**1. Inflammation**

When an organism is injured by a wound injury or infected by a pathogen, inflammation is a crucial response. Inflammation is a complex interaction with molecular mediators; it includes the function of immune cells in a microenvironment through a response that occurs at all levels of biological organisation [1]. Following previous studies, this paper illustrates that the inflammation response involves cooperation between cells and a wide range of mediators, such as cytokines, chemokines and non-enzyme factors involved in the classical immune response. The macrophage is one of the critical inflammatory immune cells involved in the uptake and degradation of infectious agents and senescent cells and also plays critical roles in tissue growth, tissue remodelling and inflammation by producing oxidants, proteinases and anti-microbial peptides [2–4]. Activated inflammatory cells are sources of reactive oxygen

© 2016 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. © 2016 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

species (ROS) and reactive nitrogen species (RNS) that can initiate changes in cell functions, including cell signalling pathways, transcription factor activation, mediator release and apoptosis. However, whether the ROS and RNS that are produced and released by neutrophils or macrophages are sufficient to diffuse through the extra-cellular matrix, enter epithelial cells and cross the cytoplasm is not clear [5–7]. Even the physiological roles of ROS and RNS in the cellular response are not clear [8–11]. The results obtained from experiments performed on the livers of tilapia showed that extra-cellular hydrogen peroxide (H2O2) attracted cell migration. These results suggested that ROS is a crucial factor in initiating the migration of macrophages that trigger cascades of phagocytic activity.

In the microenvironment of inflammation, the platelet-derived growth factor (PDGF), the tumour necrosis factors (TNF)-α and TNF-β, the hepatocyte growth factor, transforming growth factor (TGF)-β2, the epidermal growth factor (EGF) and the fibroblast growth factor all play an important role in physiological immune response. The interleukins (IL)-1, IL-6, IL-8, IL-10, and the interferon gamma (INF-γ) also detain key functions in the natural inflammatory response [12–16]. These factors hold a primordial function in fibroblast activation and regulation, also concerning reactive fibrosis that follows their continuing activation. Although these growth factors are also related to fibroblast migration and activation, particular research was recently focused on the PDGF family of growth factors and their relative receptors [17, 18]. Research has documented that PDGF exerts autocrine, mitogenic effects on keratinocytes to support epidermal proliferation and stabilisation of the epidermal junction during wound closure. In addition, it stimulates vessel maturation by recruiting and differentiating pericytes to the immature-endothelial channel [19–22]. According to these references, we investigate whether the produced ROS/RNS is related to the released factors and (if so) what type of relationship exists among ROS/RNS and these factors.
