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Received Mar 24, 2017; Revised Jul 29, 2017; Accepted Aug 20, 2017
This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
1. Introduction
Macrophages are on the first line of the host’s immune response to bacterial infection. Indeed, these cells play detrimental roles in pathogen recognition, bacterial killing, and antigen presentation, leading to further activation of adaptive immune responses (see for review [1–3]). Gram-negative bacterial strains are major pathogens causatives of severe infectious diseases in humans, associated with high mortality rates [4, 5]. This is due not only to their ability to become resistant to the available antimicrobials [4] but also depends on an effective macrophage response to these pathogens [6].
The production of oxidant species by macrophages is a hallmark of the inflammatory response to infection (see for review [7, 8]). Oxidant species such as hydrogen peroxide (H2O2) and superoxide (O2−) are produced following phagocytosis of the pathogen by these cells as part of their machinery to respond to harmful insults [9]. Alongside an excessive nitric oxide (NO) production, increased levels of prooxidant species may lead to damage and poor perfusion of vital organs of the host, contributing to multiple organ failure; thus, to counteract this response, antioxidant pathways are activated [10].
Natural antioxidants including phenolic compounds have been identified in a variety of plants. Additionally, antimicrobial properties have been attributed...