Differential expression of CCR5 and CRTH2 on infiltrated cells in colonic mucosa of patients with ulcerative colitis

Matsuzaki, Koji; Hokari, Ryota; Kato, Shingo; Tsuzuki, Yoshikazu; Tanaka, Hirofumi; Kurihara, Chie; Iwai, Atsuhiro; Kawaguchi, Atsushı; Nagao, Shigeaki; Itoh, Kazuro; Nagata, Kazuhiro; Miura, Soichiro

doi:10.1046/j.1440-1746.2003.03088.x

Cited by 26 publications

(17 citation statements)

References 42 publications

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“…There has been no report about PGD 2 in UC. We previously reported that chemoattractant receptor-homologous molecule expressed on Th2 cells (CRTH2) positive cells infiltrated to colonic mucosa of UC patients (19). Recently, it is reported that CRTH2 serves as a receptor for PGD 2 , and it induces chemotaxis in Th2 cells, eosinophils, basophils, and macrophages in response to PGD 2 .…”

mentioning

confidence: 99%

Increased expression of lipocalin-type-prostaglandin D synthase in ulcerative colitis and exacerbating role in murine colitis

Hokari

Kurihara

Nagata³

et al. 2011

American Journal of Physiology-Gastrointestinal and Liver Physi

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Miura S. Increased expression of lipocalin-type-prostaglandin D synthase in ulcerative colitis and exacerbating role in murine colitis. Am J Physiol Gastrointest Liver Physiol 300: G401-G408, 2011. First published December 16, 2010 doi:10.1152/ajpgi.00351.2010.-The pathogenesis of ulcerative colitis (UC) is unclear, but enhancement of disease activity by usage of nonsteroidal anti-inflammatory drugs suggests involvement of prostanoid in its pathophysiology. However, biological effect of prostaglandin (PG) D2 on intestinal inflammation remains unknown. We investigated the expression of enzymes for PGD2 synthesis, prostaglandin D synthase (PGDS), and its relation to the activity of colitis in UC patients. The role of lipocalin-type PGDS (L-PGDS) using a murine colitis model was also assessed. Tissue samples were obtained by colonic biopsies from patients with UC. Expression levels of mRNAs for L-PGDS and hematopoietic-type PGDS were investigated by quantitative RT-PCR. COX-2 and L-PGDS expression was investigated by immunohistochemistry. Localization of L-PGDS expression was also determined by in situ hybridization. In experimental study, mice were treated with dextran sodium sulfate in the drinking water to induce colitis. The degree of colonic inflammation was compared with L-PGDS Ϫ/Ϫ mice and control mice. The level of L-PGDS mRNA expression was increased in UC patients in parallel with disease activity. Colocalization of L-PGDS and cyclooxygenase (COX) 2 was observed in lamina proprial infiltrating cells and muscularis mucosa in UC patients. The level of hematopoietic PGDS mRNA expression did not differ from control mucosa. Dextran sodium sulfate treatment to L-PGDS Ϫ/Ϫ mice showed lower disease activity than control mice. We reported for the first time the presence of L-PGDS in the COX-2-expressing cells in the mucosa of active UC patients and that only L-PGDS increased with disease activity. An animal model study suggests that PGD 2 derived from L-PGDSexpressing cells plays proinflammatory roles in colitis. prostaglandin D2; dextran sodium sulfate; chemoattractant receptorhomologous molecule expressed on Th2 cells; ulcerative colitis THE PATHOGENESIS OF ULCERATIVE colitis (UC) is unclear, but enhancement of disease activity by usage of cyclooxygenase (COX) inhibitor suggests involvement of prostanoid in its pathophysiology (10,11). In an animal model of colitis, administration of nonsteroidal anti-inflammatory dugs to IL-10

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confidence: 99%

Increased expression of lipocalin-type-prostaglandin D synthase in ulcerative colitis and exacerbating role in murine colitis

Hokari

Kurihara

Nagata³

et al. 2011

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…In human UC, several studies of the mucosal cytokine profile, especially containing IL-4, IL-5 and IL-13, supported the hypothesis of UC as a Th2-associated inflammation [103,104,105,106,107,108,109,110]. As a histopathological characteristic of UC, mucosal IgG1 + plasma cell infiltration is observed, suggesting Th2 polarization.…”

Section: Ulcerative Colitismentioning

confidence: 83%

The Role of T-Cell Subsets in Chronic Inflammation in Celiac Disease and Inflammatory Bowel Disease Patients: More Common Mechanisms or More Differences?

Hisamatsu

Erben²,

Kühl³

2016

Inflamm Intest Dis

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Background: Chronic intestinal inflammation due to noninfectious causes represents a growing health issue all over the world. Celiac disease as well as inflammatory bowel diseases (IBD) like Crohn's disease and ulcerative and microscopic colitis involve uncontrolled T-cell activation and T-cell-mediated damage as common denominators. Therefore, diagnosis and treatment decisions clearly benefit from the knowledge of the intricacies of the systemic and the local T-cell activity. Summary: Depending on the cytokine milieu, CD4⁺ T cells can differentiate into proinflammatory T helper 1 (Th1), anti-inflammatory Th2, antimicrobial Th17, pleiotropic Th9, tissue-instructing Th22 cells, and in the regulatory compartment forkhead box protein 3⁺ Treg, suppressive Tr1 or Th3 cells. Additionally, follicular Th cells provide B-cell help in antibody class switching; cytotoxic CD8⁺ T cells target virus-infected or tumor cells. This review discusses our current knowledge on the contribution of defined T-cell subpopulations to establishing and maintaining chronic intestinal inflammation in either of the above entities. It also puts emphasis on the differences in the prevalence of these diseases between Eastern and Western countries. Key Messages: In celiac disease, the driving role of T cells in the lamina propria and in the epithelium mainly specific for two defined antigens is well established. Differences in genetics and lifestyle between Western and Eastern countries were instrumental in understanding underlying mechanisms. In IBD, the vast amount of potential antigens and the corresponding antigen-specific T cells makes it unlikely to find universal triggers. Increased mucosal CD4⁺ regulatory T cells in all four entities fail to control or abrogate local inflammatory processes. Thus, prevailing differences in the functional T-cell subtypes driving chronic intestinal inflammation in celiac disease and IBD at best allow some overlap in the treatment options for either disease.

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“…Synergy between IL-12 and IL-18 in activated macrophages may be potent regulatory mechanism driving lamina propria lymphocytes toward a Th1 response in IBD [42,43,44,45]. According to Matsuzaki et al [46], Th1 responses occur significantly in colonic mucosa with severe inflammation in patients with UC, whereas Th2 responses mainly occur with mild inflammation.…”

Section: Discussionmentioning

confidence: 99%

Interleukin-18 Gene Polymorphisms in Tunisian Patients with Inflammatory Bowel Disease

Aleya

Sfar²,

Habibi³

et al. 2011

Digestion

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Aim: Interleukin (IL)-18 can regulate the Th2-mediated immune response and it may be involved in the pathogenesis of Th1 and Th2 chronic inflammatory diseases. This study sought to detect a possible association between two single nucleotide polymorphisms (SNPs) (–137G/C and –607C/A) in the IL-18 gene promoter region and susceptibility to inflammatory bowel disease (IBD) including Crohn’s disease (CD) and ulcerative colitis (UC) in the Tunisian population. Methods: The (–137G/C and –607C/A) IL-18 polymorphism was analyzed in 105 patients with CD, 59 patients with UC, and 100 controls using the sequence-specific polymerase chain reaction method. Results: The distribution of allele and genotype frequencies illustrate that the –137G/G genotype frequency was significantly higher in UC than in controls (p value corrected (pc) = 0.038). On the other hand, we found a statistically significant association (pc = 0.033) between genotype AA of the IL-18 gene promoter (–607C/A) polymorphism in UC patients and the distal localization of the lesions. In CD, no significant differences were observed at positions –607 and –137. The analysis of IBD patients according to clinical behavior revealed no difference. Conclusion: The two SNPs at position –607 (C/A) and –137 (G/C) in the promoter region of the IL-18 gene was associated with the development of UC but not CD, providing a strong support for an IBD susceptibility gene in the region surrounding IL-18. It remains to be determined precisely how the IL-18 alleles influence the pathogenesis of IBD.

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Differential expression of CCR5 and CRTH2 on infiltrated cells in colonic mucosa of patients with ulcerative colitis

Abstract: There is a possibility that Th1 responses significantly occur in colonic mucosa with severe inflammation, while Th2 responses mainly occur with mild inflammation in UC patients. The Th1/Th2 imbalance in colonic mucosa may be related to the disease progression of UC.

Cited by 26 publications

References 42 publications

Increased expression of lipocalin-type-prostaglandin D synthase in ulcerative colitis and exacerbating role in murine colitis

Increased expression of lipocalin-type-prostaglandin D synthase in ulcerative colitis and exacerbating role in murine colitis

The Role of T-Cell Subsets in Chronic Inflammation in Celiac Disease and Inflammatory Bowel Disease Patients: More Common Mechanisms or More Differences?

Interleukin-18 Gene Polymorphisms in Tunisian Patients with Inflammatory Bowel Disease

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