Starting as a model for developmental genetics, embryology, and organogenesis, the zebrafish has become increasingly popular as a model organism for numerous areas of biology and biomedicine over the last decades. Within haematology, this includes studies on blood cell development and function and the intricate regulatory mechanisms within vertebrate immunity. Here, we review recent studies on the immediate mechanisms mounting an inflammatory response by in vivo analyses using the zebrafish. These recently revealed novel roles of the reactive oxygen species hydrogen peroxide that have changed our view on the initiation of a granulocytic inflammatory response. 1. Introduction The innate immune system comprises the cells and mechanisms that defend the host from infection by other organisms or damage to tissue integrity, in a nonspecific manner. This means that the cells of the innate system recognise and respond to pathogens and trauma in a generic way, but unlike the adaptive immune system, it does not confer long-lasting or protective immunity to the host. The innate immune system provides an immediate defence. A typical vertebrate immune response depends on the orchestrated motility and activity of various haematopoietic compartments and their interactions that ultimately control the magnitude of the response [1–3]. Inflammation is one of the first responses of the immune system to infection or irritation. Stimulated by factors released from injured cells, it serves to establish a physical barrier against the spread of infection. This further promotes healing of any damaged tissue following the clearance of pathogens or cell debris. Molecules produced during inflammation sensitise pain receptors, cause localised vasodilatation of blood vessels, and attract phagocytes, especially neutrophils and macrophages, which then trigger other parts of the immune system. Failure to initiate a response allows uncontrolled proliferation of invading microorganisms and severe tissue damage that may become fatal. Failure to resolve an immune response can also cause severe tissue damage, due to persistent degranulation, and may lead to chronic inflammation, which ceases to be beneficial to the host. Overall, inflammation is now recognised as a central feature of prevalent pathologies, such as atherosclerosis, cancer, asthma, thyroiditis, inflammatory bowel disease, autoimmune disease, as well as Alzheimer’s and Parkinson’s disease [4–6]. Hence, the regulation of an inflammatory response is an active field of research. New players or novel functions of old players
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