Expression of interleukin 6 in brain and colon of rats with TNBS-induced colitis

Wang, Kai; Yuan, Chenfeng; Wang, Wei; Yang, Zhan-Qing; Cui, Wei; Mu, Lian-Zhi; Yue, Zhan‐Peng; Yin, Xiu-Ling; Hu, Zhong-Ming; Liu, Juxiong

doi:10.3748/wjg.v16.i18.2252

Cited by 39 publications

(23 citation statements)

References 35 publications

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“…Rectal administration of TNBS resulted in the development of clinical symptoms of colitis, which manifested as a decrease in food intake and a decrease in body weight, similar to what has been observed in previous studies [33, 34, 39]. On the experimental day 0, the body weight was 352 ± 24 g and did not differ significantly between the groups (one-way ANOVA, F = 0.512, p = 0.61).…”

Section: Resultssupporting

confidence: 85%

“…TNBS-induced colitis in rats has also been used to study effects of gut inflammation on the brain. TNBS administration in rats was shown to induce activation of microglia and cytokine release in the brain [32, 33] and increased expression of intestinal TSPO receptors [40]. Therefore, we selected the TNBS-induced colitis model for this study.…”

Section: Introductionmentioning

confidence: 99%

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Evaluating [11C]PBR28 PET for Monitoring Gut and Brain Inflammation in a Rat Model of Chemically Induced Colitis

et al. 2016

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PurposeUlcerative colitis (UC) is a chronic inflammatory disease of the colon that affects an increasing number of patients. High comorbidity is observed between UC and other diseases in which inflammation may be involved, including brain diseases such as cognitive impairment, mental disorders, anxiety, and depression. To investigate the increased occurrence of these brain diseases in patients with UC, non-invasive methods for monitoring peripheral and central inflammation could be applied. Therefore, the goal of this study is to assess the feasibility of monitoring gut and brain inflammation in a rat model of chemically induced colitis by positron emission tomography (PET) with [11C]PBR28, a tracer targeting the translocator protein (TSPO), which is upregulated when microglia and macrophages are activated.ProceduresColitis was induced in rats by intra-rectal injection of 2,4,6-trinitrobenzenesulfonic acid (TNBS). Rats with colitis and healthy control animals were subjected to [11C]PBR28 PET of the abdomen followed by ex vivo biodistribution in order to assess whether inflammation in the gut could be detected. Another group of rats with colitis underwent repetitive [11C]PBR28 PET imaging of the brain to investigate the development of neuroinflammation.ResultsEleven days after TNBS injection, ex vivo biodistribution studies demonstrated increased [11C]PBR28 uptake in the inflamed cecum and colon of rats with colitis as compared to healthy controls, whereas PET imaging did not show any difference between groups at any time. Similarly, repetitive PET imaging of the brain did not reveal any neuroinflammation induced by the TNBS administration in the colon. In contrast, significantly increased [11C]PBR28 uptake in cerebellum could be detected in ex vivo biodistribution studies on day 11.ConclusionInflammation in both the gut and the brain of rats with chemically induced colitis was observed by ex vivo biodistribution. However, these effects could not be detected by [11C]PBR28 PET imaging in our colitis model, which is likely due to spill-over effects and insufficient resolution of the PET camera.

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Section: Resultssupporting

confidence: 85%

Section: Introductionmentioning

confidence: 99%

Evaluating [11C]PBR28 PET for Monitoring Gut and Brain Inflammation in a Rat Model of Chemically Induced Colitis

et al. 2016

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“…Although these studies demonstrate that epithelial Stat3 activation mediates mucosal protective functions, other evidence suggests that Stat3 hyperactivation may also contribute to inflammation. Indeed, increases in serum IL-6 concentrations and Stat3 hyperactivation were observed in IBD patients, as well as in experimental colitis models (53,54). Likewise, Stat3 is hyperphosphorylated in both colonic epithelial cells and lamina propria mononuclear cells in colitis (55).…”

Section: Discussionmentioning

confidence: 97%

Epithelial Tyrosine Phosphatase SHP-2 Protects against Intestinal Inflammation in Mice

Coulombe

Leblanc

Cagnol

et al. 2013

Molecular and Cellular Biology

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“…In FCDIIb, balloon cells expressed both IL-6 and GFAP. Additional work suggests the expression of IL-6 in neurons of the cerebral cortex and hypothalamus with trinitrobenzene sulfonic acid-induced colitis (Wang et al, 2010). Further work has demonstrated that the combination of neuronal depolarization and activation of IL-1R1 with IL-1β can induce neurons to synthesize and release IL-6 (Juttler et al, 2002; Ringheim et al, 1995; Tsakiri et al, 2008a, b).…”

Section: Discussionmentioning

confidence: 99%

Interleukin (IL)-1 and IL-6 regulation of neural progenitor cell proliferation with hippocampal injury: Differential regulatory pathways in the subgranular zone (SGZ) of the adolescent and mature mouse brain

McPherson

Aoyama

Harry

2011

Brain, Behavior, and Immunity

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Current data suggests an association between elevations in interleukin 1 (IL-1)α, IL-1β, and IL-6 and the proliferation of neural progenitor cells (NPCs) following brain injury. A limited amount of work implicates changes in these pro-inflammatory responses with diminished NPC proliferation observed as a function of aging. In the current study, adolescent (21 day-old) and 1 yr-old CD1 male mice were injected with trimethyltin (TMT, 2.3 mg/kg, i.p.) to produce acute apoptosis of hippocampal dentate granule cells. In this model, fewer 5-bromo-2′-deoxyuridine (BrdU) + NPC were observed in both naive and injured adult hippocampus as compared to the corresponding number seen in adolescent mice. At 48 h post-TMT, a similar level of neuronal death was observed across ages, yet activated amoeboid microglia were observed in the adolescent and hypertrophic process-bearing microglia in the adult. IL-1α mRNA levels were elevated in the adolescent hippocampus; IL-6 mRNA levels were elevated in the adult. In subgranular zone (SGZ) isolated by laser-capture microdissection, IL-1β was detected but not elevated by TMT, IL-1α was elevated at both ages, while IL-6 was elevated only in the adult. Naïve NPCs isolated from the hippocampus expressed transcripts for IL-1R1, IL-6Rα, and gp-130 with significantly higher levels of IL-6Rα mRNA in the adult. In vitro, IL-1α (150pg/ml) stimulated proliferation of adolescent NPCs; IL-6 (10ng/ml) inhibited proliferation of adolescent and adult NPCs. Microarray analysis of SGZ post-TMT indicated a prominence of IL-1α/IL-1R1 signaling in the adolescent and IL-6/gp130 signaling in the adult.

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Expression of interleukin 6 in brain and colon of rats with TNBS-induced colitis

Abstract: These results revealed that changes in IL-6 expression in brain and colon tissues occur in different phases of IBD. Therefore, we propose that the nerve centre regulates and controls the occurrence and development of IBD via IL-6.

Cited by 39 publications

References 35 publications

Evaluating [11C]PBR28 PET for Monitoring Gut and Brain Inflammation in a Rat Model of Chemically Induced Colitis

Evaluating [11C]PBR28 PET for Monitoring Gut and Brain Inflammation in a Rat Model of Chemically Induced Colitis

Epithelial Tyrosine Phosphatase SHP-2 Protects against Intestinal Inflammation in Mice

Interleukin (IL)-1 and IL-6 regulation of neural progenitor cell proliferation with hippocampal injury: Differential regulatory pathways in the subgranular zone (SGZ) of the adolescent and mature mouse brain

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