Infection and apoptosis as a combined inflammatory trigger

Torchinsky, Miriam Beer; Garaude, Johan; Blander, J. Magarian

doi:10.1016/j.coi.2010.01.003

Cited by 53 publications

(42 citation statements)

References 50 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The prototypical response of TLR4 following LPS activation is a degree of proinflammatory response characterized by the transcription of several inflammatory cytokines, chemokines, type 1 interferons, and immune response genes [56]. By contrast, on enterocytes, TLR4 activation has a strong role in the induction of mucosal injury in the newborn small intestine via increased enterocyte apoptosis, and an inhibition in mucosal repair, through decreased enterocyte proliferation and migration [35,57].…”

Section: Tlr4mentioning

confidence: 99%

The role of innate immune-stimulated epithelial apoptosis during gastrointestinal inflammatory diseases

Siggers

Hackam

2011

Cell. Mol. Life Sci.

View full text Add to dashboard Cite

The maintenance of mucosal barrier equilibrium in the intestine requires a delicate and dynamic balance between enterocyte loss by apoptosis and the generation of new cells by proliferation from stem cell precursors at the base of the intestinal crypts. When the balance shifts towards either excessive or insufficient apoptosis, a broad range of gastrointestinal diseases can manifest. Recent work from a variety of laboratories has provided evidence in support of a role for receptors of the innate immune system, including Toll-like receptors 2, 4, and 9 as well as the intracellular pathogen recognition receptor NOD2/CARD15, in the initiation of enterocyte apoptosis. The subsequent induction of enterocyte apoptosis in response to the activation of these innate immune receptors plays a key role in the development of various intestinal diseases, including necrotizing enterocolitis, Crohn's disease, ulcerative colitis, and intestinal cancer. This review will detail the regulatory pathways that govern enterocyte apoptosis, and will explore the role of the innate immune system in the induction of enterocyte apoptosis in gastrointestinal disease.

show abstract

Section: Tlr4mentioning

confidence: 99%

The role of innate immune-stimulated epithelial apoptosis during gastrointestinal inflammatory diseases

Siggers

Hackam

2011

Cell. Mol. Life Sci.

View full text Add to dashboard Cite

show abstract

“…Inflammatory mediators have complex roles in cancer and infectious diseases, either limiting or promoting these disorders (11)(12)(13)(14)(15). Several proinflammatory factors have been fully characterized in experimental and clinical studies, including tumor necrosis factor alpha (TNF-␣), interferon gamma (IFN-␥), interleukin-1␣ (IL-1␣), and IL-1␤.…”

mentioning

confidence: 99%

Epstein-Barr Virus BZLF1-Mediated Downregulation of Proinflammatory Factors Is Essential for Optimal Lytic Viral Replication

Long

Yang

et al. 2016

J Virol

View full text Add to dashboard Cite

Elevated secretion of inflammatory factors is associated with latent Epstein-Barr virus (EBV) infection and the pathology of EBV-asso- Infection by the Epstein-Barr virus (EBV) causes infectious mononucleosis and several malignant cancers, including Burkitt's lymphoma, Hodgkin's lymphoma, nasopharyngeal carcinoma (NPC), and gastric carcinoma, as well as posttransplant lymphomas (1-5). EBV infection is persistent worldwide, but the frequency of EBV-associated NPC is highest in southern China, while Burkitt's lymphoma is most commonly found in equatorial Africa (2, 3). Although the exact mechanism by which EBV causes tumorigenesis remains to be fully defined, two important cofactors are strongly involved in EBV pathogenesis: genetic susceptibility and local diet. Unique polymorphisms of NPC-associated EBV have been identified in Chinese individuals, indicating the existence of EBV variants with higher pathogenic potential for NPC than that seen in the typical Western strains that cause infectious mononucleosis (6-8).Latent infection with limited gene expression is the default EBV cycle, whereas the lytic cycle is essential for transmission (1, 9). Lytic replication during primary infection or reactivation from the latent cycle is initiated by the expression of the immediate early (IE) viral transactivators BZLF1 and BRLF1. BZLF1, an EBV-encoded transcription factor of the basic-leucine zipper (b-ZIP) family, activates both viral and cellular genes by binding to BZLF1-responsive elements (ZREs), including several transcription factors and inflammatory factors (10).Inflammatory mediators have complex roles in cancer and infectious diseases, either limiting or promoting these disorders (11-15). Several proinflammatory factors have been fully characterized in experimental and clinical studies, including tumor necrosis factor alpha (TNF-␣), interferon gamma (IFN-␥), interleukin-1␣ (IL-1␣), and IL-1␤. TNF-␣ serves as an antiviral immune factor operating via two different mechanisms: induction of apoptosis in infected cells and activation of the antiviral response in uninfected cells (16)(17)(18)(19). For successful infection and replication, viruses employ multiple strategies to escape or hijack the host defenses, including innate immunity and the inflammatory response (15,17,20). The EBV lytic cycle evades the host inflammatory responses through the activity of BZLF1, which inhibits both IFN-␥ signaling and tumor necrosis factor receptor 1 (TNFR1) signaling (21-23). BZLF1 suppresses the NF-B signaling pathway by directly binding the p65 subunit (24, 25), acting as an

show abstract

“…However, it is well-recognized that during viral or bacterial infection apoptotic cells are generated, but with a highly inflammatory outcome [102]. One recent study has addressed this apparent contradiction: bacterially infected apoptotic cells were highly inflammatory and induced inflammatory T cell differentiation to the T H 17 fate; in contrast, uninfected apoptotic cells induced T cell differentiation to the anti-inflammatory regulatory T cell (T reg ) fate [103], suggesting that the presence of other ligands (e.g., LPS and TLR engagement [104,105]) determines the nature of signal (pro-vs. anti-inflammatory).…”

Section: Pro-inflammatory Responses To Apoptotic Cells and Diseasementioning

confidence: 99%

A model to die for: signaling to apoptotic cell removal in worm, fly and mouse

Kinchen

2010

Apoptosis

View full text Add to dashboard Cite

Programmed cell death is used during developmental morphogenesis to eliminate superfluous cells or cells with inappropriate developmental potential (e.g., self-reactive immune cells, tumorigenic cells). Recent work in genetic models has led to a number of key observations, revealing signal transduction pathways and identifying new roles for genes previously studied in corpse removal (e.g., removal of broken synapses in the nervous system). Further, studies using mouse models have suggested a role for removal of apoptotic cells in the establishment or maintenance of immune tolerance. In this review, we survey current knowledge of phagocytic pathways derived from studies in the nematode (Caenorhabditis elegans), the fly (Drosophila melanogaster), and mouse (Mus musculus) model systems.

show abstract

Infection and apoptosis as a combined inflammatory trigger

Cited by 53 publications

References 50 publications

The role of innate immune-stimulated epithelial apoptosis during gastrointestinal inflammatory diseases

The role of innate immune-stimulated epithelial apoptosis during gastrointestinal inflammatory diseases

Epstein-Barr Virus BZLF1-Mediated Downregulation of Proinflammatory Factors Is Essential for Optimal Lytic Viral Replication

A model to die for: signaling to apoptotic cell removal in worm, fly and mouse

Contact Info

Product

Resources

About