Trauma, Regulated Cell Death, and Inflammation
Trauma is a significant regulator of cell death, which, in turn, plays an important role in the regulation of inflammation. The efficacy of tissue homeostasis includes several factors such as the removal of foreign microbial pathogens and the removal and
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Abstract Trauma is a significant regulator of cell death, which, in turn, plays an important role in the regulation of inflammation. The efficacy of tissue homeostasis includes several factors such as the removal of foreign microbial pathogens and the removal and identification of dead and dying cells. Further research has led to an enhanced knowledge on the connection between cell death and inflammation, expanding past understanding of the signaling pathways that regulate and affect different forms of cell death and inflammatory responses. This chapter presents an overview of the major types of cell death related to inflammation and the mechanisms underlying trauma regulation of cell death. The impact of these cell death pathways allows for the identification of a therapeutic target for inflammatory diseases.
Keywords Alveolar macrophages Apoptosis Autophagy Caspases Cell death Cold-inducible RNA binding proteins (CIRP) Damage-associated molecular patterns (DAMPs) Inflammasome Necrosis Necroptosis Netosis Pyronecrosis Pyroptosis
1 Introduction Cell death is an important factor in the development and maintenance of an organism. The early 1960s saw the classification of apoptosis as the only form of cell death [1, 2], while necrosis was seen as a form of ‘accidental’ cell death that would only occur in response to harmful chemical or physical stimuli. Further J. Fan (&) School of Medicine and Veterans Affairs Pittsburgh Healthcare System, University of Pittsburgh, Pittsburgh, PA 15240, USA e-mail: [email protected] L. Fan School of Medicine, Case Western Reserve University, Cleveland, OH 44106, USA e-mail: [email protected] © Springer Nature Singapore Pte Ltd. 2017 X. Fu and L. Liu (eds.), Advanced Trauma and Surgery, DOI 10.1007/978-981-10-2425-2_16
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development in cell death research allowed for the observation of the relationship between cell death and inflammation that is that, in host defense, cell death can be used defensively, reducing infections by separating unaffected cells from infected cells. However, cell death can also increase inflammation. Trauma regulates cell death through the damage and destruction of tissue and cells, but also through the release of signals that induce cell death and thus affect inflammation and organ dysfunction following trauma. Two criteria were proposed by the Nomenclature Committee on Cell Death (NCCD) in 2015 for the identification of dead cells. These criteria include: (1) the permanent loss of the barrier function of the plasma membrane; and (2) the destruction of cells into discrete, separate pieces, called apoptotic bodies [3, 4]. There are two categories that instances of cell death and by classified into: “accidental” and “regulated”. Accidental cell death (ACD) and regulated cell death (RCD) are contrasted by the factors that initiate these types of cell death. ACD is causes by severe physical (e.g. high temperatures and pressures), chemical (e.g. variations in pH and detergents), and mechanical (e.g. shearing) i
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