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Inflammation, Stem Cell Therapy, and Cardiac Repair
Published in Shyam S. Bansal, Immune Cells, Inflammation, and Cardiovascular Diseases, 2022
Marcus J. Wagner, Jacob T. Menzer, Sadia Mohsin
Mesenchymal stem cells produce a paracrine secretome that can directly modulate the recruitment, retention, and viability of neutrophil populations. MSC secretome is enriched in chemotactic signaling molecules CXCL1, CXCL2, CXCL5, and CXCL8 – all of which elicit neutrophil recruitment.27 Additionally, MSC-mediated production of IL-6 has been shown to directly affect neutrophil viability in co-culture systems.28 Exposure of neutrophils to MSC cultures that are deficient in IL-6 compromises neutrophil viability.29 Understanding how stem cells mediate the viability, recruitment, and phenotype of neutrophil populations in the infarcted heart can provide insight into how cell-based therapies can modulate the clearance of necrotic myocardium, cardiac rupture, and establishment of a pro-reparative state that promotes myocardial wound healing.
Inflammation and Infection
Published in Karl H. Pang, Nadir I. Osman, James W.F. Catto, Christopher R. Chapple, Basic Urological Sciences, 2021
Judith Hall, Christopher K. Harding
Newly recruited Ly6C+ macrophages produce TNF.TNF stimulates resident macrophages to secrete CXCL2.CXCL2 induces circulatory neutrophils to produce metalloproteinases, which allows them to penetrate basement membranes and move transepithelially.
Cancer Immunology
Published in John C Watkinson, Raymond W Clarke, Louise Jayne Clark, Adam J Donne, R James A England, Hisham M Mehanna, Gerald William McGarry, Sean Carrie, Basic Sciences Endocrine Surgery Rhinology, 2018
Osama Al Hamarneh, John Greenman
Immune suppressive cytokines, whether produced by tumour cells or by stromal cells, seem to control the cross-talk between cells within the TME during tumour progression (Figure 16.1). Furthermore the release of such cytokines induces ECM remodelling, basement membrane degradation, tumour cell proliferation and angiogenesis, and hence favours tumour progression and metastasis. In studies on HNSCC cell lines, fibroblasts and stromal endothelial cells have been shown to express a suppressive cytokine/chemokine milieu when co-cultured with HNSCC cells.39 CAF showed an increase in the expression of a number of pro-inflammatory cytokines and chemokines including CCL7, CXCL1, CXCL2, CXCL3 and CXCL8 when compared with CAF cultured alone.40 Similarly, type I collagen was found to markedly stimulate immune-suppressive cytokine expression such as IL-1α, IL-1β, IL-6, TNF-α, TGF-β and MMP-2 in metastatic HNSCC cell lines compared with that of the primary cancer cell lines.41
Identification of genes and miRNAs in paclitaxel treatment for breast cancer
Published in Gynecological Endocrinology, 2021
Jie Wu, Yijian Zhang, Maolan Li
CXCL2, an antimicrobial gene, is a member of the chemokine superfamily that encodes secreted proteins involved in immunoregulatory and inflammatory processes [19]. Accumulating evidence suggests that chemokines play an important role in cancer development and carcinogenesis. Ding et al. reported that the CXCL2 was downregulated in the hepatocelluar carcinoma (HCC) samples, and overexpression of CXCL2 suppressed the HCC cell proliferation and induced apoptosis; they also found CXCL2 might negatively regulate the cell cycle of HCC cells via the ERK1/2 signaling pathway [20]. Similarly, Rollins also indicated that exogenous expression of CXCL2 could suppress cell proliferation by enhancing apoptosis [21]. In the present study, paclitaxel treatment led to the increase in CXCL2 and high expression level of CXCL2 had longer survival time. Additionally, the TF–miRNA–mRNA network showed that CXCL2 was regulated by TF–FOXA2. As we known, FOXA2 has a tumor suppressor function through inhibition of pancreatic cancer cell growth and migration [22]. In addition, study pointed out that the stable overexpression of FOXA2 abolished metastasis of breast cancer cells in vivo [23]. Although the function of CXCL2 and its role in the pathophysiology of breast cancer remained to be elucidated, the above findings indicated their role in inhibiting cancer cell growth. Taken together, we speculated paclitaxel might play a therapeutic role via regulating CXCL2 expression.
Cryptotanshinone enhances wound healing in type 2 diabetes with modulatory effects on inflammation, angiogenesis and extracellular matrix remodelling
Published in Pharmaceutical Biology, 2020
Min Song, Lu Chen, Lusha Zhang, Chunxiao Li, Joel Wake Coffie, Zhirui Fang, Liyuan Zhang, Shaoxia Wang, Xiumei Gao, Hong Wang
Appropriate inflammatory response can promote cell recruitment and tissue regeneration. However, excessive inflammatory response will lead to delayed wound healing in diabetes. To verify whether CT could inhibit the excessive inflammatory response, CD45 staining and relative gene expression were detected by immunohistochemistry and qRT-PCR. The results showed that leukocyte infiltrates were significantly decreased in group receiving CT (Figure 3(A)). CXCL1 and CXCL2 are pro-inflammatory chemokines, which are expressed in inflammatory stage of wound healing. Inhibition of inflammatory cytokines is a main principle for diabetic wounds treatment in the whole process of therapy. CT can significantly reduce the expression of CXCL1 and CXCL2 at day 16 post-injury compared with those in vehicle group (Figure 3(B–E); p < 0.01 or p < 0.001, respectively), which is compatible with the reduction of the lesion observed in Figure 1, indicating CT may accelerate wound healing through inhibiting inflammation.
Staphylococcus aureus infected embolic stroke upregulates Orm1 and Cxcl2 in a rat model of septic stroke pathology
Published in Neurological Research, 2019
Lærke Boye Astrup, Kerstin Skovgaard, Rune Skovgaard Rasmussen, Tine Moesgaard Iburg, Jørgen Steen Agerholm, Bent Aalbæk, Henrik Elvang Jensen, Ole Lerberg Nielsen, Flemming Fryd Johansen, Peter Mikael Helweg Heegaard, Páll Skúli Leifsson
As mentioned Cxcl2 is as powerful chemoattracants for neutrophils, possibly explaining its role in abscess formation [8]. Thus both abscess formation and increased mortality in the septic group may be directly linked to pro-inflammatory actions of especially Orm1 and Cxcl2.