PMID- 28409543
OWN - NLM
STAT- MEDLINE
DCOM- 20170512
LR  - 20180116
IS  - 1753-4267 (Electronic)
IS  - 1753-4259 (Linking)
VI  - 23
IP  - 4
DP  - 2017 May
TI  - CCR-2 neutralization augments murine fresh BMC activation by Staphylococcus 
      aureus via two distinct mechanisms: at the level of ROS production and cytokine 
      response.
PG  - 345-372
LID - 10.1177/1753425917697806 [doi]
AB  - 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-kappaB/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-kappaB or p-38-MAPK 
      blocker induced less CCL-2, suggesting that NF-kappaB or p-38-MAPK is required for 
      CCL-2 production by FBMCs. Moreover, blocking of CCR-2 along with NF-kappaB 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.
FAU - Nandi, Ajeya
AU  - Nandi A
AD  - Department of Physiology, Immunology Laboratory, University of Calcutta, 
      University Colleges of Science and Technology, West Bengal, India.
FAU - Bishayi, Biswadev
AU  - Bishayi B
AD  - Department of Physiology, Immunology Laboratory, University of Calcutta, 
      University Colleges of Science and Technology, West Bengal, India.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20170310
PL  - United States
TA  - Innate Immun
JT  - Innate immunity
JID - 101469670
RN  - 0 (Antibodies, Neutralizing)
RN  - 0 (Ccr2 protein, mouse)
RN  - 0 (Cytokines)
RN  - 0 (Reactive Oxygen Species)
RN  - 0 (Receptors, CCR2)
SB  - IM
MH  - Animals
MH  - Antibodies, Neutralizing/pharmacology
MH  - Bacteriolysis/*drug effects
MH  - Bone Marrow Cells/drug effects/*physiology
MH  - Cell Differentiation/drug effects
MH  - Cell Movement/drug effects
MH  - Cells, Cultured
MH  - Cytokines/metabolism
MH  - Humans
MH  - Male
MH  - Mice
MH  - Monocytes/drug effects/*physiology
MH  - Oxidative Stress/drug effects
MH  - Reactive Oxygen Species/metabolism
MH  - Receptors, CCR2/metabolism
MH  - Signal Transduction/drug effects
MH  - Staphylococcal Infections/drug therapy/*immunology
MH  - Staphylococcus aureus/*immunology
OTO - NOTNLM
OT  - Antioxidant
OT  - S. aureus
OT  - chemokine
OT  - fresh BMC
OT  - reactive oxygen species
EDAT- 2017/04/15 06:00
MHDA- 2017/05/13 06:00
CRDT- 2017/04/15 06:00
PHST- 2017/04/15 06:00 [entrez]
PHST- 2017/04/15 06:00 [pubmed]
PHST- 2017/05/13 06:00 [medline]
AID - 10.1177/1753425917697806 [doi]
PST - ppublish
SO  - Innate Immun. 2017 May;23(4):345-372. doi: 10.1177/1753425917697806. Epub 2017 
      Mar 10.