Cytokines, IBD, and Colitis-associated Cancer

Francescone, Ralph; Hou, Vivianty; Grivennikov, Sergei I.

doi:10.1097/mib.0000000000000236

Cited by 247 publications

(208 citation statements)

References 111 publications

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“…The presence of deregulated cytokines and chemokines has been previously reported in cases of IBD, primarily in studies performed at the level of the inflamed mucosa, while studies on the circulating levels of cytokines and chemokines in IBD are less frequent (14)(15)(16)(17). Among the panel of cytokines and chemokines investigated in the present study, 10 proteins, including IL-1β, IL-5, IL-7, IFN-α2, IFN-γ, IP-10, CTACK, IL-16, MIG and LIF, were shown to be significantly upregulated in the group of pediatric IBD patients, as compared with the age-matched controls.…”

Section: Discussionmentioning

confidence: 99%

Pediatric patients with inflammatory bowel disease exhibit increased serum levels of proinflammatory cytokines and chemokines, but decreased circulating levels of macrophage inhibitory protein-1β, interleukin-2 and interleukin-17

Kleiner¹,

Zanin²,

Monasta³

et al. 2015

Experimental and Therapeutic Medicine

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Abstract. Inflammatory bowel disease (IBD) is a chronic and progressive inflammatory condition of the gastrointestinal tract. Although the causative events that lead to the onset of IBD are yet to be fully elucidated, deregulation of immune and inflammatory mechanisms are hypothesized to significantly contribute to this disorder. Since the onset of IBD is often during infancy, in the present study, the serum values of a large panel of cytokines and chemokines in pediatric patients (<18 years; n=26) were compared with age-matched controls (n=37). While elevations in the serum level of several proinflammatory and immune regulating cytokines were confirmed, such as interleukin (IL)-1β, IL-5, IL-7, interferon (IFN)-γ-inducible protein-10, IL-16, cutaneous T-cell-attracting chemokine, leukemia inhibitory factor, monokine induced by γ-IFN, IFN-α2 and IFN-γ, notably decreased levels of IL-2, IL-17 and macrophage inhibitory protein-1β were also observed. Therefore, while a number of proinflammatory cytokines exhibit increased levels in IBD patients, pediatric IBD patients may also exhibit certain aspects of a reduced immunological response.

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Section: Discussionmentioning

confidence: 99%

Pediatric patients with inflammatory bowel disease exhibit increased serum levels of proinflammatory cytokines and chemokines, but decreased circulating levels of macrophage inhibitory protein-1β, interleukin-2 and interleukin-17

Kleiner¹,

Zanin²,

Monasta³

et al. 2015

Experimental and Therapeutic Medicine

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“…Allelic variants in cytokine genes have been shown to influence gene expression and subsequently the susceptibility to and severity of inflammation diseases (23). There is increasing evidence that TNF-α is key in the pathogenesis of IBD and may represent novel therapeutic targets (12). Studies indicate the TNF-α gene as an appropriate and functional candidate for IBD treatment (24,25).…”

Section: Discussionmentioning

confidence: 99%

“…There is direct evidence for the role of genetics in IBD, associated with the family history of patients, as well as increased rates of IBD in monozygotic twins (10,11). The predominant genetic association in IBD is divided into genes that contribute to innate and adaptive immune responses (12). Tumor necrosis factor (TNF)-α is a multifunctional cytokine involved in the advancement of inflammatory responses and is critical in the pathogenesis of inflammatory, autoimmune and malignant diseases (13).…”

Section: Introductionmentioning

confidence: 99%

Evaluation of tumor necrosis factor (TNF)-α mRNA expression level and the rs1799964 polymorphism of the TNF-α gene in peripheral mononuclear cells of patients with inflammatory bowel diseases

et al. 2017

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“…Chronic intestinal inflammation is well known to increase the risk of colon cancers (10,47,48). Chronically inflamed tissues which are continuously regenerating are at an increased risk for mutagenesis and tumor transformation.…”

Section: Fig 6 (A) H Saguini-infected Monoassociated Il-10mentioning

confidence: 99%

Helicobacter saguini, a Novel Helicobacter Isolated from Cotton-Top Tamarins with Ulcerative Colitis, Has Proinflammatory Properties and Induces Typhlocolitis and Dysplasia in Gnotobiotic IL-10 ^−/− Mice

Shen

Mannion

et al. 2016

Infect Immun

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A urease-negative, fusiform, novel bacterium named Helicobacter saguini was isolated from the intestines and feces of cottontop tamarins (CTTs) with chronic colitis. Helicobacter sp. was detected in 69% of feces or intestinal samples from 116 CTTs. The draft genome sequence, obtained by Illumina MiSeq sequencing, for H. saguini isolate MIT 97-6194-5, consisting of ϳ2.9 Mb with a G؉C content of 35% and 2,704 genes, was annotated using the NCBI Prokaryotic Genomes Automatic Annotation Pipeline. H. saguini contains homologous genes of known virulence factors found in other enterohepatic helicobacter species (EHS) and H. pylori. These include flagellin, ␥-glutamyl transpeptidase (ggt), collagenase, the secreted serine protease htrA, and components of a type VI secretion system, but the genome does not harbor genes for cytolethal distending toxin (cdt). H. saguini MIT 97-6194-5 induced significant levels of interleukin-8 (IL-8) in HT-29 cell culture supernatants by 4 h, which increased through 24 h. mRNAs for the proinflammatory cytokines IL-1␤, tumor necrosis factor alpha (TNF-␣), IL-10, and IL-6 and the chemokine CXCL1 were upregulated in cocultured HT-29 cells at 4 h compared to levels in control cells. At 3 months postinfection, all H. saguini-monoassociated gnotobiotic C57BL/129 IL-10 ؊/؊ mice were colonized and had seroconverted to H. saguini antigen with a significant Th1-associated increase in IgG2c (P < 0.0001). H. saguini induced a significant typhlocolitis, associated epithelial defects, mucosa-associated lymphoid tissue (MALT) hyperplasia, and dysplasia. Inflammatory cytokines IL-22, IL-17a, IL-1␤, gamma interferon (IFN-␥), and TNF-␣, as well as inducible nitric oxide synthase (iNOS) were significantly upregulated in the cecal tissues of infected mice. The expression of the DNA damage response molecule ␥-H2AX was significantly higher in the ceca of H. saguini-infected gnotobiotic mice than in the controls. This model using a nonhuman primate Helicobacter sp. can be used to study the pathogenic potential of EHS isolated from primates with naturally occurring inflammatory bowel disease (IBD) and colon cancer. C otton-top tamarins (CTTs) are New World primates indigenous to the rain forests of Colombia and were imported into the United States for biomedical research beginning in the 1960s, until their classification as endangered species in 1976 (1). Approximately 50% of colony-maintained tamarins develop idiopathic chronic colitis, with 20 to 40% of cases evolving into colonic adenocarcinomas (2). The clinical and histopathological manifestations of colitis in CTTs resemble human inflammatory bowel disease (IBD), particularly ulcerative colitis (UC), making the CTT an attractive animal model of naturally occurring IBD. The etiology of colitis in CTTs remains unknown but has been speculated to be caused by genetic predispositions and/or conditions related to captivity, such as husbandry, the environment (temperature, humidity, and sanitation), abnormal diet, stress, and infectious agents (Escherichia coli, C...

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Cytokines, IBD, and Colitis-associated Cancer

Cited by 247 publications

References 111 publications

Pediatric patients with inflammatory bowel disease exhibit increased serum levels of proinflammatory cytokines and chemokines, but decreased circulating levels of macrophage inhibitory protein-1β, interleukin-2 and interleukin-17

Pediatric patients with inflammatory bowel disease exhibit increased serum levels of proinflammatory cytokines and chemokines, but decreased circulating levels of macrophage inhibitory protein-1β, interleukin-2 and interleukin-17

Evaluation of tumor necrosis factor (TNF)-α mRNA expression level and the rs1799964 polymorphism of the TNF-α gene in peripheral mononuclear cells of patients with inflammatory bowel diseases

Helicobacter saguini, a Novel Helicobacter Isolated from Cotton-Top Tamarins with Ulcerative Colitis, Has Proinflammatory Properties and Induces Typhlocolitis and Dysplasia in Gnotobiotic IL-10 ^−/− Mice

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Cytokines, IBD, and Colitis-associated Cancer

Cited by 247 publications

References 111 publications

Pediatric patients with inflammatory bowel disease exhibit increased serum levels of proinflammatory cytokines and chemokines, but decreased circulating levels of macrophage inhibitory protein-1β, interleukin-2 and interleukin-17

Pediatric patients with inflammatory bowel disease exhibit increased serum levels of proinflammatory cytokines and chemokines, but decreased circulating levels of macrophage inhibitory protein-1β, interleukin-2 and interleukin-17

Evaluation of tumor necrosis factor (TNF)-α mRNA expression level and the rs1799964 polymorphism of the TNF-α gene in peripheral mononuclear cells of patients with inflammatory bowel diseases

Helicobacter saguini, a Novel Helicobacter Isolated from Cotton-Top Tamarins with Ulcerative Colitis, Has Proinflammatory Properties and Induces Typhlocolitis and Dysplasia in Gnotobiotic IL-10 −/− Mice

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Helicobacter saguini, a Novel Helicobacter Isolated from Cotton-Top Tamarins with Ulcerative Colitis, Has Proinflammatory Properties and Induces Typhlocolitis and Dysplasia in Gnotobiotic IL-10 ^−/− Mice