli accumulated in tumor tissue, induced some inflammatory responses, but failed to Nitroprusside disodium dihydrate confer protection.