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Anti-cxcl9, anti-cxcl10, anti-cxcl11, anti-cxcl13, anti-cxcr3 and anti-cxcr5 agents for inhibition of inflammation

A technology of -CXCL11, -CXCR3, applied in the direction of anti-inflammatory agents, antibodies, antibacterial drugs, etc., can solve the problem that the exact mechanism of chemokine-mediated events is not clear

Inactive Publication Date: 2015-08-26
JYANT TECH
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  • Summary
  • Abstract
  • Description
  • Claims
  • Application Information

AI Technical Summary

Problems solved by technology

However, the precise mechanism of chemokine-mediated events remains unclear

Method used

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  • Anti-cxcl9, anti-cxcl10, anti-cxcl11, anti-cxcl13, anti-cxcr3 and anti-cxcr5 agents for inhibition of inflammation
  • Anti-cxcl9, anti-cxcl10, anti-cxcl11, anti-cxcl13, anti-cxcr3 and anti-cxcr5 agents for inhibition of inflammation
  • Anti-cxcl9, anti-cxcl10, anti-cxcl11, anti-cxcl13, anti-cxcr3 and anti-cxcr5 agents for inhibition of inflammation

Examples

Experimental program
Comparison scheme
Effect test

Embodiment 1

[0176] Example 1: Up-regulation of chemokines and their receptors in inflammatory diseases

[0177] Materials and Method

[0178] Primer design. CXCL9, CXCL10, CXCL11, CCRL1, CCRL2, CCR5, CCL1, CCL2, CCL3, CCL4, CCL4L1, CCL5, CCL7, CCL8, CCL14-1, CCL14-2, CCL14-3, CCL15-1, CCL15-2, CCL16, The messenger RNA sequences of CCL19, CCL23-1, CCL23-2, CCL24, CCL26, CCR6, CCL20 and CCL25, CCL25-1, CCL25-2 were obtained from the NIH-NCBI gene database (Table 1). Use BeaconJ 2.0 computer program to design primers. The computer programs Primer PremierJ and MIT Primer 3 were used for thermodynamic analysis of the primers. The resulting primer set was compared with the entire human genome to confirm specificity.

[0179] Real-time PCR analysis. Culture lymphocytes or inflammatory tissue in RMPI-1640, which contains 10% fetal bovine serum, 2% human serum, supplemented with non-essential amino acids L-glutamate and sodium pyruvate (complete medium ). In addition, primary inflammatory and nor...

Embodiment 2

[0194] Example 2: IFN-γ, CXCL10, MIG, I-TAC, CXCR3 in murine MRNA expression in colitis

[0195] figure 1 The mRNA expression of IFN-γ, CXCL10, MIG, I-TAC and CXCR3 during murine colitis is shown. IL-10 housed in a cage with a C57BL / 6 background - / - Mice remove laminar flow barrier to naturally develop colitis. After sacrifice, total RNA was isolated from the colon or mesenteric lymph nodes of the mice before the onset of colitis (sterile conditions, blank rectangular bars) and after contracting colitis (filled rectangular bars). The mRNA expression levels of IFN-γ, IP-10, MIG, I-TAC and CXCR3 were determined after RT-PCT analysis capable of detecting more than 20 copies of transcribed cDNA. in figure 1 In the Log of the transcript 10 The copy is expressed relative to the true copy of 18S rRNA.

[0196] Such as figure 1 As shown, IL-10 with colitis - / - A significant increase in the expression of CXCR3 and CXCL10 was observed in the inflamed colon of mice. Moreover, IL-10 with ...

Embodiment 3

[0197] Example 3: Accept CD45RB through inherited transfer HI Or CXCR3 + CD4 + T thin Cell TCR β x δ - / - Histological analysis of IBD in mice

[0198] Figure 2 shows the acceptance of CD45RB through inherited transfer HI Or CXCR3 + CD4 + TCR of T cells β x δ - / - Histological analysis of IBD in mice. Receive CD45RB from normal C57BL / 6 mice Lo -(Figure A), CD45RB Hi -(Figure B) or CXCR3 + -CD4 + TCR β x δ of T cells (Figure C) - / - 60x magnification of enteritis in mice. 6μm paraffin sections were stained with hematoxylin-eosin, and cross-section sections of the intestines showed differences in wall thickness, mucosal layer enlargement, crypt deformation, and leukocyte infiltration.

[0199] This analysis shows that CXCR3, which is composed of the CD45RB population + CD4 + T cells in TCR β x δ - / - Induction of colitis in mice (Figure C)

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Abstract

Methods for preventing or inhibiting inflammation in a subject are disclosed. In one aspect, the method comprises administering to a subject diagnosed with an inflammatory disease an effective amount of an anti-inflammatory agent that (1) inhibits the expression of CXCL9, CXCL10, CXCL11, CXCL13, CXCR3 and / or CXCR5, or (2) inhibits the interaction between CXCR3 and CXCL9, CXCL10 or CXCL11, or between CXCR5 and CXCLl 3, or (3) inhibits a biological activity of CXCL9, CXCL10, CXCL11, CXCL13, CXCR3 and / or CXCR5, wherein the agent comprises an antibody, antibody fragment, short interfering RNA (siRNA), aptamer, synbody, binding agent, peptide, aptamer-siRNA chimera, single stranded antisense oligonucleotide, triplex forming oligonucleotide, ribozyme, external guide sequence, or an agent-encoding expression vector.

Description

Technical field [0001] This application mainly relates to methods and compositions for inhibiting inflammation. More specifically, this application relates to the use of anti-CXCL9, anti-CXCL10, anti-CXCL11, anti-CXCL13, anti-CXCR3 and anti-CXCR5 agents and / or other anti-inflammatory agents for the prevention and treatment of inflammatory diseases . Background technique [0002] Although recent progress has been made in research related to the inflammatory process, there are still many unclear therapies for the treatment of chronic inflammatory diseases. This may be because there are many and complex factors that trigger and maintain the inflammatory state in the host. Current treatments have disadvantages associated with them, including suppression of the immune system that may make the host more susceptible to bacterial, viral and parasitic infections. For example, the use of steroids is a traditional method of treating chronic inflammation. This treatment may result in sup...

Claims

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Application Information

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IPC IPC(8): A61K39/395A61K48/00A61P29/00
CPCC07K16/24A61K2039/505A61P1/04A61P3/10A61P5/14A61P9/10A61P11/00A61P11/02A61P11/06A61P13/08A61P13/10A61P13/12A61P17/00A61P17/06A61P19/02A61P21/04A61P25/00A61P29/00A61P31/04A61P37/02A61P37/06A61P37/08
Inventor 詹姆斯·W·利拉德
Owner JYANT TECH
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