scholarly journals C-Kit+ Cells Can Modulate Asthmatic Condition via Differentiation Into Pneumocyte-Like Cells and Alteration of Inflammatory Responses via ERK/NF-κB Pathway

2021 ◽  
Author(s):  
Fatemeh Mirershadi ◽  
Mahdi Ahmadi ◽  
Reza Rahbarghazi ◽  
Hossein Heiran ◽  
Rana Keyhanmanesh
Keyword(s):  
Progenitor Cell ◽  
Cellular Differentiation ◽  
Inflammatory Responses ◽  
Cell Types ◽  
Male Rats ◽  
Exact Role ◽  
Pulmonary Tissue ◽  
Cell Counts ◽  
Phosphate Buffered Saline

Abstract Background The exact role of the progenitor cell types in the dynamic healing of asthmatic lungs is lacking. This investigation was proposed to evaluate the effect of intra-tracheally administered rat bone marrow-derived c-kit⁺ cells on ovalbumin-induced sensitized male rats. Methods Forty rats were randomly divided into 4 groups; healthy rats received phosphate-buffered saline (PBS) (C); sensitized rats received PBS (S); PBS containing C-kitˉ cells (S + C-kit−); and PBS containing C-kit⁺ cells (S + C-kit⁺). After two weeks, circulatory CD4⁺/CD8⁺ T-cell counts and pulmonary ERK/NF-κB signaling pathway as well as the probability of cellular differentiation were assessed. Results The results showed that transplanted C-Kit+ cells were engrafted into pulmonary tissue and differentiated into epithelial cells. C-Kit+ cells could increase the number of CD4+ cells in comparison with S group (p < 0.001); however, diminished the level of CD8+ cells (p < 0.01). Moreover, data showed increased p-ERK/ERK ratio (p < 0.001) and NF-ƙB level (p < 0.05) in sensitized rats compared to C group. The administration of C-kit+, but not C-Kit−, decreased p-ERK/ERK ratio and NF-ƙB level than those of S group (p < 0.05). Conclusions The study showed that C-Kit+ cells engrafted into pulmonary tissue reduced NF-ƙB protein level and diminished p-ERK/ERK ratio, leading to suppression of inflammatory response in asthmatic lungs.

scholarly journals The Emerging Role of Galectins and O-GlcNAc Homeostasis in Processes of Cellular Differentiation

Cells ◽  
2020 ◽  
Vol 9 (8) ◽  
pp. 1792 ◽  
Author(s):  
Rada Tazhitdinova ◽  
Alexander V. Timoshenko
Keyword(s):  
Cancer Biology ◽  
Cellular Differentiation ◽  
Current Knowledge ◽  
Expression Profiles ◽  
Cell Types ◽  
Innovative Strategies ◽  
Protein Levels ◽  
Differentiated Cells ◽  
Independent Functions

Galectins are a family of soluble β-galactoside-binding proteins with diverse glycan-dependent and glycan-independent functions outside and inside the cell. Human cells express twelve out of sixteen recognized mammalian galectin genes and their expression profiles are very different between cell types and tissues. In this review, we summarize the current knowledge on the changes in the expression of individual galectins at mRNA and protein levels in different types of differentiating cells and the effects of recombinant galectins on cellular differentiation. A new model of galectin regulation is proposed considering the change in O-GlcNAc homeostasis between progenitor/stem cells and mature differentiated cells. The recognition of galectins as regulatory factors controlling cell differentiation and self-renewal is essential for developmental and cancer biology to develop innovative strategies for prevention and targeted treatment of proliferative diseases, tissue regeneration, and stem-cell therapy.

scholarly journals Non-Alcoholic Steatohepatitis: Clinical and Translational Research

2016 ◽  
Vol 19 (1) ◽  
pp. 8 ◽  
Author(s):  
Manuela G Neuman ◽  
Mihai Voiculescu ◽  
Radu M Nanau ◽  
Yaakov Maor ◽  
Ehud Melzer ◽  
...  
Keyword(s):  
Fatty Liver ◽  
Liver Damage ◽  
Immune Modulation ◽  
Inflammatory Responses ◽  
Cell Types ◽  
Organ Injury ◽  
Alcoholic Fatty Liver ◽  
Neuropsychological Disorders ◽  
Alcoholic Steatohepatitis

The present review includes translational and clinical research that characterize non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH). Clinical and experimental evidence led to the recognition of the key toxic role played by lipotoxicity in the pathogenesis of NAFLD. The current understanding of lipotoxicity suggests that organ injury is initiated by the generation of oxidative metabolites and the translocation of gut-derived endotoxin. These processes lead to cellular injury and stimulation of the inflammatory responses mediated through a variety of molecules. The injury progresses through impairment of tissue regeneration and extracellular matrix turnover, leading to fibrogenesis and cirrhosis. Several cell types are involved in this process, predominantly stellate cells, macrophages and parenchymal cells. In response to inflammation, cytokines activate many signaling cascades that regulate fibrogenesis. This examination brings together research focusing on the underlying mechanisms of injury. It highlights the various processes and molecules that are likely involved in inflammation, immune modulation, and fibrogenesis in the liver. We searched electronic databases (Medline, Embase) for this review. This integrative work investigates different aspects of liver damage and possible repair. We aim to (1) determine the immuno-pathology of liver damage due to steatosis, (2) suggest diagnostic markers of NASH, (3) examine the role of behaviour in the development of NASH, and (4) develop common tools to study steatosis-induced effects in clinical studies. Special accent is put on co-morbidities with renal and neuropsychological disorders. Moreover, we review the evidence in literature on the role of moderate alcohol consumption in individuals that present NAFLD/NASH.Key Words: behavior, diet, imaging, non-alcoholic fatty liver, nonalcoholic steatohepatitis, laboratory markers.This article is open to POST-PUBLICATION REVIEW. Registered readers (see “For Readers”) may comment by clicking on ABSTRACT on the issue’s contents page.

scholarly journals Phagocytosis in Mesocestoides vogae-induced peritoneal monocytes/macrophages via opsonin-dependent or independent pathways

2016 ◽  
Vol 53 (1) ◽  
pp. 3-13 ◽  
Author(s):  
G. Hrčková ◽  
E. Vendelova ◽  
S. Velebný
Keyword(s):  
Phagocytic Activity ◽  
Inflammatory Responses ◽  
Cell Types ◽  
Phagocytic Cells ◽  
Monocytic Cells ◽  
Latex Beads ◽  
Oral Inoculation ◽  
Intraperitoneal Infection ◽  
Mesocestoides Vogae

SummaryIntraperitoneal infection with larvae of cestode Mesocestoides vogae offers the opportunity to study dynamic changes in the proportion and functions of individual cell types under a direct influence of parasites. The phagocytic activity is one of the basic effector functions of professional phagocytes and receptor-mediated uptake is a central in implementation of inflammatory responses. Present study extends information on this issue by exploring several phagocytosis pathways in M. vogae-induced myelo-monocytic cells. In addition, we analyzed proportions of morphologically distinct phenotypes within macrophage compartments after oral inoculation of larvae to mice. In gradually elevated population of peritoneal exudate cells, monocytes/ macrophages and giant cell were dominant cell types from day 21 p.i. Phagocytic activity of these cells had biphasic behaviour for both opsonin-dependent and independent pathways, whereas uptake by multinucleated macrophages was profoundly reduced. Highly elevated proportions of activated phagocytic cells were found from day 7 to 14 p.i., regardless particle type (latex beads, HEMA, liposomes) and opsonisation. Source of opsonins used for coating of liposomes suggested higher expression of complement receptors than Fc receptors on these cells, although the uptake of non-opsonized liposomes had different kinetics and was very high by activated cells early p.i. Present data indicate that early recruited macrophages/monocytes attain pro-inflammatory functions as indicated by highly elevated phagocytosis of immunologically inert particles as well as opsonized liposomes what is down-regulated once larvae start to proliferate in the peritoneal cavity, suggesting the role of parasite-derived molecules in modulation of this key phagocytes function.

scholarly journals The Role of IL-33 in Host Response toCandida albicans

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
C. Rodríguez-Cerdeira ◽  
A. Lopez-Bárcenas ◽  
B. Sánchez-Blanco ◽  
R. Arenas
Keyword(s):  
Defense Mechanisms ◽  
Fungal Pathogens ◽  
Inflammatory Responses ◽  
Inflammatory Diseases ◽  
Case Reports ◽  
Pathogenic Fungi ◽  
Cell Types ◽  
Immune Defense ◽  
Beneficial Role

Background. Interleukin (IL) 33 is a recently identified pleiotropic cytokine that influences the activity of multiple cell types and orchestrates complex innate and adaptive immune responses.Methods. We performed an extensive review of the literature published between 2005 and 2013 on IL-33 and related cytokines, their functions, and their regulation of the immune system followingCandida albicanscolonization. Our literature review included cross-references from retrieved articles and specific data from our own studies.Results. IL-33 (IL-1F11) is a recently identified member of the IL-1 family of cytokines. Accumulating evidence suggests a pivotal role of the IL-33/ST2 axis in host immune defense against fungal pathogens, includingC. albicans. IL-33 induces a Th2-type inflammatory response and activates both innate and adaptive immunity. Studies in animal models have shown that Th2 inflammatory responses have a beneficial role in immunity against gastrointestinal and systemic infections byCandidaspp.Conclusions. This review summarizes the most important clinical studies and case reports describing the beneficial role of IL-33 in immunity and host defense mechanisms against pathogenic fungi. The finding that the IL-33/ST2 axis is involved in therapeutic target has implications for the prevention and treatment of inflammatory diseases, including acute or chronic candidiasis.

scholarly journals Putative positive role of inflammatory genes in fat deposition supported by altered gene expression in purified human adipocytes and preadipocytes from lean and obese adipose tissues

2020 ◽  
Author(s):  
Sang-Hyeop Lee ◽  
Nak-Hyeon Choi ◽  
In-Uk Koh ◽  
Bong-Jo Kim ◽  
Song Lee ◽  
...  
Keyword(s):  
Gene Expression ◽  
Inflammatory Responses ◽  
Cell Types ◽  
Deposition Process ◽  
Fat Deposition ◽  
Low Grade ◽  
Positive Role ◽  
Inflammatory Genes ◽  
Altered Gene

Abstract BackgroundObesity is a chronic low-grade inflammatory disease that is generally characterized by enhanced inflammation in obese adipose tissue (AT). Here, we investigated alterations in gene expression between lean and obese conditions using mRNA-Seq data derived from human purified adipocytes (ACs) and preadipocytes (preACs). ResultsWe defined four classes of differentially expressed genes (DEGs) by comparing gene expression between 1) lean and obese ACs, 2) lean and obese preACs, 3) lean ACs and lean preACs, and 4) obese ACs and obese preACs. Based on an analysis of comparison 1, numerous canonical obesity-related genes, particularly inflammatory genes including IL6, TNF- and IL-1, i.e., the genes that are expected to be upregulated in obesity conditions, were found to be expressed at significantly lower levels in obese ACs than in lean ACs. In contrast, some inflammatory genes were found to be expressed at higher levels in obese preACs than lean preACs in the analysis of comparison 2. These two results indicate that (1) up-/downregulation of genes in ACs and preACs is inversely controlled during the fat deposition process and (2) preACs rather than ACs have increased inflammatory response genes in comparisons of lean and obese conditions for each of these cell types. Analysis of comparisons 3 and 4 showed that inflammatory gene classes were expressed at higher levels in differentiated ACs than undifferentiated preACs under both lean and obese conditions; however, the degree of upregulation was greater for lean than for obese conditions.ConclusionsTaken together, our analyses may suggest that lean fat differentiation involves even greater enhancement of inflammatory responses than does obese fat differentiation.

scholarly journals Prion Protein in Stem Cells: A Lipid Raft Component Involved in the Cellular Differentiation Process

2020 ◽  
Vol 21 (11) ◽  
pp. 4168 ◽  
Author(s):  
Stefano Martellucci ◽  
Costantino Santacroce ◽  
Francesca Santilli ◽  
Valeria Manganelli ◽  
Maurizio Sorice ◽  
...  
Keyword(s):  
Stem Cells ◽  
Prion Protein ◽  
Lipid Raft ◽  
Cellular Differentiation ◽  
Cell Types ◽  
Pleiotropic Effect ◽  
Cellular Prion Protein ◽  
Differentiation Process ◽  
Differentiation Degree

The prion protein (PrP) is an enigmatic molecule with a pleiotropic effect on different cell types; it is localized stably in lipid raft microdomains and it is able to recruit downstream signal transduction pathways by its interaction with various biochemical partners. Since its discovery, this lipid raft component has been involved in several functions, although most of the publications focused on the pathological role of the protein. Recent studies report a key role of cellular prion protein (PrPC) in physiological processes, including cellular differentiation. Indeed, the PrPC, whose expression is modulated according to the cell differentiation degree, appears to be part of the multimolecular signaling pathways of the neuronal differentiation process. In this review, we aim to summarize the main findings that report the link between PrPC and stem cells.

Critical role of microglia in the inflammatory response after spinal injury

2015 ◽  
Vol 3 (3) ◽  
pp. 453-462
Author(s):  
Ya-Yun Shi
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Inflammatory Responses ◽  
Spinal Injury ◽  
Critical Role ◽  
Cell Types ◽  
Inflammatory Factors ◽  
Cytokines And Chemokines ◽  
Cord Injury

Spinal cord injury induces a robust neuroinflammatory response that includes marked changes in the variety of endogenous CNS cell types specially microglia. In response to spinal injury, microglia undergo dramatic changes in cell morphology and promote inflammatory responses, which result in production of inflammatory factors and oxidative stress including reactive oxygen species. Further pro-inflammatory cytokines and chemokines are also rapidly up-regulated and likely contribute to microglial activation. This topic review will explore the current research on microglial responses to spinal injury and the recent progress in the pharmacologic and molecular targeting of microglia in spinal injury. Finally, we explore the argument for a positive versus negative role of microglia after spinal cord injury.

Role of endothelial cells in bovine mammary gland health and disease

2015 ◽  
Vol 16 (2) ◽  
pp. 135-149 ◽  
Author(s):  
Valerie E. Ryman ◽  
Nandakumar Packiriswamy ◽  
Lorraine M. Sordillo
Keyword(s):  
Endothelial Cells ◽  
Mammary Gland ◽  
Endothelial Dysfunction ◽  
Milk Production ◽  
Inflammatory Responses ◽  
Cell Types ◽  
Mammary Tissue ◽  
Bovine Mammary Gland ◽  
Affected Tissue

AbstractThe bovine mammary gland is a dynamic and complex organ composed of various cell types that work together for the purpose of milk synthesis and secretion. A layer of endothelial cells establishes the blood–milk barrier, which exists to facilitate the exchange of solutes and macromolecules necessary for optimal milk production. During bacterial challenge, however, endothelial cells divert some of their lactation function to protect the underlying tissue from damage by initiating inflammation. At the onset of inflammation, endothelial cells tightly regulate the movement of plasma components and leukocytes into affected tissue. Unfortunately, endothelial dysfunction as a result of exacerbated or sustained inflammation can negatively affect both barrier integrity and the health of surrounding extravascular tissue. The objective of this review is to highlight the role of endothelial cells in supporting milk production and regulating optimal inflammatory responses. The consequences of endothelial dysfunction and sustained inflammation on milk synthesis and secretion are discussed. Given the important role of endothelial cells in orchestrating the inflammatory response, a better understanding of endothelial function during mastitis may support development of targeted therapies to protect bovine mammary tissue and mammary endothelium.

Directed Cellular Dynamics on Aligned STEP Fibrous Mechanistic Microenvironments

2011 ◽  
Author(s):  
Kevin Sheets ◽  
Amrinder Nain
Keyword(s):  
Cell Types ◽  
Polymeric Fibers ◽  
Exact Role ◽  
Cellular Behavior ◽  
Current State ◽  
Dry Spinning ◽  
Spatial Parameters ◽  
Different Cell Types

Cells attach to and interact with their immediate mechanistic native microenvironment. However, the current state-the-art in vitro cell studies are performed on flat substrates of glass, plastic or gel. [1]. The native environment consisting of an assembly of protein nanofibers forming the extracellular matrix (ECM) offers different mechanistic environments for different tissues, which elicits diverse cellular behavior [2]. Recently, there is increased interest in mimicking the ECM by depositing polymeric fibers in single and multiple layers using electrospinning, template synthesis, and micro dry-spinning. The key fibrous spatial parameters (diameter, alignment, spacing, and orientation) can be designed to generate microenvironments of varying mechanical properties. However, the exact role of these parameters on cellular behavior is not clearly understood. Hence, in this study we explore the topological-mechanistic effects of fibrous scaffolds on dynamics of different cell types.

scholarly journals Why does inflammation persist: a dominant role for the stromal microenvironment?

2002 ◽  
Vol 4 (25) ◽  
pp. 1-18 ◽  
Author(s):  
Michael R. Douglas ◽  
Karen E. Morrison ◽  
Michael Salmon ◽  
Christopher D. Buckley
Keyword(s):  
Inflammatory Disease ◽  
Stromal Cells ◽  
Inflammatory Responses ◽  
Dominant Role ◽  
Cell Types ◽  
Stromal Microenvironment ◽  
Causative Agents ◽  
Mononuclear Cell Infiltrates ◽  
Temporal Interactions

Inflammatory responses occur within tissue microenvironments, with functional contributions from both haematopoietic (lymphocytic) cells and stromal cells (including macrophages and fibroblasts). These environments are complex – a compound of many different cell types at different stages of activation and differentiation. Traditional models of inflammatory disease highlight the role of antigen-specific lymphocyte responses and attempt to identify causative agents. However, recent studies have indicated the importance of tissue microenvironments and the innate immune response in perpetuating the inflammatory process. The prominent role of stromal cells in the generation and maintenance of these environments has begun to challenge the primacy of the lymphocyte in regulating chronic inflammatory processes. Sensible enquiries into factors regulating the persistence of inflammatory disease necessitate an understanding of the mechanisms regulating tissue homeostasis and remodelling during inflammation. This article highlights recent insights into the factors regulating dynamic aspects of inflammation, focusing particularly on mononuclear cell infiltrates, their interactions with stromal cells in tissues and the relevance of these interactions to existing and possible future therapies. A key feature of current research has been a growing appreciation that disordered spatial and temporal interactions between infiltrating immune cells and resident stromal cells lie at the heart of disease persistence.

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