Host antioxidant enzymes and TLR-2 neutralization modulate intracellular survival of Staphylococcus aureus: Evidence of the effect of redox balance on host pathogen relationship during acute staphylococcal infection

• SOD, catalase and TLR-2 receptor was blocked in isolated fresh bone marrow cells.
• Moderate level of ROS and cytokine was produced in acute Staphylococcal infection.
• Blocking host anti-oxidants modulated TLR-2 expression in S. aureus infection.
• Host TLR-2 and redox modulation may alleviate S. aureus infection and bone loss.

Staphylococcus aureus is an important pathogen in bone disease and innate immune recognition receptor, TLR-2 is reported to be crucial for inflammatory bone loss. Role of TLR-2 in bacterial clearance and cytokine response to S. aureus infection in murine bone marrow macrophages has been reported but the role of host derived ROS in host–pathogen relationship still remains an obvious question. In the present study, blocking of SOD and catalase in TLR-2 neutralized fresh bone marrow cells (FBMC) with Diethyldithiocarbamic acid (DDC) and 3-Amino-1,2,4-triazole (ATZ), separately, during acute S. aureus infection, produces moderate level of ROS and limits inflammation as compared with only TLR-2 non-neutralized condition and leads to decreased bacterial count compared with only TLR-2 neutralized condition. In summary, host SOD and catalase modulates ROS generation, cytokine levels and TLR-2 expression in FBMCs during acute S. aureus infection which might be useful in the alleviation of S. aureus infection and bone loss.

Figure optionsDownload as PowerPoint slide