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Rehn M, Krarup PM, Christensen LH, Seidelin JB, Ågren MS, Syk I. GM6001 Increases Anastomotic Leakage following Colonic Obstruction Possibly by Impeding Epithelialization. Surg Infect (Larchmt) 2015; 16:702-8. [PMID: 26171681 DOI: 10.1089/sur.2014.248] [Citation(s) in RCA: 7] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/16/2023] Open
Abstract
BACKGROUND Emergency operations performed on an obstructed colon are accompanied by an increased risk of anastomotic insufficiency. Tissue-destructive matrix metalloproteinase (MMP) activity is elevated in the obstructed colon and contributes to a loss of suture-holding submucosal collagen, which may be mediated by tumor necrosis factor (TNF)-α. Our aim was to study the effect of the non-selective MMP and TNF-α converting enzyme (TACE) inhibitor GM6001 (30 mg/kg) on anastomosis repair in obstructed left colon. GM6001 has been proved to be highly efficacious in elective anastomosis rodent models. METHODS A partial obstruction of the distal colon was induced in male Sprague-Dawley rats. After 4 d the obstructed colonic segment was resected, and an end-to-end anastomosis was constructed. Seven days later, the anastomoses were evaluated for clinical leakage. Histopathological and immunohistochemical assessments were also performed. Finally, the direct effect of GM6001 on epithelialization was studied in cultured colonic epithelial cells. RESULTS Unlike the robust beneficial effect on anastomosis under uncomplicated conditions, here GM6001 had a negative impact on anastomotic wound healing following colonic obstruction and substantially (p=0.004) more rats in the GM6001 group (75%) than in the control group (11%) had developed anastomotic leakage. In the anastomotic wounds, the myofibroblast abundance and cell proliferation were similar in the two groups. Histologically, GM6001 treatment resulted in wider and minimally epithelialized wounds that were commonly necrotic on the luminal side and infiltrated with numerous granulocytes. In vitro, GM6001 also delayed (p=0.026) epithelialization of denuded intestinal epithelium grown on type I collagen. CONCLUSIONS Non-selective MMP/TACE inhibition with GM6001 increased the anastomotic complications following colon obstruction. Inhibition of epithelialization is one possible mechanism responsible for the increased leakage following GM6001 treatment.
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Affiliation(s)
- Martin Rehn
- 1 Department of Surgery, Skåne University Hospital , Malmö, Sweden
| | - Peter-Martin Krarup
- 2 Digestive Disease Center, Bispebjerg Hospital, University of Copenhagen , Copenhagen, Denmark
| | - Lise H Christensen
- 3 Department of Pathology, Bispebjerg Hospital, University of Copenhagen , Copenhagen, Denmark
| | - Jakob B Seidelin
- 2 Digestive Disease Center, Bispebjerg Hospital, University of Copenhagen , Copenhagen, Denmark
| | - Magnus S Ågren
- 2 Digestive Disease Center, Bispebjerg Hospital, University of Copenhagen , Copenhagen, Denmark .,4 Copenhagen Wound Healing Center, Bispebjerg Hospital, University of Copenhagen , Copenhagen, Denmark .,5 Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen , Copenhagen, Denmark
| | - Ingvar Syk
- 1 Department of Surgery, Skåne University Hospital , Malmö, Sweden
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Human colonic crypts in culture: segregation of immunochemical markers in normal versus adenoma-derived. J Transl Med 2014; 94:222-34. [PMID: 24365748 PMCID: PMC4108175 DOI: 10.1038/labinvest.2013.145] [Citation(s) in RCA: 36] [Impact Index Per Article: 3.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/09/2013] [Revised: 11/04/2013] [Accepted: 11/11/2013] [Indexed: 01/09/2023] Open
Abstract
In order to advance a culture model of human colonic neoplasia, we developed methods for the isolation and in vitro maintenance of intact colonic crypts from normal human colon tissue and adenomas. Crypts were maintained in three-dimensional Matrigel culture with a simple, serum-free, low Ca(2+) (0.15 mM) medium. Intact colonic crypts from normal human mucosa were viably maintained for 3-5 days with preservation of the in situ crypt-like architecture, presenting a distinct base and apex. Abnormal structures from adenoma tissue could be maintained through multiple passages (up to months), with expanding buds/tubules. Immunohistochemical markers for intestinal stem cells (Lgr5), growth (Ki67), differentiation (E-cadherin, cytokeratin 20 (CK20) and mucin 2 (MUC2)) and epithelial turnover (Bax, cleaved Caspase-3), paralleled the changes in function. The epithelial cells in normal crypts followed the physiological sequence of progression from proliferation to differentiation to dissolution in a spatially and temporally appropriate manner. Lgr5 expression was seen in a few basal cells of freshly isolated crypts, but was not detected after 1-3 days in culture. After 24 h in culture, crypts from normal colonic tissue continued to show strong Ki67 and MUC2 expression at the crypt base, with a gradual decrease over time such that by days 3-4 Ki67 was not expressed. The differentiation marker CK20 increased over the same period, eventually becoming intense throughout the whole crypt. In adenoma-derived structures, expression of markers for all stages of progression persisted for the entire time in culture. Lgr5 showed expression in a few select cells after months in culture. Ki67 and MUC2 were largely associated with the proliferative budding regions while CK20 was localized to the parent structure. This ex vivo culture model of normal and adenomatous crypts provides a readily accessible tool to help understand the growth and differentiation process in human colonic epithelium.
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Lecce L, Kaneko Y, Madawala RJ, Murphy CR. ICAM1 and fibrinogen-γ are increased in uterine epithelial cells at the time of implantation in rats. Mol Reprod Dev 2011; 78:318-27. [PMID: 21448983 DOI: 10.1002/mrd.21307] [Citation(s) in RCA: 14] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/07/2010] [Accepted: 02/25/2011] [Indexed: 11/07/2022]
Abstract
Uterine epithelial cells transform into a receptive state to adhere to an implanting blastocyst. Part of this transformation includes the apical concentration of cell adhesion molecules at the time of implantation. This study, for the first time, investigates the expression of ICAM1 and fibrinogen-γ (FGG) in uterine epithelial cells during normal pregnancy, pseudopregnancy and in hormone-treated rats. An increase (P < 0.05) in ICAM1 was seen at the apical membrane of uterine epithelial cells at the time of implantation compared with day 1 of pregnancy. ICAM1 was also increased (P < 0.05) on day 6 of pseudopregnancy as well as in ovariectomized rats treated with progesterone plus oestrogen. These results show that ICAM1 up-regulation at the time of implantation is under the control of progesterone, and is not dependent on cytokine release from the blastocyst or in semen. FGG dimerization increased (P < 0.05) on day 6 of pregnancy compared with day 1, and was not up-regulated in day 6 pseudopregnant animals, suggesting this increase is dependent on a developing blastocyst. The presence of ICAM1 and FGG in the uterine epithelium at the time of implantation in the rat is similar to that seen in lymphocyte-endothelium adhesion, and we suggest a similar mechanism in embryo-uterine epithelium adhesion is utilized.
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Affiliation(s)
- Laura Lecce
- Cell and Reproductive Biology Laboratory, School of Medical Sciences and Bosch Institute, The University of Sydney, Sydney, NSW, Australia.
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Vainer B. Intercellular adhesion molecule-1 (ICAM-1) in ulcerative colitis: presence, visualization, and significance. APMIS 2010:1-43. [PMID: 20653648 DOI: 10.1111/j.1600-0463.2010.02647.x] [Citation(s) in RCA: 11] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/14/2023]
Affiliation(s)
- Ben Vainer
- Department of Pathology, Rigshospitalet, University of Copenhagen, Blegdamsvej 9, DK-2100 Copenhagen, Denmark.
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Seidelin JB, Nielsen OH. Attenuated apoptosis response to Fas-ligand in active ulcerative colitis. Inflamm Bowel Dis 2008; 14:1623-9. [PMID: 18680199 DOI: 10.1002/ibd.20629] [Citation(s) in RCA: 15] [Impact Index Per Article: 0.9] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/09/2022]
Abstract
BACKGROUND From mainly carcinoma cell line studies, apoptosis has been thought to play a major role in the pathogenesis of ulcerative colitis (UC). Apoptosis has been suggested to be due to a Fas ligand / Fas receptor interaction, but has never been studied in cells from patients with active UC. The aim was to investigate both the spontaneous and the cell death receptor ligand-induced apoptosis in UC. METHODS Twenty patients with UC and 16 control subjects who underwent routine colonoscopy either for the control or surveillance of their disease or where the diagnosis of irritable bowel syndrome was subsequently reached were included. Cultures of isolated colonic crypts were obtained from biopsies and cultured for 4 to 16 hours with Fas ligand or Fas ligand and costimulation with interferon-gamma (IFN-gamma). Control experiments were performed on HT29 cells. Apoptosis was assessed by independent methods. RESULTS Isolated colonocytes from healthy subjects or patients with remission in UC had a dose-dependent response to Fas ligand. This response was abolished in patients with active UC (P < 0.002), and costimulation with IFN-gamma did not alter this response. Patients with active UC had an increased apoptosis rate of 9.5% compared with controls (P < 0.05). CONCLUSIONS The current study indicates that colonocytes do not respond to cytokine exposure and inflammation by an increased vulnerability, as previously thought. Colonocytes seem to activate cytoprotective programs in response to inflammation. Apart from supporting the regeneration process during inflammation, this response could additionally cause an increased susceptibility to neoplastic transformation.
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Affiliation(s)
- Jakob B Seidelin
- Department of Medical Gastroenterology C, Herlev Hospital, University of Copenhagen, Denmark.
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Youn H, Hong K, Yoo JW, Lee CH. ICAM-1 expression in vaginal cells as a potential biomarker for inflammatory response. Biomarkers 2008; 13:257-69. [PMID: 18415799 DOI: 10.1080/13547500701843338] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 10/22/2022]
Abstract
This study aimed to elucidate the mechanisms that may lead to an efficient strategy to induce a suitable host response of the vaginal mucosa upon exposure to intravaginally delivered exogenous compounds. It was hypothesized that the upregulation of intercellular adhesion molecule (ICAM)-1 gene expression may reflect the inflammatory response evoked by exogenous compounds. Major emphasis was placed on ethylenediamine tetraacetic acid (EDTA) which was added as a synergistic agent to conventional spermicidal agents or anti-HIV drugs. The levels of ICAM-1 mRNA were examined as a surrogate marker for inflammatory response in human vaginal epithelial cells upon exposure to EDTA or interleukin (IL)-1beta (i.e. positive control, 25 mM). The effects of estrogen on EDTA-induced ICAM-1 expression were also evaluated for the estrogen involvement in the inflammatory process of the vaginal mucosa. ICAM-1 expression in human vaginal cells (VK2/E6E7 cells) increased as EDTA concentration added to human vaginal cell lines increased. The effects of estrogen on EDTA-induced ICAM-1 expression in human vaginal epithelial cells were estrogen-concentration dependent; estrogen at lower concentrations (approximately 1-10 nM) did not affect ICAM-1 expression, whereas estrogen at higher concentrations (approximately 100 nM-1 microM) attenuated ICAM-1 expression. The influence of estrogen in ICAM-1 expression suggests the beneficial effects of estrogen on the regulation of vaginal homeostasis. Identification and quantification of specific surrogate markers for the inflammatory response evoked by exogenous compounds and their regulation by estrogen will lead to an efficient strategy against sexually transmitted diseases including AIDS.
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Affiliation(s)
- Hyewon Youn
- Department of Urology, University of Kansas Medical Center, Kansas City, KS, USA
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Celecoxib modulates adhesion of HT29 colon cancer cells to vascular endothelial cells by inhibiting ICAM-1 and VCAM-1 expression. Br J Pharmacol 2007; 153:1153-61. [PMID: 18084316 DOI: 10.1038/sj.bjp.0707636] [Citation(s) in RCA: 21] [Impact Index Per Article: 1.2] [Reference Citation Analysis] [Abstract] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/22/2022] Open
Abstract
BACKGROUND AND PURPOSE Cyclooxygenase-2 (COX-2) is highly expressed during inflammation and can promote the progression of colorectal cancer. Interactions between cancer cells and vascular endothelial cells are key events in this process. Recently, the selective COX-2 inhibitor, celecoxib, was shown to inhibit expression of the adhesion molecules, ICAM-1 and VCAM-1, in the human colon cancer cell line HT29 and to inhibit adhesion of HT29 cells to FCS-coated plastic wells. Here, we evaluated the effects of celecoxib on adhesion of HT29 cells to human umbilical vein endothelial cells (HUVEC), mediated by ICAM-1 and VCAM-1, to assess further the potential protective effects of celecoxib on cancer development. EXPERIMENTAL APPROACH Celecoxib was incubated for 4 h with HT29 cells and HUVEC and adhesion was quantified by a computerized micro-imaging system. Expression analysis of ICAM-1 and VCAM-1 cell adhesion molecules was performed by western blot. KEY RESULTS Celecoxib (1 nM-10 microM) inhibited, with the same potency, adhesion of HT29 cells to resting HUVEC or to HUVEC stimulated by tumour necrosis factor-alpha (TNF-alpha), mimicking inflammatory conditions. Analysis of ICAM-1 and VCAM-1 expression showed that celecoxib inhibited expression of both molecules in TNF-alpha-stimulated HUVEC, but not in resting HUVEC; inhibition was concentration-dependent and maximal (about 50%) at 10 microM celecoxib. CONCLUSIONS AND IMPLICATIONS In conclusion, our data show that celecoxib inhibits HT29 cell adhesion to HUVEC and expression of ICAM-1 and VCAM-1, in stimulated endothelial cells. These effects may contribute to the chemopreventive activity of celecoxib in the development of colorectal cancer.
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Taglia L, Matusiak D, Matkowskyj KA, Benya RV. Gastrin-releasing peptide mediates its morphogenic properties in human colon cancer by upregulating intracellular adhesion protein-1 (ICAM-1) via focal adhesion kinase. Am J Physiol Gastrointest Liver Physiol 2007; 292:G182-90. [PMID: 16920698 DOI: 10.1152/ajpgi.00201.2006] [Citation(s) in RCA: 27] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/31/2023]
Abstract
Gastrin-releasing peptide (GRP) and its receptor (GRPR) act as morphogens when expressed in colorectal cancer (CRC), promoting the assumption of a better differentiated phenotype by regulating cell motility in the context of remodeling and retarding tumor cell metastasis by enhancing cell-matrix attachment. Although we have shown that these processes are mediated by focal adhesion kinase (FAK), the downstream target(s) of GRP-induced FAK activation are not known. Since osteoblast differentiation is mediated by FAK-initiated upregulation of ICAM-1 (Nakayamada S, Okada Y, Saito K, Tamura M, Tanaka Y. J Biol Chem 278: 45368-45374, 2003), we determined whether GRP-induced activation of FAK alters ICAM-1 expression in CRC and, if so, determined the contribution of ICAM-1 to mediating GRP's morphogenic properties. Caco-2 and HT-29 cells variably express GRP/GRPR. These cells only express ICAM-1 when GRPR are present. In human CRC, GRPR and ICAM-1 are only expressed by better differentiated tumor cells, with ICAM-1 located at the basolateral membrane. ICAM-1 expression was only observed subsequent to GRPR signaling via FAK. To study the effect of ICAM-1 expression on tumor cell motility, CRC cells expressing GRP, GRPR, and ICAM-1 were cultured in the presence and absence of GRPR antagonist or monoclonal antibody to ICAM-1. CRC cells engaged in directed motility in the context of remodeling and were highly adherent to the extracellular matrix, only in the absence of antagonist or ICAM-1 antibody. These data indicate that GRP upregulation of ICAM-1 via FAK promotes tumor cell motility and attachment to the extracellular matrix.
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Affiliation(s)
- Lauren Taglia
- Department of Medicine, University of Illinois at Chicago, 840 South Wood St., Chicago, IL 60612, USA
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Vainer B, Horn T, Nielsen OH. Colonic epithelial cell expression of ICAM-1 relates to loss of surface continuity: a comparative study of inflammatory bowel disease and colonic neoplasms. Scand J Gastroenterol 2006; 41:318-25. [PMID: 16497620 DOI: 10.1080/00365520510024241] [Citation(s) in RCA: 15] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/04/2023]
Abstract
OBJECTIVE Intercellular adhesion molecule-1 (ICAM-1) is important in ulcerative colitis (UC) by mediating the arrest and further migration of neutrophils. In vitro studies have shown that colonocytes from chronically inflamed colon and cultured colon cancer cells are capable of expressing ICAM-1. The aim of this study was to assess the ICAM-1 expression in human colonic tissue representing UC, Crohn's disease (CD), adenomas, and adenocarcinomas, with special attention to the epithelium. MATERIAL AND METHODS Formalin-fixed and paraffin-embedded tissue from the archives of the Department of Pathology of Rigshospitalet University of Copenhagen was examined. Colonic tissue from 10 patients with UC, 10 with CD, 32 adenomas, 27 adenocarcinomas, and 10 lymph node metastases were included. The expression of ICAM-1 was assessed by using the EnVision(+)technique (DakoCytomation). RESULTS Endothelial ICAM-1 was up-regulated in areas with dense lymphocyte infiltration and near crypt abscesses and ulcerations. Ulcerations were covered by a continuous layer of macrophages and epithelial cells expressing ICAM-1. Similar observations were made in the case of adenomas and adenocarcinomas, but in adenocarcinomas the epithelial ICAM-1 was more diffuse and not related solely to sites of surface destruction. CONCLUSIONS In the colon, endothelial cells, macrophages, and epithelial cells are in certain conditions capable of expressing ICAM-1. Although the ICAM-1 expression was related to both the degree and the nature of inflammation, the data indicate increased susceptibility of cancer cells to express ICAM-1. Epithelial and macrophage ICAM-1 might be involved in the immune surveillance and the first-line defense of the diseased colon.
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Affiliation(s)
- Ben Vainer
- Department of Pathology, Herlev Hospital, Herlev, Denmark.
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Bruno MEC, Kaetzel CS. Long-Term Exposure of the HT-29 Human Intestinal Epithelial Cell Line to TNF Causes Sustained Up-Regulation of the Polymeric Ig Receptor and Proinflammatory Genes through Transcriptional and Posttranscriptional Mechanisms. THE JOURNAL OF IMMUNOLOGY 2005; 174:7278-84. [PMID: 15905574 DOI: 10.4049/jimmunol.174.11.7278] [Citation(s) in RCA: 34] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 12/15/2022]
Abstract
Transport of IgA Abs across intestinal epithelial cells into gut secretions is mediated by the polymeric Ig receptor (pIgR). The cytokine TNF plays a central role in initiating and amplifying inflammatory reactions, and is implicated in the pathogenesis of inflammatory bowel diseases. Acute exposure of intestinal epithelial cell lines to TNF has been shown to up-regulate transcription of genes encoding pIgR and a number of proinflammatory factors, but the effects of chronic exposure to TNF have not been studied. We found that exposure of HT-29 human colon carcinoma cells to TNF for up to 20 days reduced the rate of cell proliferation, but did not cause gross morphological changes. Expression of mRNA encoding pIgR and several proinflammatory genes increased acutely, and then diminished but remained elevated above control levels throughout the experiment. Changes in gene expression were paralleled by increased expression of the transcription factors IFN regulatory factor-1 and the RelB subunit of NF-kappaB. HT-29 cells activated the endogenous TNF gene in response to TNF treatment, but the level of TNF production was insufficient to maintain pIgR and proinflammatory gene expression after withdrawal of exogenous TNF. Chronic exposure to TNF caused a marked increase in pIgR mRNA stability and a small but significant decrease in TNF mRNA stability, but no change in the half-lives of IL-8, c-Myc, and GAPDH. In summary, we observed different effects of acute vs chronic exposure to TNF on gene expression, and found evidence for transcriptional and posttranscriptional regulation of expression of the pIgR.
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Affiliation(s)
- Maria E C Bruno
- Department of Microbiology, Immunology, and Molecular Genetics, University of Kentucky, Lexington, 40536, USA
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Guo SM, Tong HB, Bai LS, Yang W. Effect of traditional Chinese medicinal enemas on ulcerative colitis of rats. World J Gastroenterol 2004; 10:1914-7. [PMID: 15222036 PMCID: PMC4572230 DOI: 10.3748/wjg.v10.i13.1914] [Citation(s) in RCA: 8] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/15/2022] Open
Abstract
AIM: To investigate the effects of traditional Chinese medicinal enema (TCME) on inflammatory and immune response of colonic mucosa of rats with ulcerative colitis (UC), and to observe the pathogenic mechanism.
METHODS: Thirty UC rats, induced by intestinal enema together with 2.4-dinitrochlorobenzene (DNCB) and acetic acid, were randomly divided into 3 groups, i.e., G I, G II and G III. Groups G I and G II were administered with TCME and salazosulfapyridine enema (SASPE), respectively. Group G III was clystered with only normal saline (NSE), served as control. Group G IV was taken from normal rats as reference, once daily, from the 7th day after the establishment of UC for total 28 d. Interleukin-6 (IL-6) in the colonic mucosa was assayed by 3H-TdR incorporation assay. Colonic mucosal lymphocyte subpopulation adhesive molecules, CD4+CD11a+, CD4+CD18+, CD8+CD11a+, CD8+CD18+ (LSAM), tumor necrosis factor (TNF)-α, and interferon-γ (IFN-γ), were detected by enzyme linked immunosorbent assay (ELISA). Moreover, the expression of TNF-α mRNA and IFN-γ mRNA in colonic mucosa were detected by polymerase chain reaction (RT-PCR).
RESULTS: Before therapies, in model groups, G I, G II and G III, levels of IL-6, TNF-α, IFN-γ, CD8+CD11a+ and CD8+CD18+ were significantly different (38.29 ± 2.61 U/mL, 16.54 ± 1.23 ng/L, 8.61 ± 0.89 ng/L, 13.51% ± 2.31% and 12.22% ± 1.13%, respectively) compared to those in G IV group (31.56 ± 2.47 U/mL, 12.81 ± 1.38 ng/L, 5.28 ± 0.56 ng/L, 16.68% ± 1.41% and 16.79% ± 1.11%, respectively). After therapeutic enemas, in G I group, the contents of IL-6 (32.48 ± 2.53 U/m), TNF-α (13.42 ± 1.57 ng/L) and IFN-γ (5.87 ± 0.84 ng/L) were reduced; then, the contents of CD8+CD11a+ (16.01% ± 1.05 %) and CD8+CD18+ (16.28% ± 0.19%) were raised. There was no significant difference between groups G I and G IV, but the difference between groups G I and G II was quite obvious (P < 0.05). The expressions of TNF-α mRNA and IFN-γ mRNA in group G III were much higher than those of group G IV, but those in group G I were significantly suppressed by TCME therapy.
CONCLUSION: Ulcerative colitis is related to colonic regional mucosal inflammatory factors and immune imbalance. TCME can effectively inhibit regional mucosal inflammatory factors and improve their disorder of immunity.
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Affiliation(s)
- Song-Ming Guo
- Department of Traditional Chinese Medicine, Tongji Hospital, Tongji University, Shanghai 200065, China.
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