Role of programmed necrosis and cell death in intestinal inflammation

Dagenais, Maryse; Douglas, Todd; Saleh, Maya

doi:10.1097/mog.0000000000000117

Cited by 26 publications

(18 citation statements)

References 73 publications

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“…Here our purposes are thus simply to recognise that the genes induced or repressed via transcription factors such as NF-kB can be pro-or antiapoptotic, and which ones are activated depend on all prevailing conditions. As well as apoptosis, there is a less tightly (but partly) regulated form of cell death known as 'programmed necrosis' or 'necroptosis', [425][426][427][428][429][430][431][432][433][434][435][436][437] that may be induced by inflammatory ligands such as TNF, especially during infection, and that sometimes also involve NF-kB. Another important mode of cell death induced by related stimuli is pyroptosis [438][439][440][441][442][443][444][445][446][447][448][449][450] (that involves the caspase 1-dependent production of IL-1b).…”

Section: Lps Induction Of Apoptotic Programmed Necrotic and Pyroptotmentioning

confidence: 99%

On the translocation of bacteria and their lipopolysaccharides between blood and peripheral locations in chronic, inflammatory diseases: the central roles of LPS and LPS-induced cell death

Kell

Pretorius

2015

Integrative Biology

146

178

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We have recently highlighted (and added to) the considerable evidence that blood can contain dormant bacteria. By definition, such bacteria may be resuscitated (and thus proliferate). This may occur under conditions that lead to or exacerbate chronic, inflammatory diseases that are normally considered to lack a microbial component. Bacterial cell wall components, such as the endotoxin lipopolysaccharide (LPS) of Gram-negative strains, are well known as potent inflammatory agents, but should normally be cleared. Thus, their continuing production and replenishment from dormant bacterial reservoirs provides an easy explanation for the continuing, low-grade inflammation (and inflammatory cytokine production) that is characteristic of many such diseases. Although experimental conditions and determinants have varied considerably between investigators, we summarise the evidence that in a great many circumstances LPS can play a central role in all of these processes, including in particular cell death processes that permit translocation between the gut, blood and other tissues. Such localised cell death processes might also contribute strongly to the specific diseases of interest. The bacterial requirement for free iron explains the strong co-existence in these diseases of iron dysregulation, LPS production, and inflammation. Overall this analysis provides an integrative picture, with significant predictive power, that is able to link these processes via the centrality of a dormant blood microbiome that can resuscitate and shed cell wall components.

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Section: Lps Induction Of Apoptotic Programmed Necrotic and Pyroptotmentioning

confidence: 99%

On the translocation of bacteria and their lipopolysaccharides between blood and peripheral locations in chronic, inflammatory diseases: the central roles of LPS and LPS-induced cell death

Kell

Pretorius

2015

Integrative Biology

146

178

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“…Since the discovery and naming of necroptosis in 2005, it has been demonstrated that necroptosis may participate in the pathology of a number of inflammation diseases, such as acute pancreatitis (Wang, Qu, Li, Lv, & Sun, ), ischemia–reperfusion injury (Zhang et al., ), inflammatory bowel disease (IBD) (Dagenais, Douglas, & Saleh, ), and skin diseases (Panayotova‐Dimitrova et al., ). In addition, human cytomegalovirus (Omoto et al., ), as well as herpes simplex virus I and II (Guo et al., ), inhibited necroptosis to facilitate the intracellular proliferation and growth, whereas interaction of HSV‐1 protein ICP6 with RIPK1 and RIPK3 triggers necroptosis, thus limiting viral propagation in experimental animals (Huang et al., ), which demonstrated a different role of necroptosis in virus infection‐related diseases.…”

Section: Necroptosis In the Homeostasis Of Periodontal Tissuementioning

confidence: 99%

Necroptosis in the periodontal homeostasis: Signals emanating from dying cells

Yan

et al. 2017

Oral Diseases

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Periodontal tissues are constantly exposed to microbial stimuli. The equilibrium between microbes and host defense system helps maintain the homeostasis in the periodontal microenvironment. Growth of pathogenic bacteria in dental biofilms may induce proinflammatory cytokine production to recruit sentinel cells, mainly neutrophils and monocytes into the gingival sulcus or the periodontal pocket. Moreover, dysbiosis with overgrowth of anaerobic pathogens, such as Porphyromonas gingivalis and Tannerella forsythia, may induce death of both immune cells and host resident cells. Necroptosis is one newly characterized programmed cell death mediated by receptor-interacting protein kinase (RIPK)-1, RIPK3, and mixed lineage kinase like (MLKL). With its release of death-associated molecular patterns (DAMPs) into extracellular environment, necroptosis may help transmit the danger signal and amplify the inflammatory responses. In this review, we present recent advances on how necroptosis influences bacterial infection progression and what a role necroptosis plays in maintaining the homeostasis in the periodontal niche. Until we fully decipher the signals emanated from dying cells, we cannot completely understand the mechanism of disease progression.

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“…Accumulating evidence implicates both apoptosis and a novel form of regulated necrosis termed necroptosis in intestinal chronic inflammation and pathology. 5 A key inducer of both cell death forms is the proinflammatory cytokine tumor necrosis factor-a (TNFa) that exerts important pathological effects in IBD. Indeed, anti-TNFa monoclonal antibody therapy is currently the main biological treatment for IBD patients.…”

Section: Introductionmentioning

confidence: 99%

A critical role for cellular inhibitor of protein 2 (cIAP2) in colitis-associated colorectal cancer and intestinal homeostasis mediated by the inflammasome and survival pathways

et al. 2016

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Cellular inhibitors of apoptosis proteins (cIAPs) are critical arbiters of cell death and key mediators of inflammation and innate immunity. cIAP2 is frequently overexpressed in colorectal cancer and in regenerating crypts of ulcerative colitis patients. However, its corresponding functions in intestinal homeostasis and underlying mechanisms in disease pathogenesis are poorly understood. We found that mice deficient in cIAP2 exhibited reduced colitis-associated colorectal cancer tumor burden but, surprisingly, enhanced susceptibility to acute and chronic colitis. The exacerbated colitis phenotype of cIAP2-deficient mice was mediated by increased cell death and impaired activation of the regenerative inflammasome-interleukin-18 (IL-18) pathway required for tissue repair following injury. Accordingly, administration of recombinant IL-18 or pharmacological inhibition of caspases or the kinase RIPK1 protected cIAP2-deficient mice from colitis and restored intestinal epithelial barrier architecture. Thus, cIAP2 orchestrates intestinal homeostasis by exerting a dual function in suppressing cell death and promoting intestinal epithelial cell proliferation and crypt regeneration.

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Role of programmed necrosis and cell death in intestinal inflammation

Abstract: The role of cell death in the intestine is complex and its potential implication in intestinal diseases, and inflammatory bowel disease in particular, needs to be reevaluated.

Cited by 26 publications

References 73 publications

On the translocation of bacteria and their lipopolysaccharides between blood and peripheral locations in chronic, inflammatory diseases: the central roles of LPS and LPS-induced cell death

On the translocation of bacteria and their lipopolysaccharides between blood and peripheral locations in chronic, inflammatory diseases: the central roles of LPS and LPS-induced cell death

Necroptosis in the periodontal homeostasis: Signals emanating from dying cells

A critical role for cellular inhibitor of protein 2 (cIAP2) in colitis-associated colorectal cancer and intestinal homeostasis mediated by the inflammasome and survival pathways

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