Blockade of CXCL10 protects mice from acute colitis and enhances crypt cell survival

Sasaki, Seiki; Yoneyama, Hiroyuki; Suzuki, Kenji; Suriki, H.; Aiba, Tsuneo; Watanabe, Shiro; Kawauchi, Yusuke; Kawachi, Hiroshi; Shimizu, Fujio; Matsushima, Kouji; Asakura, Hitoshi; Narumi, Shosaku

doi:10.1002/1521-4141(200211)32:11<3197::aid-immu3197>3.0.co;2-1

Cited by 118 publications

(96 citation statements)

References 39 publications

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“…In contrast, TGF-β is a typical negative regulator which inhibit proliferation of intestinal epithelial cells. Additionally, as we described above, we found that IP-10 is another negative regulator of crypt epithelial proliferation (Sasaki et al, 2002). In normal intestine, the net balance between these two factors is well balanced, and normal intestinal epithelial renewing is maintained (Fig.…”

Section: Blockade Of Ip-10 Ameliorated Maids Colitissupporting

confidence: 76%

“…3b). Therefore, theoretically, blocking IP-10 is an ideal therapeutic approach for UC as we reported using two mouse models (Sasaki et al, 2002;Suzuki et al, 2007). We think that blockade of IP-10 promotes crypt epithelial cell proliferation and regeneration as well as inhibiting differentiation of Th1 cells and their trafficking into the diseased colon (Fig.…”

Section: Blockade Of Ip-10 Ameliorated Maids Colitismentioning

confidence: 89%

“…We have revealed that the endogenously produced chemokine IP-10 regulates crypt cell proliferation (Sasaki et al, 2002). IP-10 was constitutively expressed by basal crypts in normal mouse colon, but the expression of IP-10 as well as CXCR3 was enhanced in the proliferative zone during acute phase of the colitis after oral administration of DSS.…”

Section: Blockade Of Ip-10 Ameliorated Acute Colitis and Enhances Crymentioning

confidence: 99%

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Role of Interferon -γ-Inducible Protein (IP)-10/ (IP-10/CXCL10) in Ulcerative Colitis; A Review of the Present Status

Suzuki¹,

Yoneyama²,

Asakura³

2011

Ulcerative Colitis - Epidemiology, Pathogenesis and Complications

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Section: Blockade Of Ip-10 Ameliorated Maids Colitissupporting

confidence: 76%

Section: Blockade Of Ip-10 Ameliorated Maids Colitismentioning

confidence: 89%

Section: Blockade Of Ip-10 Ameliorated Acute Colitis and Enhances Crymentioning

confidence: 99%

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Role of Interferon -γ-Inducible Protein (IP)-10/ (IP-10/CXCL10) in Ulcerative Colitis; A Review of the Present Status

Suzuki¹,

Yoneyama²,

Asakura³

2011

Ulcerative Colitis - Epidemiology, Pathogenesis and Complications

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“…CXCLs are induced by infl ammatory cytokines in human colonic enterocyte cells and pharyngeal epithelium and increased in the colons of IBD patients (Cole et al, 2001;Kwon et al, 2005;Egesten et al, 2009). Additionally, the inhibition of CXCL10 protects DSS-induced and IL-10 knockout colitic mice (Shimoyama et al, 2001;Sasaki et al, 2002). CCL4 is …”

Section: Discussionmentioning

confidence: 99%

Evaluation of Anti-Colitic Effect of Chung-Jang-Hwan (C-mix) in Mice

Lee¹,

Ahn²,

Park³

et al. 2011

Biomolecules and Therapeutics

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The inhibitory effect of Chung-Jang-Hwan (C-mix) consisted of Geranium nepalense subsp. thunbergii, Saururus chinensis, and Rubus coreanus were investigated in dextran sulfate sodium (DSS)-induced colitic mice by microarray analysis. Treatment with Cmix improved colitic symptoms, including colon shortening and myeloperoxidase activity. Treatment with DSS alone upregulated the expression levels of infl ammation-related genes, including IL-1β, CCL2, CCL4, CCL5, CCL7, CCL8, CCL24, CXCL1, CXCL2, CXCL5, CXCL9 and CXCL10, and other colitis-related genes such as COX-2, PAP, MMP family, S100a8, S100a9 and DEFA1 in mice. However, treatment with C-mix inhibited the expression levels of infl ammation-associated genes induced by DSS. The increased expression levels of COX-2 and IL-1β, representative infl ammatory genes, were confi rmed by a quantitative realtime polymerase chain reaction analysis. These results indicate that C-mix may ameliorate colitis by the inhibitory regulation of infl ammation-associated genes. 52-58 (2011) www.biomolther.org Abstract

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“…Regarding cell proliferation, our previous studies indicated that CXCL10 neutralization induced a cellular proliferative response (24,41), whereas some suggested that CXCL10 itself was associated with regeneration of tissues (42). Regarding the opposite effect of CXCL10 among the reports, it has been reported that an alternatively splicing variant of CXCR3 (renamed CXCR3-A), named CXCR3-B, was identified, and that CXCR3-A mediates the increase in survival of vascular endothelial cells, whereas CXCR3-B mediates the inhibition of cell growth induced by ligands of CXCR3 (42).…”

Section: Discussionmentioning

confidence: 99%

CXCL10 DNA Vaccination Prevents Spontaneous Diabetes through Enhanced β Cell Proliferation in NOD Mice

Shigihara

Shimada

Oikawa

et al. 2005

The Journal of Immunology

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CXCL10, a chemokine for Th1 cells, is involved in the pathogenesis of various Th1-dominant autoimmune diseases. Type 1 diabetes is considered to be a Th1-dominant autoimmune disease, and a suppressive effect of CXCL10 neutralization on diabetes development has been reported in a cyclophosphamide-induced accelerated diabetes model through induction of β cell proliferation. However, intervention in a diabetes model might bring about opposite effects, depending on the timing, amount, or method of treatment. In the present study, we examined the effect of CXCL10 neutralization in a “spontaneous diabetes” model of NOD mice, using CXCL10 DNA vaccination (pCAGGS-CXCL10). pCAGGS-CXCL10 treatment in young NOD mice induced the production of anti-CXCL10 Ab in vivo and suppressed the incidence of spontaneous diabetes, although this treatment did not inhibit insulitis or alter the immunological response. pCAGGS-CXCL10 treatment enhanced the proliferation of pancreatic β cells, resulting in an increase of β cell mass in this spontaneous diabetes model as well. Therefore, CXCL10 neutralization is suggested to be useful for maintaining β cell mass at any stage of autoimmune diabetes.

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Blockade of CXCL10 protects mice from acute colitis and enhances crypt cell survival

Cited by 118 publications

References 39 publications

Role of Interferon -γ-Inducible Protein (IP)-10/ (IP-10/CXCL10) in Ulcerative Colitis; A Review of the Present Status

Role of Interferon -γ-Inducible Protein (IP)-10/ (IP-10/CXCL10) in Ulcerative Colitis; A Review of the Present Status

Evaluation of Anti-Colitic Effect of Chung-Jang-Hwan (C-mix) in Mice

CXCL10 DNA Vaccination Prevents Spontaneous Diabetes through Enhanced β Cell Proliferation in NOD Mice

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