Lipid Signaling and Metabolism in Inflammation-Associated Diseases

Dear Colleagues,

When the human body is challenged by pathogens, cell damage or irritants, a complex counteracting response of the immune system is initiated. This response is aimed at eliminating the inflammatory stimuli and at reestablishing tissue homeostasis. Although the inflammatory response is beneficial for the entire body, it involves locally destructive processes leading to cell injury and tissue damage. During the phase of inflammatory resolution (healing phase) the inflamed tissue is cleaned up and the original tissue structure is reestablished. In principle, inflammation can affect all organs, and thus can impact organ-specific functions. However, despite tissue-specific differences, the basic mechanisms are always similar. In most cases, inflammation starts as an acute process which either heals completely (restitution ad integrum) or turns into chronic inflammation when the healing process is incomplete. A key event in acute inflammation is the local activation of immune cells, particularly of neutrophils and pro-inflammatory M1 macrophages. Lymphocytes (B- and T- cells) are rare in acutely inflamed tissue, but occur more frequently in chronic inflammation. Inflammatory cells are attracted by pro-inflammatory signals produced in inflamed tissue. They leave the vasculature and actively migrate towards the center of inflammation following the gradient of pro-inflammatory mediators. Acute inflammation and inflammatory resolution are characterized by specific profiles of lipid mediators, which are biosynthesized by different cell types. It is the major aim of this Special Issue to summarize our current knowledge on lipid signaling and lipid metabolism in all types of inflammation-associated diseases, which includes the biosynthesis and modes of action of pro- and anti-inflammatory lipid mediators. 

Prof. Dr. Hartmut Kühn
Guest Editor

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