scholarly journals The use of Dermacell® in Fingertip Injury

2019 ◽  
Vol 1 (2) ◽  
pp. 14-22 ◽  
Author(s):  
Wu, Tsung-Hsuan ◽  
Giampietro Bertasi
Keyword(s):  
Immune Response ◽  
Collagen Scaffold ◽  
Tissue Scaffolds ◽  
Cellular Growth ◽  
Collagen Structure ◽  
Tissue Remodelling ◽  
Fingertip Injury ◽  
Viable Cells ◽  
Native Collagen ◽  
Immunogenic Response

Matrices or tissue scaffolds provide a collagen structure for tissue remodelling while the removal of viable cells aims to minimize or prevent inflammatory or immunogenic response. Allograft collagen scaffold can support the patient’s own cellular ingrowth, ingeneered to minimize an immune response and to yeld a bio-compatible matrix and support incoming cellular growth. The decellyularized dermis retains its growth factors, native collagen scaffold, and elastin, thanks to a LifeNet Health proprietaryprocessin technology.

scholarly journals Kaposi's Sarcoma-Associated Herpesvirus Inhibits Interleukin-4-Mediated STAT6 Phosphorylation To Regulate Apoptosis and Maintain Latency

2010 ◽  
Vol 84 (21) ◽  
pp. 11134-11144 ◽  
Author(s):  
Qiliang Cai ◽  
Subhash C. Verma ◽  
Ji-Young Choi ◽  
Michelle Ma ◽  
Erle S. Robertson
Keyword(s):  
Immune Response ◽  
Kaposi's Sarcoma ◽  
Primary Effusion Lymphoma ◽  
Kaposi’S Sarcoma ◽  
Cellular Growth ◽  
Interleukin 4 ◽  
Nuclear Antigen ◽  
Viral Agent ◽  
Kaposi's Sarcoma Associated Herpesvirus ◽  
Kaposi’S Sarcoma Associated Herpesvirus

ABSTRACT Cytokine-mediated JAK/STAT signaling controls numerous important biologic responses like immune function, cellular growth, and differentiation. Inappropriate activation of this signaling pathway is associated with a range of malignancies. Kaposi's sarcoma-associated herpesvirus (KSHV) is the infectious viral agent associated with Kaposi's sarcoma and may also contribute to B-cell disorders, which include primary effusion lymphoma (PEL) and multicentric Castleman's disease. However, regulation of cytokine-mediated lymphocytic immune response by KSHV is not fully understood. In this report, we demonstrate that KSHV suppresses the interleukin-4 (IL-4)-stimulated immune response of B-lymphocyte activation and cell proliferation. Moreover, we show that the latency-associated nuclear antigen (LANA) encoded by KSHV is essential for viral blocking of IL-4-induced signaling. LANA reduces phosphorylation of the signal transducers and activators of transcription 6 (STAT6) on Y-641 and concomitantly its DNA binding ability. Importantly, knockdown of endogenous STAT6 dramatically increases the sensitivity of PEL cells to low-serum stress or chemical-mediated cellular apoptosis and reactivation of KSHV from latent replication. Thus, these findings suggest that the IL-4/STAT6 signaling network is precisely controlled by KSHV for survival, maintenance of latency, and suppression of the host cytokine immune response of the virus-infected cells.

scholarly journals Specific immune response in neonate Holstein heifer calves fed fresh or frozen colostrum

2017 ◽  
Vol 37 (12) ◽  
pp. 1385-1394 ◽  
Author(s):  
Sylvia M.F. Novo ◽  
Juliana F. dos R. Costa ◽  
Camila C. Baccili ◽  
Natália M. Sobreira ◽  
Milena A. Maia ◽  
...  
Keyword(s):  
Immune Response ◽  
Cytokine Production ◽  
Clinical History ◽  
Immune Memory ◽  
Steady Increase ◽  
Peripheral Blood Mononuclear ◽  
Whole Cell ◽  
E Coli ◽  
Cell Antigen ◽  
Viable Cells

ABSTRACT: The objective of this study was to evaluate the influence of viable cells from colostrum on immune development in dairy heifer calves during the first 28 days of life. The animals were distributed between 2 groups: COL+ (n=9) receiving fresh whole colostrum from their own damns; and COL- (n=10) receiving pooled frozen colostrum, containing no viable cells, from a pool of donor cows. These calves were assessed before colostrum intake (D0), 48 hours of age (D2), and weekly from D7 to D28. The development of immunity was evaluated by assessment of the phenotype of blood leukocyte subsets, and induced cytokine production after 72 hours of stimulation in culture with concanavalin A (ConA), killed Staphylococcus aureus (S.aureus) and killed Escherichia coli (E. coli) by peripheral blood mononuclear cell (PBMC). The clinical history of these calves was marked by a high frequency of diarrhea in both groups. However, COL- had greater diarrhea intensity scores (fecal score~3 of 4), and rectal temperature on D7 than COL+ calves. Moreover, bronchopneumonia (n=1) and navel inflammation were observed only in COL- calves. COL- had a lower concentration of serum iron, and a higher absolute number of lymphocytes on D7 than COL+. COL- also had a higher percentage of anemic calves than the COL+ calves on D21 and D28. In general, the percent of cells within each subset of leukocytes was similar between the groups over the experiment, except on week 1 when COL- calves had a higher percentage of lymphocytes expressing CD45RO+ (P=0.07). A steady increase in CD45RO+ and concomitant decline in CD45RO- leukocytes was observed over the course of the study, indicating the development of immune memory. The proportion of CD14MHCII+ leukocytes increased with age (P≤0.05). The median background cytokine production by PBMC that were not stimulated was below the level of detection of the assays used for both groups. The PBMC from COL+ calves stimulated with ConA secreted a larger quantity of IL-17 week 2 (COL+=2060.0pg/mL and COL-=0.0pg/mL, P=0.00). PBMC from COL+ calves stimulated with killed S. aureus whole cell antigen (P=0.05) and killed E. coli whole cell antigen (P=0.05) also secreted higher levels of IL17 than COL- calves at week 4. Clear production of IL17 was observed in PBML from COL+ calves at week 2, but the difference was not statistical different between groups. In conclusion, calves fed fresh and frozen colostrum showed no difference in cells subset profile overall. The increased percentage of leukocytes expressing the memory CD45RO+ or CD14MHCII+ over the course of the experiment indicated a maturation of the adaptive immune response after natural exposure to pathogens in the environment of the calf. The enhanced IL17 secretion by COL+ calves indicated that viable maternal cells modulated T-cell Th17 production that was primed by bacterial antigens. This mechanism could be responsible for quick and efficient activation of neutrophils for bacterial clearance. The differences in cytokine production observed between groups may help to explain the different clinical pictures observed for calves COL+ and COL- calves.

Collagenous Biocomposites for the Repair of Soft Tissue Injury

1991 ◽  
Vol 252 ◽  
Author(s):  
David Christiansen ◽  
George Pins ◽  
Ming Che Wang ◽  
Michael G. Dunn ◽  
Frederick H. Silver
Keyword(s):  
Tissue Regeneration ◽  
Type I Collagen ◽  
Tissue Injury ◽  
Soft Tissue Injury ◽  
Collagen Scaffold ◽  
High Strength ◽  
Tissue Scaffolds ◽  
Animal Tissue ◽  
Type I ◽  
Tissue Models

ABSTRACTResults of implantation studies in a variety of animal tissue models demonstrate that the rate of biogradation of a collagen scaffold should parallel the rate of wound healing observed in particular anatomic sites. This rapid degradation maximizes tissue regeneration and minimizes encapsulation of the implant. The following paper reviews the effects of crosslinking on the rate of tissue ingrowth and regeneration. In addition, preliminary mechanical data on newly developed soluble type I collagen fibers is presented as a possible advance in the production of high strength collagen based tissue scaffolds.

scholarly journals Glycosaminoglycan content of a mineralized collagen scaffold promotes mesenchymal stem cell secretion of factors to modulate angiogenesis and monocyte differentiation

2021 ◽  
Author(s):  
Marley J Dewey ◽  
Vasiliki Kolliopoulos ◽  
Mai Ngo ◽  
Brendan Harley
Keyword(s):  
Immune Response ◽  
Collagen Scaffold ◽  
Bone Defects ◽  
Tube Formation ◽  
Osteogenic Potential ◽  
Monocyte Differentiation ◽  
Endogenous Production ◽  
Endothelial Tube Formation ◽  
Mineralized Collagen

Effective design of biomaterials to aid regenerative repair of craniomaxillofacial (CMF) bone defects requires approaches that modulate the complex interplay between exogenously added progenitor cells and cells in the wound microenvironment, such as osteoblasts, osteoclasts, endothelial cells, and immune cells. We are exploring the role of the glycosaminoglycan (GAG) content in a class of mineralized collagen scaffolds recently shown to promote osteogenesis and healing of craniofacial bone defects. We previously showed that incorporating chondroitin-6-sulfate or heparin improved mineral deposition by seeded human mesenchymal stem cells (hMSCs). However, improved healing requires angiogenic processes as well as an immune response. Here, we examine the effect of varying scaffold GAG content on hMSC behavior, specifically with regards to their ability to act as endogenous factories of biomolecules that modulate processes associated with osteoclastogenesis, vasculogenesis, and the immune response. We report the role of hMSC-conditioned media produced in mineralized scaffolds containing chondroitin-6-sulfate (CS6), chondroitin-4-sulfate (CS4), or heparin (Heparin) GAGs on biomarkers of endothelial tube formation and monocyte differentiation towards macrophage and osteoclast lineages. Notably, endogenous production by hMSCs within Heparin scaffolds most significantly inhibits osteoclastogenesis via secreted osteoprotegerin (OPG), while the secretome generated by CS6 scaffolds reduced pro-inflammatory immune response and increased endothelial tube formation. Modulation of endogenous factor production by seeded hMSCs via scaffold GAG content is sufficient to down-regulate many pro- and anti-inflammatory cytokines, such as IL6, IL-1β, and CCL18 and CCL17 respectively. Together, these findings demonstrate that modifying mineralized collagen scaffold GAG content can both directly (hMSC activity) and indirectly (endogenous production of secreted factors) influence overall osteogenic potential and mineral biosynthesis as well as angiogenic potential and monocyte differentiation towards osteoclastic and macrophage lineages. Scaffold GAG content is therefore a powerful stimulus to modulate reciprocal signaling between multiple cell populations within the bone healing microenvironment.

scholarly journals Shape-memory collagen scaffold for enhanced cartilage regeneration: native collagen versus denatured collagen

2018 ◽  
Vol 26 (10) ◽  
pp. 1389-1399 ◽  
Author(s):  
L.-B. Jiang ◽  
D.-H. Su ◽  
P. Liu ◽  
Y.-Q. Ma ◽  
Z.-Z. Shao ◽  
...  
Keyword(s):  
Shape Memory ◽  
Collagen Scaffold ◽  
Cartilage Regeneration ◽  
Native Collagen ◽  
Collagen Versus

Cell signalling pathways

2016 ◽  
pp. 23-30
Author(s):  
Stefan Knapp
Keyword(s):  
Tumour Growth ◽  
Cell Signalling ◽  
Tumour Microenvironment ◽  
The Body ◽  
Cellular Growth ◽  
Regulatory Mechanisms ◽  
Signalling Pathways ◽  
Tissue Remodelling ◽  
Cellular Replication ◽  
Key Pathways

Development and progression of cancer is driven by dysfunctional signalling pathways that promote tumour growth and invasion. The combined effect of a variety of deregulated key pathways leads to the acquisition of capabilities in cancer that are tightly controlled in normal cells. These altered cellular properties strongly promote cancer cell proliferation and the evasion of cellular growth suppression mechanisms and apoptosis. Cancer-specific alterations in signalling pathways also overcome limitations of cellular replication potential. In late-stage cancers, communication of cancer cells with the tumour microenvironment leads to tissue remodelling and reprogramming, including the formation of new blood vessels and the spread of tumour cells in the body. These complex cellular changes are controlled by a myriad of cellular signalling pathways. The chapter reviews the principal regulatory mechanisms that control key cancer signalling pathways, particularly focusing on pathways that have been successfully targeted in cancer therapy.

scholarly journals Identification of Regulatory Functions of LncRNAs Associated With T. circumcincta Infection in Adult Sheep

2021 ◽  
Vol 12 ◽  
Author(s):  
Praveen Krishna Chitneedi ◽  
Rosemarie Weikard ◽  
Juan J. Arranz ◽  
María Martínez-Valladares ◽  
Christa Kuehn ◽  
...  
Keyword(s):  
Immune Response ◽  
Functional Role ◽  
Defense Mechanism ◽  
Nematode Infection ◽  
Cellular Growth ◽  
Differentially Expressed ◽  
Differential Host ◽  
Adult Sheep ◽  
Gene Enrichment

Several recent studies have demonstrated the role of long non-coding RNAs (lncRNAs) in regulating the defense mechanism against parasite infections, but no studies are available that investigated their relevance for immune response to nematode infection in sheep. Thus, the aim of the current study was to (i) detect putative lncRNAs that are expressed in the abomasal lymph node of adult sheep after an experimental infection with the gastrointestinal nematode (GIN) Teladorsagia circumcincta and (ii) to elucidate their potential functional role associated with the differential host immune response. We hypothesized that putative lncRNAs differentially expressed (DE) between samples from animals that differ in resistance to infection may play a significant regulatory role in response to nematode infection in adult sheep. To obtain further support for our hypothesis, we performed co-expression and functional gene enrichment analyses with the differentially expressed lncRNAs (DE lncRNAs). In a conservative approach, we included for this predictive analysis only those lncRNAs that are confirmed and supported by documentation of expression in gastrointestinal tissues in the current sheep gene atlas. We identified 9,105 putative lncRNA transcripts corresponding to 7,124 gene loci. Of these, 457 were differentially expressed lncRNA loci (DELs) with 683 lncRNA transcripts. Based on a gene co-expression analysis via weighted gene co-expression network analysis, 12 gene network modules (GNMs) were found significantly correlated with at least one of 10 selected target DE lncRNAs. Based on the principle of “guilt-by-association,” the DE genes from each of the three most significantly correlated GNMs were subjected to a gene enrichment analysis. The significant pathways associated with DE lncRNAs included ERK5 Signaling, SAPK/JNK Signaling, RhoGDI Signaling, EIF2 Signaling, Regulation of eIF4 and p70S6K Signaling and Oxidative Phosphorylation pathways. They belong to signaling pathway categories like Cellular Growth, Proliferation and Development, Cellular Stress and Injury, Intracellular and Second Messenger Signaling and Apoptosis. Overall, this lncRNA study conducted in adult sheep after GIN infection provided first insights into the potential functional role of lncRNAs in the differential host response to nematode infection.

scholarly journals Identification of differentially expressed genes for fescue toxicosis in high and low tolerant Angus cows

2019 ◽  
Author(s):  
Piush Khanal ◽  
Leticia P Sanglard ◽  
Kyle Mayberry ◽  
Jeffery Sommer ◽  
Matthew H Poore ◽  
...  
Keyword(s):  
Immune Response ◽  
Differentially Expressed Genes ◽  
Gene Networks ◽  
Cardiovascular Function ◽  
Cellular Growth ◽  
Differentially Expressed ◽  
Fescue Toxicosis ◽  
Biological Processes ◽  
Q Value ◽  
Beef Industry

Abstract Background Fescue toxicosis (FT) is the multifaceted syndrome that causes the major loss of revenue in beef industry. Management of FT has been substantial challenge for the beef industry. Little research has been conducted to identify host genetic variation for FT response. Therefore, the objectives of this study were 1) to identify differentially expressed genes (DEG) in animals with contrasting response to fescue toxicosis, 2) to assess the biological relevance of DEG and 3) to investigate the relationships of DEG through gene networks in Angus cows. Results Genotype-by-location-by-time interaction was evident, with one location (2,296) having much greater number of DEG (q-value < 0.1) between HT and LT animals than the other (554). In addition, there was a greater number of DEG (q-value < 0.1) between HT and LT animals on week 5 (3,892) than on weeks 1(1,413), 9 (1,384), and 13 (573). So, further analyses focused on DEG between HT and LT animals on week 5 at the most toxic location. The most significant DEG between HT and LT animals had relevant functions associated with FT: cellular growth (SPDYC, HEYL, ANXA13), cardiovascular function (FGB, HBA, WNT11, BPIFB4, MESP2), protein metabolism (ENPP6, MMP8), and immune response (CTBS, SDC2, CXCL13, IL-13, JAKMIP2). The strongest positive partial correlation (0.99) was between CTBS and CXCL13, where CTBS is involved in carbohydrate metabolism and immune function, and CXCL13 is involved in immune, inflammatory, and defense response, and G-protein coupled pathway. The regulation of the most significant DEG between HT and LT animals on week 5 are highly correlated, indicating a complex interaction between. When all DEG were analyzed, the enriched biological processes associated with fescue toxicosis included immune response, cardiovascular function and development, metabolic, cellular and biological processes, and fertilization. Conclusions These findings provide potential biomarkers that should be evaluated for selection of cattle with greater tolerance to fescue toxicosis which will help to establish the herd with fescue tolerant cows in regions where high endophyte infected pasture is present.

scholarly journals The MYC oncogene is a global regulator of the immune response

Blood ◽  
2018 ◽  
Vol 131 (18) ◽  
pp. 2007-2015 ◽  
Author(s):  
Stephanie C. Casey ◽  
Virginie Baylot ◽  
Dean W. Felsher
Keyword(s):  
Immune Response ◽  
Cellular Growth ◽  
Therapeutic Interventions ◽  
Immune Checkpoints ◽  
Immune Effector ◽  
Effector Cells ◽  
Myc Oncogene ◽  
Induced Tumors ◽  
Programmed Death ◽  
Immune Detection

Abstract The MYC proto-oncogene is a gene product that coordinates the transcriptional regulation of a multitude of genes that are essential to cellular programs required for normal as well as neoplastic cellular growth and proliferation, including cell cycle, self-renewal, survival, cell growth, metabolism, protein and ribosomal biogenesis, and differentiation. Here, we propose that MYC regulates these programs in a manner that is coordinated with a global influence on the host immune response. MYC had been presumed to contribute to tumorigenesis through tumor cell–intrinsic influences. More recently, MYC expression in tumor cells has been shown to regulate the tumor microenvironment through effects on both innate and adaptive immune effector cells and immune regulatory cytokines. Then, MYC was shown to regulate the expression of the immune checkpoint gene products CD47 and programmed death-ligand 1. Similarly, other oncogenes, which are known to modulate MYC, have been shown to regulate immune checkpoints. Hence, MYC may generally prevent highly proliferative cells from eliciting an immune response. MYC-driven neoplastic cells have coopted this mechanism to bypass immune detection. Thus, MYC inactivation can restore the immune response against a tumor. MYC-induced tumors may be particularly sensitive to immuno-oncology therapeutic interventions.

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