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Volume 6, Issue 6(Suppl) J Clin Toxicol 2016
ISSN: 2161-0495, JCT an open access journal
Page 93
Notes:
Euro Toxicology 2016
October 24-26, 2016
conferenceseries.com
Toxicology & Applied Pharmacology
October 24-26, 2016 Rome, Italy
7th Euro-Global Summit on
CCR-2 neutralization augments murine fresh bone marrow cells activation by S. aureus via ROS
production and cytokine response
Ajeya Nandi and Biswadev Bishayi
University of Calcutta, India
Recruitment of monocytes from the bone marrow into the bloodstream and then to the sites of infection is regulated by CCL-
2/CCR-2 signaling. But, involvement of CCL-2/CCR-2 signaling in the killing of S. aureus by murine fresh bone marrow
cells is a pertinent question. The intermittent link of ROS and NF-κB/p38-MAPK mediated MCP-1 production in CCR-2
signaling has prompted to determine whether neutralization of CCR-2 augments the response of murine fresh bone marrow
cells (FBMC) after S. aureus infection utilizing ROS production and cytokines in the killing of S. aureus. It was observed that
FBMCs treated with anti-CCR-2 antibody released less ROS and NO on encountering S. aureus infection compared to CCR-
2 non-neutralized FBMCs also correlating with reduced killing of S. aureus in CCR-2 neutralized FBMCs. Staphylococcal
catalase and SOD also found to play a role in protecting S. aureus from the ROS mediated killing of FBMC. CCR-2 neutralized
FBMCs infected with S. aureus exhibit less production of TNF-α, IFN-γ and IL-6 with increased IL-10 as compared to CCR-2
intact FBMCs. S. aureus infection to CCR-2 intact FBMCs pretreated with either NF-κB or p-38-MAPK blocker caused less
MCP-1 suggesting that NF-κB or p-38-MAPK is required for MCP-1 production by FBMCs. Moreover, blocking of CCR-2
along with NF-κB or p-38-MAPK showed elevated MCP-1 production and reduced CCR-2 expression. Therefore, inhibition
of CCR-2 exacerbates the murine fresh bone marrow cells response to S. aureus infection by utilizing the ROS production and
by regulating the cytokine response.
Biography
Ajeya Nandi has gained her Post-graduate degree in Human Physiology from University of Calcutta, India in 2013. She is working as DST-INSPIRE Fellow in
the Immunology Laboratory of University of Calcutta since 2013 and submitted her PhD thesis. She has published quite a good number of research articles. Her
research has focused on the role of TLR-2 and CCR-2 in the host pathogen interaction during acute Staphylococcal infection.
Ajeya Nandi et al., J Clin Toxicol 2016, 6:6(Suppl)