Association of CCL11, CCL24 and CCL26 with primary biliary cholangitis

Lin, Feng; Shi, Hong; Liu, Donghong; Zhang, Zhencheng; Luo, Wanwan; Mao, Panying; Zhong, Renqian; Liang, Yan; Yang, Zaixing

doi:10.1016/j.intimp.2018.12.026

Cited by 9 publications

(10 citation statements)

References 17 publications

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“…Likewise, our study illustrated that the plasma level of CCL26 was approximately 3 times higher in PBC patients than that in healthy volunteers. This profound up‐regulation of CCL26 in PBC patients has also been identified in prior reports, suggesting potential significance of CCL26 in PBC 20,21 . In 2019, Lin et al found a negative correlation between serum CCL26 and fibrosis indicators in PBC patients 21 .…”

Section: Discussionsupporting

confidence: 73%

“…This profound up‐regulation of CCL26 in PBC patients has also been identified in prior reports, suggesting potential significance of CCL26 in PBC 20,21 . In 2019, Lin et al found a negative correlation between serum CCL26 and fibrosis indicators in PBC patients 21 . Considering the limited number of subjects with liver fibrosis and lack of data regarding fibrosis indicators, this study could not evaluate the association of CCL26 with PBC staging or fibrosis progression.…”

Section: Discussionmentioning

confidence: 56%

“…In 2010, chemokine CCL26 was found to be another functional ligand to CX3CR1 19 . Previous literature reported a significantly higher serum level of CCL26 in PBC patients compared with healthy volunteers and patients with chronic hepatitis B or hepatitis C infection, suggesting the possibility of CCL26 being involved in the pathogenesis of PBC 20,21 . However, studies regarding the role of CCL26 in the immune mechanism of PBC are scarce.…”

Section: Introductionmentioning

confidence: 99%

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CCL26 in primary biliary cholangitis – Is it a novel disease mediator?

et al. 2023

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Aim:To verify the role of CX3C chemokine ligand 1 -CX3C chemokine receptor 1 (CX3CL1-CX3CR1) pathway in the pathogenesis of primary biliary cholangitis (PBC).To explore whether CCL26, a novel functional ligand to CX3CR1, participates in the immunological mechanism of PBC.Methods: Fifty-nine PBC patients and 54 healthy controls were recruited. Enzymelinked immunosorbent assay and flow cytometry were used to measure CX3CL1 and CCL26 concentrations in plasma and CX3CR1 expression on peripheral lymphocytes, respectively. Chemotactic effects of CX3CL1 and CCL26 toward lymphocytes were detected by Transwell cell migration assays. CX3CL1 and CCL26 expressions in liver were assessed by immunohistochemical staining. Effects of CX3CL1 and CCL26 on stimulating cytokine production from lymphocytes were evaluated using intracellular flow cytometry.Results: Significantly elevated CX3CL1 and CCL26 plasma concentration and CX3CR1 expression on CD4 + and CD8 + T cells were noted in PBC patients. CX3CL1 exhibited chemotactic activity toward CD8 + T, natural killer (NK) and NKT cells in a dosedependent manner while such chemotactic effects were not detected for CCL26. In PBC patients, CX3CL1 and CCL26 were both increasingly expressed in biliary tracts and a concentration gradient of CCL26 in hepatocytes around portal areas was observed. Immobilized CX3CL1 could enhance interferonγ production from T and NK cells while such effect was not exhibited by soluble CX3CL1 or CCL26.Conclusions: CCL26 expression is significantly elevated in plasma and biliary duct of PBC patients, yet does not appear to attract CX3CR1-expressing immune cells. CX3CL1-CX3CR1 pathway promotes the infiltration of T, NK and NKT cells into bile ducts and forms a positive feedback loop with T-helper 1 type cytokines in PBC.

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Section: Discussionsupporting

confidence: 73%

Section: Discussionmentioning

confidence: 56%

Section: Introductionmentioning

confidence: 99%

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CCL26 in primary biliary cholangitis – Is it a novel disease mediator?

et al. 2023

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“…Therefore, the identification of crucial autocrine inflammatory factors could aid the identification of potential targets and inhibitors to block the regulatory loop that continuously activates intratumoral pathways 13 . C-C motif chemokine ligand 24 (CCL24, also named eotaxin-2), a type of inflammatory chemokine, has been reported to be associated with various diseases, such as primary biliary cholangitis, allergies, and eosinophilic esophagitis 14,15 . Furthermore, CCL24 is strongly associated with primary and metastatic tumors of colorectal origin and the poor prognosis of patients, and serves as a potential target in immune therapy 16 .…”

Section: Introductionmentioning

confidence: 99%

Blocking the autocrine regulatory loop of Gankyrin/STAT3/CCL24/CCR3 impairs the progression and pazopanib resistance of clear cell renal cell carcinoma

Wang

Hong

et al. 2020

Cell Death Dis

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The poor prognosis of clear-cell renal cell carcinoma (ccRCC) patients is due to progression and targeted drug resistance, but the underlying molecular mechanisms need further elucidation. This study examined the biological function and related mechanisms of gankyrin in ccRCC based on the results of our previous study. To this end, in vitro functional experiments; in vivo models of subcutaneous tumor formation, lung metastasis, and orthotopic ccRCC; and antibody chip detection, co-IP, ChIP assays were performed to examine the biological role and molecular mechanisms of gankyrin in ccRCC. Two hundred fifty-six ccRCC patients were randomly divided into training and validation cohorts to examine the prognostic value of gankyrin and other markers through IHC and statistical analyses. We observed that the gankyrin-overexpressing ccRCC cell lines 786-O and 769-P exhibited increased proliferation, invasion, migration, tumorigenicity, and pazopanib resistance and decreased apoptosis, while gankyrin knockdown achieved the opposite results. Mechanistically, gankyrin recruited STAT3 via direct binding, and STAT3 binding to the CCL24 promoter promoted its expression. Reciprocally, an increase in autocrine CCL24 enhanced the expression of gankyrin and STAT3 activation via CCR3 in ccRCC, forming a positive autocrine-regulatory loop. Furthermore, in vivo experimental results revealed that blocking the positive loop through gankyrin knockdown or treatment with the CCR3 inhibitor SB328437 reversed the resistance to pazopanib and inhibited lung metastasis in ccRCC. Moreover, a positive correlation between gankyrin and STAT3 or CCL24 expression in ccRCC specimens was observed, and improved accuracy for ccRCC patient prognosis was achieved by combining gankyrin and STAT3 or CCL24 expression with existing clinical prognostic indicators, including the TNM stage and SSIGN score. In summary, targeting the gankyrin/STAT3/CCL24/CCR3 autocrine-regulatory loop may serve as a remedy for patients with advanced ccRCC, and combining gankyrin and STAT3 or CCL24 expression with the current clinical indicators better predicts ccRCC patient prognosis.

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“…CCL3, CCL4, and CCL5 promote macrophage and natural killer (NK) cell chemotaxis [ 43 , 44 ]. CCL11 and CCL24 promote inflammatory monocyte chemotaxis [ 45 ]. Other chemokines, such as CXCL1, CXCL2, and CXCL5, promote the chemotactic migration of neutrophils [ 46 ].…”

Section: Discussionmentioning

confidence: 99%

Transcriptome analysis of a newly established mouse model of Toxoplasma gondii pneumonia

et al. 2023

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Background Toxoplasmosis is a zoonotic parasitic disease caused by Toxoplasma gondii. Toxoplasma gondii infection of the lungs can lead to severe pneumonia. However, few studies have reported Toxoplasma pneumonia. Most reports were clinical cases due to the lack of a good disease model. Therefore, the molecular mechanisms, development, and pathological damage of Toxoplasma pneumonia remain unclear. Methods A mouse model of Toxoplasma pneumonia was established by nasal infection with T. gondii. The model was evaluated using survival statistics, lung morphological observation, and lung pathology examination by hematoxylin and eosin (H&E) and Evans blue staining at 5 days post-infection (dpi). Total RNA was extracted from the lung tissues of C57BL/6 mice infected with T. gondii RH and TGME49 strains at 5 dpi. Total RNA was subjected to transcriptome analysis by RNA sequencing (RNA-seq) followed by quantitative real-time polymerase chain reaction (qRT–PCR) validation. Transcript enrichment analysis was performed using the Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) databases to assess the biological relevance of differentially expressed transcripts (DETs). Results C57BL/6 mice infected with T. gondii via nasal delivery exhibited weight loss, ruffled fur, and respiratory crackles at 5 dpi. The clinical manifestations and lethality of RH strains were more evident than those of TGME49. H&E staining of lung tissue sections from mice infected with T. gondii at 5 dpi showed severe lymphocytic infiltration, pulmonary edema, and typical symptoms of pneumonia. We identified 3167 DETs and 1880 DETs in mice infected with the T. gondii RH and TGME49 strains, respectively, compared with the phosphate-buffered saline (PBS) control group at 5 dpi. GO and KEGG enrichment analyses of DETs showed that they were associated with the immune system and microbial infections. The innate immune, inflammatory signaling, cytokine-mediated signaling, and chemokine signaling pathways displayed high gene enrichment. Conclusion In this study, we developed a new mouse model for Toxoplasma pneumonia. Transcriptome analysis helped to better understand the molecular mechanisms of the disease. These results provided DETs during acute T. gondii lung infection, which expanded our knowledge of host immune defenses and the pathogenesis of Toxoplasma pneumonia. Graphical Abstract

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Association of CCL11, CCL24 and CCL26 with primary biliary cholangitis

Cited by 9 publications

References 17 publications

CCL26 in primary biliary cholangitis – Is it a novel disease mediator?

CCL26 in primary biliary cholangitis – Is it a novel disease mediator?

Blocking the autocrine regulatory loop of Gankyrin/STAT3/CCL24/CCR3 impairs the progression and pazopanib resistance of clear cell renal cell carcinoma

Transcriptome analysis of a newly established mouse model of Toxoplasma gondii pneumonia

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