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• W1560175330 abstract "Inflammation is a complex pathophysiological phenomenon orchestrated by immune cells in response to infection and/or tissue damage (Nathan, 2002; Foster & Medzhitov, 2009). It serves protective mechanism against pathological insults and aims to re-instate homeostasis. Monocytes/macrophages are the first line of immune cells to detect and response to ‘‘danger signals’’ in an organism (e.g. pathogens, tissue damage). The detection of pathogens and/or endotoxins by these cells is mediated through pattern recognition receptors (PRRs) such as Toll-like receptors (TLRs) which triggers a robust and inflammatory reaction (Figure 1). However, uncontrolled inflammation can lead to extensive tissue damage and manifestation of pathological states like sepsis, autoimmune diseases, metabolic diseases and cancer (Foster & Medzhitov, 2009). Thus, the innate immune cells ‘adapt’ themselves in the later phase of inflammation to tune down this response and promote resolution of inflammation leading to healing and tissue repair (Figure 1). Organisms as well as their immune cells have developed mechanisms to protect themselves from excessive inflammation in response to endotoxins. Endotoxin tolerance (ET) is such an adaptation wherein organisms or their innate immune cells (like monocytes/macrophages) show diminished response to endotoxins as a result of prior exposure to low doses of endotoxins (Foster & Medzhitov, 2009; Biswas et al., 2007; Dobrovolskaia & Vogel, 2002; Fan & Cook, 2004; Cavaillon & Adib-Conquy, 2006). In other words, the organism or their immune cells have developed a ’’tolerance” to endotoxin. Clinically, this phenomenon can be observed in monocytes/macrophages in patients with sepsis, trauma, surgery or pancreatitis (Cavaillon et al., 2003; Monneret et al., 2008). In most of these cases ET contributes to immunosuppression, while in sepsis it has been linked to mortality as well (Figure 1) (Monneret et al., 2008). These and other facts have suggested ET as a key mechanism for immunosuppression associated with diverse pathological conditions. In this chapter, we will review the in vitro and in vivo evidences for ET, as well as an insight into the cellular and molecular basis of this phenomenon. In addition, the pathophysiological implications of ET will be also discussed." @default.
• W1560175330 created "2016-06-24" @default.
• W1560175330 creator A5006185510 @default.
• W1560175330 creator A5080409424 @default.
• W1560175330 date "2012-02-24" @default.
• W1560175330 modified "2023-09-24" @default.
• W1560175330 title "Endotoxin Tolerance as a Key Mechanism for Immunosuppression" @default.
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