Mucosal cytokine expression, cellular markers and adhesion molecules in inflammatory bowel disease

Woywodt, Alexander; Ludwig, D.; Neustock, Petra; Kruse, Andrea; Schwarting, Karsten; Jantschek, Günter; Kirchner, Holger; Stange, Eduard F.

doi:10.1097/00042737-199903000-00010

Cited by 78 publications

(50 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…During acute flares of UC or CD there is a massive infiltration of NGs into the affected mucosa, which is manifested clinically by an increase in stool NGs. In IBD there is also a marked infiltration of macrophages into the inflamed mucosa, manifested by an increase in macrophage-derived inflammatory cytokines IL-1β, IL-6 and TNF-α during acute flares [18]. IBD are characterized by a dense infiltration of tissue by CD-68…”

Section: Introductionmentioning

confidence: 99%

Identification of CD68+ neutrophil granulocytes in in vitro model of acute inflammation and inflammatory bowel disease

Amanzada¹,

Malik²,

Ramadori³

et al. 2013

Z Gastroenterol

View full text Add to dashboard Cite

CD-68 is widely regarded as a selective marker for human monocytes and macrophages and is commonly used in human pathology studies. The purpose of this study was to investigate the expression of CD-68 in human peripheral blood mononuclear cells (PBMCs), neutrophil granulocytes (NGs) and in inflamed intestinal tissue samples for comparison. PBMCs and NGs were isolated from heparinized human blood samples. Intestinal biopsies were obtained during routine endoscopic procedures from patients with inflammatory bowel disease (IBD), e.g. ulcerative colitis and Crohn's disease. Gene and protein expression was analyzed by real-time RT-PCR, Western blot and immunohistochemistry. Both PBMCs and NGs preparations contained cells that were positive for CD-68 and either neutrophil elastase (NE), or myeloperoxidase (MPO). CD-68 + /NE -/MPO -cells were regarded as monocytes. CD-68 mRNA expression was detected in PBMCs and NGs preparations. With Western blot and by performing immunoprecipitation of cell lysate, we could clearly detect CD-68 in NGs, U-937, THP-1, Hep-G2, Jurkat cells and PBMCs. Identification of inflammatory cells in acutely inflamed colonic mucosa obtained from patients with IBD revealed a strong accumulation of CD-68 + /MPO + cells compared to normal colonic mucosa. The uptake of the marker by phagocytosis was excluded by performing a double staining with CD-163/NE and CD-163/MPO in PBMCs, NGs cultures and in inflamed colonic mucosa. These results identify CD-68 + NGs in peripheral blood and inflamed colonic mucosa. CD-68 is not only a marker for the macrophages-monocytes but also for NGs.

show abstract

Section: Introductionmentioning

confidence: 99%

Identification of CD68+ neutrophil granulocytes in in vitro model of acute inflammation and inflammatory bowel disease

Amanzada¹,

Malik²,

Ramadori³

et al. 2013

Z Gastroenterol

View full text Add to dashboard Cite

show abstract

“…Although etiology and pathogenesis of IBD are still unknown, there is evidence that proinflammatory cytokines like interleukin-1β (IL1β) and interleukin-6 (IL6) are involved in the establishment of IBD [16,17]. IL1β and IL6 mRNA were found in large numbers of cells throughout the inflamed intestine of patients with CD but also in some macroscopically unaffected tissue specimens of the same patients [18]. Organ cultures of intestinal biopsy specimens taken from areas of affected mucosa from patients with CD spontaneously produced increased amounts of IL1β and IL6 (and TNFα) compared with controls [19].…”

Section: Introductionmentioning

confidence: 99%

Down-regulation of <i>TFF</i> Expression in Gastrointestinal Cell Lines by Cytokines and Nuclear Factors

Dossinger¹,

Kayademir²,

Blin³

et al. 2002

Cell Physiol Biochem

View full text Add to dashboard Cite

Background and Aims: Trefoil peptides (TFF1, TFF2 and TFF3) are acute phase proteins up-regulated in response to gastrointestinal mucosal damage. They promote cell migration, protect and heal the mucosa and may function as tumorsuppressors. We assumed them to be regulated by the proinflammatory cytokines interleukin-1β (IL1β) and interleukin-6 (IL6), which trigger the transcriptional factors NF-ĸB and C/EBPβ. Methods: Following IL1β and IL6 stimulation, expression of TFF genes was analyzed in gastrointestinal cell lines HT-29 and KATO III by reporter gene assays using TFF promoter constructs and by quantitative real-time PCR. NF-ĸB and C/EBPβ were transiently co-expressed. Results: We have functionally identified transcription factors NF-ĸB and C/EBPβ to inhibit transcription of human TFF genes. Down-regulation of TFF transcription is also observed by IL1β and IL6, suggesting crosstalk with or in response to the immune system. IL1β and IL6 caused a 3- to 11-fold reduction in TFF mRNA expression, displayed in real-time PCR. Conclusions: Down-regulation of intestinal trefoil factor TFF3 due to transcriptional repression by IL1β through NF-ĸB as well as by IL6 through C/EBPβ activation in vitro may reflect the situation in vivo and may contribute to ulceration and decreased wound healing during inflammatory bowel disease. Additionally, IL1 and IL6 over-expression in chronic gastritis may lead to mucosal damage and gastric carcinogenesis through transcriptional repression of TFF1 and TFF2.

show abstract

“…Previously, it was demonstrated that macrophages heavily infiltrate the colon following TNBS-induced colitis [26], and that the removal of macrophages using either anti-CD1lb or anti-CD18 antibodies prevented TNBS -colitis in mice [29,30]. In addition to cellular infiltrates, the mRNA expression of macrophage-derived inflammatory cytokines such as TNF-α, IL-6, and MCP-1 [31,32] was elevated in the TNBS-injured colon on day 2. These findings indicate that DTCM-G inhibits TNBS-induced inflammatory responses in the colon by inhibiting macrophage activation.…”

Section: Discussionmentioning

confidence: 98%

Novel anti-inflammatory agent 3-[(dodecylthiocarbonyl)-methyl]-glutarimide ameliorates murine models of inflammatory bowel disease

et al. 2015

View full text Add to dashboard Cite

Objective and design To examine the effect of 3-[(dodecylthiocarbonyl)-methyl]-glutarimide (DTCM-G), a novel anti-inflammatory agent that inhibits lipopolysaccharide (LPS) -activation of RAW264.7 macrophages, on murine models of colitis and RAW264.7 cells. Materials and MethodsColitis was induced by rectally infusing trinitrobenzenesulfonic acid (TNBS) (1.5 mg in 50% ethanol) in BALB/c mice or orally administering 3% dextran sulfate sodium (DSS) for 5 days in C57BL/6 mice. The severity of colitis was assessed after intraperitoneally injecting DTCM-G (40 mg/kg). The anti-inflammatory properties of DTCM-G and its mechanisms were investigated in LPS-stimulated RAW264.7 cells.Results DTCM-G significantly ameliorated TNBS-induced colitis, according to the body weight loss, disease activity index, colonic obstruction, macroscopic colonic inflammation score, mucosal myeloperoxidase activity, and histopathology. Immunohistochemistry and isolated lamina propria mononuclear cells showed significantly reduced colonic F4/80 + and CD11b + macrophage infiltration. DTCM-G significantly suppressed tumor necrosis factor (TNF)-α and interleukin (IL)-6 messenger RNA expression in the colon, and attenuated DSS-induced colitis, according to the disease activity index and histopathology. In RAW264.7 cells, DTCM-G suppressed LPS-induced TNF-α/IL-6 production and enhanced glycogen synthase kinase-3β phosphorylation.

show abstract

Mucosal cytokine expression, cellular markers and adhesion molecules in inflammatory bowel disease

Cited by 78 publications

References 0 publications

Identification of CD68+ neutrophil granulocytes in in vitro model of acute inflammation and inflammatory bowel disease

Identification of CD68+ neutrophil granulocytes in in vitro model of acute inflammation and inflammatory bowel disease

Down-regulation of <i>TFF</i> Expression in Gastrointestinal Cell Lines by Cytokines and Nuclear Factors

Novel anti-inflammatory agent 3-[(dodecylthiocarbonyl)-methyl]-glutarimide ameliorates murine models of inflammatory bowel disease

Contact Info

Product

Resources

About