The Role of Heparan Sulfate in CCL26-Induced Eosinophil Chemotaxis

Pum, Alexandra; Ennemoser, Maria; Gerlza, Tanja; Kungl, Andreas J.

doi:10.3390/ijms23126519

Cited by 4 publications

(3 citation statements)

References 53 publications

(58 reference statements)

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“…As both chemokines have similar HS binding but different TNC binding affinities, we speculate that TNC acts as an attenuator in monocyte (PBMC) and as an amplifier in eosinophil mobilization by preventing CCL2 from binding to HS on the one hand and by enabling CCL26 to bind to HS on the other [62,63]. This is supported by our recent finding that HS on monocytes as well as eosinophils is important for chemotaxis [52,53]. The different TNC binding affinities of the two chemokines might thus suggest different binding sites on TNC.…”

Section: Chemotaxissupporting

confidence: 70%

“…We have recently shown that GAGs present on target immune cells contribute to chemotaxis, in addition to GAGs located at the site of vessels where immune cells extravasate into affected tissues [52,53]. Chemokine secretion, immobilization, and receptor activation are apparently mediated by GAGs situated on both sites of the immunological reaction, that is, on the epithelial/endothelial vessel cells as well as on the blood-resident immune cells.…”

Section: Introductionmentioning

confidence: 99%

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Chemokine Binding to Tenascin-C Influences Chemokine-Induced Immune Cell Migration

Domaingo,

Jokesch,

Schweiger

et al. 2023

IJMS

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Tenascin-C (TNC) is a complex glycoprotein of the extracellular matrix (ECM) involved in a plethora of (patho-)physiological processes, such as oncogenesis and inflammation. Since chemokines play an essential role in both disease processes, we have investigated here the binding of TNC to some of the key chemokines, namely CCL2, CCL26, CXCL8, CXCL10, and CXCL12. Thereby, a differential chemokine-TNC binding pattern was observed, with CCL26 exhibiting the highest and CCL2 the lowest affinity for TNC. Heparan sulfate (HS), another member of the ECM, proved to be a similarly high-affinity ligand of TNC, with a Kd value of 730 nM. Chemokines use glycosa-minoglycans such as HS as co-receptors to induce immune cell migration. Therefore, we assumed an influence of TNC on immune cell chemotaxis due to co-localization within the ECM. CCL26- and CCL2-induced mobilization experiments of eosinophils and monocytes, respectively, were thus performed in the presence and the absence of TNC. Pre-incubation of the immune cells with TNC resulted in a 3.5-fold increase of CCL26-induced eosinophil chemotaxis, whereas a 1.3-fold de-crease in chemotaxis was observed when monocytes were pre-incubated with CCL2. As both chemokines have similar HS binding but different TNC binding affinities, we speculate that TNC acts as an attenuator in monocyte and as an amplifier in eosinophil mobilization by impeding CCL2 from binding to HS on the one hand, and by reinforcing CCL26 to bind to HS on the other hand.

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Section: Chemotaxissupporting

confidence: 70%

Section: Introductionmentioning

confidence: 99%

Chemokine Binding to Tenascin-C Influences Chemokine-Induced Immune Cell Migration

Domaingo,

Jokesch,

Schweiger

et al. 2023

IJMS

Self Cite

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“…Chemokine ligand 26 (CCL26) interacts with CCR3 to attract eosinophils to sites of in ammation [13] and mediates trans-endothelial migration of eosinophils by binding to and activating G protein-coupled (GPC) chemotaxis of CCR3 on the surface of eosinophils [14]. It was found that signi cantly elevated levels of the CCL26 gene were found in eosinophilia-related diseases.…”

Section: Discussionmentioning

confidence: 99%

RNA-seq analysis of chlorogenic acid intervention in duck embryo fibroblasts infected with duck plague virus

Yang,

Zhang,

Cai

et al. 2023

Preprint

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Introduction Chlorogenic acid is the main active ingredient of honeysuckle, with anti-inflammatory and antiviral effects. At present, duck plague virus causes a large number of waterfowl disease, seriously affecting the development of the breeding industry, there is an urgent need for the prevention and treatment of drugs with unique efficacy. Methods In order to investigate the effect of chlorogenic acid on duck embryo fibroblasts infected with duck plague virus, in this study, maintenance medium containing different final concentrations of chlorogenic acid (0, 0.125, 0.250, 0.500, 1.000, 2.000, and 4.000 mg/mL) was added to 96-well plates, and the plates were incubated for 24 h, and cellular activity was measured by using a CCK-8 kit in order to determine the safe concentration of the drug; cell control group, chlorogenic acid control group, virus-infected group, and chlorogenic acid intervention group were set up. Cell control group, chlorogenic acid control group, virus-infected group and chlorogenic acid intervention group were set up. Cell samples were collected at 24 h, 36 h and 48 h after treatment. qRT-PCR was used to detect the viral content, and transcriptomic sequencing was used to screen the differentially expressed genes, and GO functional classification and KEGG signaling pathway analysis were utilized; In addition, 90 ducks were randomly divided into blank control group, virus infection group and chlorogenic acid intervention group. Ducks in virus infection group and chlorogenic acid intervention group were injected with DPV (0.2 mL/only) and chlorogenic acid intervention group were manually dosed with 0.6±0.02 g chlorogenic acid capsule at the same time until the end of the experiment in 5 d. Clinical symptoms were observed every day and 10 ducks were killed in each group at 24 h, 36 h and 48 h after the infection. At 24 h, 36 h and 48 h after infection, 10 ducks were killed, and samples of each immune organ were collected aseptically for the preparation of pathological sections and the detection of DPV load by fluorescence quantitative PCR. Ducks were observed for the clinical symptoms every day, and 10 ducks were dissected and killed in each group at 24 h, 36 h and 48 h, respectively, and the samples of each immune organ were collected in aseptic condition. The samples were collected aseptically from each immune organ for the preparation of pathological sections and the load of DPV was detected by fluorescence quantitative PCR. Results CCK-8 assay showed that the highest cellular activity was observed at a chlorogenic acid concentration of 0.250 mg/mL. qRT-PCR assay showed that DPV load in DEF cells after chlorogenic acid intervention showed a significant decrease compared with that of the DEV-infected group. IL-16, CHCHD10, ROR2 and GNG10 were down-regulated, while TNFSF15 expression was up-regulated, and it was basically consistent with the qRT-PCR validation results; GO and KEGG analyses showed that chlorogenic acid inhibited DPV proliferation in DEF cells by up-regulating the activity of the Toll-like receptor signaling pathway, the TNF signaling pathway and by down-regulating the NF-κB signaling pathway. CCK-8 assay showed that the safe concentration of chlorogenic acid drug was 0.250 mg/mL; qRT-PCR assay showed that DPV load in DEF cells after chlorogenic acid intervention appeared to be significantly decreased from the DPV-infected group (P<0.05); transcriptomics sequencing showed that there were 8 differential genes in the chlorogenic acid intervention group, among which TNFAIP2, IFNAR1, CCL26, IL-16, CHCHD10, ROR2 and GNG10 expression was down-regulated, while TNFSF15 expression was up-regulated, and it was basically consistent with the results of qRT-PCR validation; GO and KEGG analyses showed that chlorogenic acid inhibited DPV proliferation in DEF cells through up-regulation of the Toll-like receptor signaling pathway, the activity of the TNF signaling pathway, and down-regulation of the NF-κB signaling pathway Histopathological observation showed that compared with the DPV-infected group, the damage of all immune organs in the ducks in the chlorogenic acid intervention group was reduced to different degrees, and the lesions such as cellular nuclear consolidation and nuclear fragmentation were alleviated; in vivo fluorescence quantitative PCR results showed that compared with the DPV-infected group, the DPV load in all immune organs in the ducks in the chlorogenic acid intervention group was decreased. Conclusions This study provides a theoretical basis for the screening of targeted anti-DPV drugs and a scientific basis for the clinical guidance of drug administration.

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Heparan sulfates and heparan sulfate proteoglycans in hematopoiesis

Piszczatowski,

Bülow,

Steidl

2024

Blood

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From signaling mediators in stem cells, to markers of differentiation and lineage commitment, to facilitators for the entry of viruses like HIV-1, cell surface heparan sulfate (HS) glycans with their distinct modification patterns play important roles in hematopoietic biology. In this review, we provide an overview of the importance of HS and the proteoglycans (HSPGs) to which they are attached, within the major cellular subtypes of the hematopoietic system. We summarize the roles of HSPGs, HS, and HS modifications within each main hematopoietic cell lineage of both myeloid and lymphoid arms. Lastly, we discuss the biological advances of the detection of HS modifications, and their potential to further discriminate cell types within hematopoietic tissue.

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The Role of Heparan Sulfate in CCL26-Induced Eosinophil Chemotaxis

Cited by 4 publications

References 53 publications

Chemokine Binding to Tenascin-C Influences Chemokine-Induced Immune Cell Migration

Chemokine Binding to Tenascin-C Influences Chemokine-Induced Immune Cell Migration

RNA-seq analysis of chlorogenic acid intervention in duck embryo fibroblasts infected with duck plague virus

Heparan sulfates and heparan sulfate proteoglycans in hematopoiesis

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