Oral Cell Lysates Reduce the Inflammatory Response of Activated Macrophages

Panahipour, Layla; Abbasabadi, Azarakhsh Oladzad; Gruber, Reinhard

doi:10.3390/jcm12041701

Cited by 3 publications

(3 citation statements)

References 32 publications

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“…For instance, in immortalized human oral keratinocytes, LPS from p. gingivalis caused a robust increase of CXCL1, CXCL8, and CCL20 [ 55 ], and in OKF6/TERT-2 oral keratinocytes, LPS increased IL6 [ 56 ]. In our in vitro setting, however, LPS at 100 ng/mL from E. coli [ 57 ] and 1 µg/mL from P. gingivalis [ 48 ] failed to considerably change chemokines in HSC2 cells, comparable to findings observed by others with the same cell line [ 58 ]. This lack of LPS response might be explained by the fact that HSC2 cells, similar to other oral epithelial cells, do not express relevant CD14 required for the LPS-induced signaling via TLR4 [ 59 , 60 ].…”

Section: Discussionsupporting

confidence: 86%

Enamel Matrix Derivative Suppresses Chemokine Expression in Oral Epithelial Cells

Panahipour,

Botta,

Abbasabadi

et al. 2023

IJMS

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Epithelial cells in periodontitis patients increasingly express chemokines, suggesting their active involvement in the inflammatory process. Enamel matrix derivative (EMD) is an extract of porcine fetal tooth germs clinically applied to support the regrowth of periodontal tissues. Periodontal regeneration might benefit from the potential anti-inflammatory activity of EMD for epithelial cells. Our aim was, therefore, to set up a bioassay where chemokine expression is initiated in the HSC2 oral squamous carcinoma cell line and then test EMD for its capacity to lower the inflammatory response. To establish the bioassay, HSC2 cells being exposed to TNFα and LPS from E. coli (Escherichia coli) or P. gingivalis (Porphyromonas gingivalis) were subjected to RNAseq. Here, TNFα but not LPS caused a robust increase of chemokines, including CXCL1, CXCL2, CXCL8, CCL5, and CCL20 in HSC2 cells. Polymerase chain reaction confirmed the increased expression of the respective chemokines in cells exposed to TNFα and IL-1β. Under these conditions, EMD reduced the expression of all chemokines at the transcriptional level and CXCL8 by immunoassay. The TGF-β receptor type I kinase-inhibitor SB431542 reversed the anti-inflammatory activity. Moreover, EMD-activated TGF-β-canonical signaling was visualized by phosphorylation of smad3 and nuclear translocation of smad2/3 in HSC2 cells and blocked by SB431542. This observation was confirmed with primary oral epithelial cells where EMD significantly lowered the SB431542-dependent expression of CXCL8. In summary, our findings suggest that TGF-β signaling mediates the effects of EMD to lower the forced expression of chemokines in oral epithelial cells.

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Section: Discussionsupporting

confidence: 86%

Enamel Matrix Derivative Suppresses Chemokine Expression in Oral Epithelial Cells

Panahipour,

Botta,

Abbasabadi

et al. 2023

IJMS

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“…There is thus a rational to make DAMPs activating TLR4 signaling in bone marrow cells responsible for the blocking of osteoclastogenesis. However, this is unlikely as the respectively lysates reduce LPS-induced in ammatory response of RAW264.7 macrophages in vitro (43). Thus, the molecular mechanisms of how the lysates reduce in vitro osteoclastogenesis remains puzzling.…”

Section: Discussionmentioning

confidence: 99%

Oral cell lysates reduce osteoclastogenesis in murine bone marrow cultures

Panahipour

Abbasabadi

Shao

et al. 2023

Preprint

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Mechanical and thermal cell damage can occur as a consequence of invasive procedures related to drilling, the insertion of dental implants, as well as periodontal treatments. Necrotic cells release the content of their cytoplasm and membrane fragments thereby signaling the need for repair, a process that includes bone resorption by osteoclasts and inflammation. Here we screened lysates from human gingival fibroblasts, HSC2 and TR146 oral squamous carcinoma cell lines, as well as murine IDG-SW3 osteocytic and RAW264.7 macrophage cell lines for their potential to modulate in vitro osteoclastogenesis in murine bone marrow cultures. We also tested the impact of necrotic lysates to modulate the expression of inflammatory cues in murine ST2 bone marrow stromal cells. We report here that independent of human or murine origin, all cell lysates significantly reduced in vitro osteoclastogenesis in bone marrow cultures; as indicated by the expression of the osteoclast marker genes cathepsin K and tartrate-resistant acid phosphatase, and the respective histochemical staining in multinucleated cells. We also found that lysates from HSC2 and TR146 cells greatly pushed the expression of CCL2, CCL5, CXCL1, IL1, and IL6 in ST2 cells. These findings suggest that oral cell lysates reduce in vitro osteoclastogenesis but only damaged oral squamous carcinoma cells can force stromal cells to produce an inflammatory environment.

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“…In vitro, platelet-tumor interactions have been studied with Ca9.22 and HSC3 cells originating from OSCC [26]. We have previously implemented our established oral squamous carcinoma cell line HSC2 as a bioassay for testing the responsiveness to lysates prepared from PRF membranes, however, in the context of inflammation research [27,28]. Today's attempts to assess the response of HSC2 and other cell types to PRF lysates are based on RNA sequencing, an omics technology that provides insight into how the genetic signature of cells changes [29].…”

Section: Introductionmentioning

confidence: 99%

PRF Lysates Enhance the Proliferation and Migration of Oral Squamous Carcinoma Cell Lines

Panahipour,

Croci,

Guarnieri

et al. 2023

Dentistry Journal

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Platelet-rich fibrin (PRF) is an autologous fibrin-rich matrix where activated platelets and leucocytes accumulate. PRF has a wide spectrum of clinical indications with the overall aim of supporting tissue regeneration which in dentistry includes the healing of healthy oral mucosa with epithelial cells. In oral squamous cell carcinoma lesions, however, epithelial cells undergo malignant transformation, indicated by their unrestricted proliferation and migration potential, which should not be further enhanced by a wound-healing formula. Yet, little is known about how oral squamous cell carcinomas respond to PRF lysates. The aim of the present study was, therefore, to test the capacity of PRF lysates to change the transcriptome of HSC2 oral squamous carcinoma cells and perform bioassays to support the findings. Based on the RNAseq analysis, PRF lysates caused an increase in the genes functionally linked to cell replication and migration. In support of this screening approach, PRF lysates enhanced the proliferation of HSC2 oral squamous carcinoma cells, as indicated by 3[H]-thymidine incorporation, cell counting, and the expression of proliferation-related genes. Moreover, PRF lysates sped up cell migration in a scratch assay requiring actin polymerization. Taken together, our data showing that PRF lysates are mitogenic and stimulate motility of oral squamous carcinoma cell lines could be an indication that treatment with PRF in cases of oral carcinoma should be carefully considered.

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Oral Cell Lysates Reduce the Inflammatory Response of Activated Macrophages

Cited by 3 publications

References 32 publications

Enamel Matrix Derivative Suppresses Chemokine Expression in Oral Epithelial Cells

Enamel Matrix Derivative Suppresses Chemokine Expression in Oral Epithelial Cells

Oral cell lysates reduce osteoclastogenesis in murine bone marrow cultures

PRF Lysates Enhance the Proliferation and Migration of Oral Squamous Carcinoma Cell Lines

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