scholarly journals Regulation of Staphylococcus aureus Infection of Macrophages by CD44, Reactive Oxygen Species, and Acid Sphingomyelinase

2018 ◽  
Vol 28 (10) ◽  
pp. 916-934 ◽  
Author(s):  
Cao Li ◽  
Yuqing Wu ◽  
Andrea Riehle ◽  
Véronique Orian-Rousseau ◽  
Yang Zhang ◽  
...  
2020 ◽  
Vol 5 (3) ◽  
pp. 526-526 ◽  
Author(s):  
Sarah E. Rowe ◽  
Nikki J. Wagner ◽  
Lupeng Li ◽  
Jenna E. Beam ◽  
Alec D. Wilkinson ◽  
...  

2019 ◽  
Vol 5 (2) ◽  
pp. 282-290 ◽  
Author(s):  
Sarah E. Rowe ◽  
Nikki J. Wagner ◽  
Lupeng Li ◽  
Jenna E. Beam ◽  
Alec D. Wilkinson ◽  
...  

2021 ◽  
Vol 204 (1) ◽  
Author(s):  
Sharmistha Das ◽  
Payel Paul ◽  
Sudipta Chatterjee ◽  
Poulomi Chakraborty ◽  
Ranojit K. Sarker ◽  
...  

2017 ◽  
Vol 23 (4) ◽  
pp. 345-372 ◽  
Author(s):  
Ajeya Nandi ◽  
Biswadev Bishayi

CCR-2 signaling regulates recruitment of monocytes from the bone marrow into the bloodstream and then to sites of infection. We sought to determine whether CCL-2/CCR-2 signaling is involved in the killing of Staphylococcus aureus by murine bone marrow cells (BMCs). The intermittent link of reactive oxygen species (ROS)–NF-κB/p38–MAPK-mediated CCL-2 production in CCR-2 signaling prompted us to determine whether neutralization of CCR-2 augments the response of murine fresh BMCs (FBMCs) after S. aureus infection. It was observed that anti-CCR-2 Ab-treated FBMCs released fewer ROS on encountering S. aureus infection than CCR-2 non-neutralized FBMCs, also correlating with reduced killing of S. aureus in CCR-2 neutralized FBMCs. Staphylococcal catalase and SOD were also found to play a role in protecting S. aureus from the ROS-mediated killing of FBMC. S. aureus infection of CCR-2 intact FBMCs pre-treated with either NF-κB or p-38-MAPK blocker induced less CCL-2, suggesting that NF-κB or p-38-MAPK is required for CCL-2 production by FBMCs. Moreover, blocking of CCR-2 along with NF-κB or p-38-MAPK resulted in elevated CCL-2 production and reduced CCR-2 expression. Inhibition of CCR-2 impairs the response of murine BMCs to S. aureus infection by attenuation ROS production and modulating the cytokine response.


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