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 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 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 A large panel of chicken cells are invaded in vivo by Salmonella Typhimurium even when depleted of all known invasion factors

Open Biology ◽  
2021 ◽  
Vol 11 (11) ◽  
Author(s):  
S. M. Roche ◽  
S. Holbert ◽  
Y. Le Vern ◽  
C. Rossignol ◽  
A. Rossignol ◽  
...  
Keyword(s):  
Gall Bladder ◽  
Cell Types ◽  
Human Infection ◽  
Cell Tropism ◽  
Wild Type ◽  
Phagocytic Cells ◽  
Bladder Cells ◽  
First Time

Poultry are the main source of human infection by Salmonella . As infected poultry are asymptomatic, identifying infected poultry farms is difficult, thus controlling animal infections is of primary importance. As cell tropism is known to govern disease, our aim was therefore to identify infected host–cell types in the organs of chicks known to be involved in Salmonella infection and investigate the role of the three known invasion factors in this process (T3SS-1, Rck and PagN). Chicks were inoculated with wild-type or isogenic fluorescent Salmonella Typhimurium mutants via the intracoelomic route. Our results show that liver, spleen, gall bladder and aortic vessels could be foci of infection, and that phagocytic and non-phagocytic cells, including immune, epithelial and endothelial cells, are invaded in vivo in each organ. Moreover, a mutant defective for the T3SS-1, Rck and PagN remained able to colonize organs like the wild-type strain and invaded non-phagocytic cells in each organ studied. As the infection of the gall bladder had not previously been described in chicks, invasion of gall bladder cells was confirmed by immunohistochemistry and infection was shown to last several weeks after inoculation. Altogether, for the first time these findings provide insights into cell tropism of Salmonella in relevant organs involved in Salmonella infection in chicks and also demonstrate that the known invasion factors are not required for entry into these cell types.

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.

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.

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.

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 A functional role for eicosanoid-lysophospholipids in activating monocyte signaling

2020 ◽  
Vol 295 (34) ◽  
pp. 12167-12180
Author(s):  
Gao-Yuan Liu ◽  
Sung Ho Moon ◽  
Christopher M. Jenkins ◽  
Harold F. Sims ◽  
Shaoping Guan ◽  
...  
Keyword(s):  
Inflammatory Responses ◽  
Enzyme Inhibitor ◽  
Ether Linkage ◽  
Monocytic Cells ◽  
Factor Α ◽  
Normal Processing ◽  
Hydrolysis Of ◽  
Catalyzed Oxidation ◽  
Necrosis Factor

Recently, eicosanoid-lysophospholipids were identified as novel metabolites generated from the direct cyclooxygenase- or lipoxygenase-catalyzed oxidation of 2-arachidonoyl-lysophospholipids produced from either phospholipase A1-mediated hydrolysis of diacyl arachidonoyl-phospholipids or through the cytochrome c-catalyzed oxidative hydrolysis of the vinyl ether linkage of arachidonoyl-plasmalogens. Although the metabolic pathways generating eicosanoid-lysophospholipids have been increasingly appreciated, the signaling functions of eicosanoid-lysophospholipids remain largely unknown. Herein, we demonstrate that 2-12(S)-HETE-lysophospholipids as well as nonesterified 12(S)-HETE are potent lipid mediators that activate THP-1 human monocytic cells to generate tumor necrosis factor α (TNFα) and interleukin 8 (IL8). Remarkably, low nanomolar concentrations of 12(S)-HETE-lysophospholipids, but not other oxidized signaling lipids examined activated THP-1 cells resulting in the production of large amounts of TNFα. Moreover, TNFα release induced by 12(S)-HETE-lysophospholipids was inhibited by the TNFα converting enzyme inhibitor TAPI-0 indicating normal processing of TNFα in THP-1 cells stimulated with these agonists. Western blotting analyses revealed that 12(S)-HETE-lysophospholipids activated the phosphorylation of NFκB p65, suggesting activation of the canonical NFκB signaling pathway. Importantly, activation of THP-1 cells to release TNFα was stereoselective with 12(S)-HETE favored over 12(R)-HETE. Furthermore, the EC50 of 2-12(S)-HETE-lysophosphatidylcholine in activating THP-1 cells was 2.1 nm, whereas the EC50 of free 12(S)-HETE was 23 nm. Additionally, lipid extracts of activated platelets were separated by RP-HPLC demonstrating the coelution of 12(S)-HETE with fractions initiating TNFα release. Collectively, these results demonstrate the potent signaling properties of 2-12(S)-HETE-lysophospholipids and 12(S)-HETE by their ability to release TNFα and activate NFκB signaling thereby revealing a previously unknown role of 2-12(S)-HETE-lysophospholipids in mediating inflammatory responses.

Substrate Stiffness Modulates the Crosstalk Between Mesenchymal Stem Cells and Macrophages

2020 ◽  
Vol 143 (3) ◽  
Author(s):  
Rukmani Sridharan ◽  
Daniel J. Kelly ◽  
Fergal J. O'Brien
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Inflammatory Responses ◽  
Macrophage Polarization ◽  
Cell Types ◽  
Substrate Stiffness ◽  
Positive Interactions ◽  
Inflammatory Stimulus ◽  
Underlying Substrate

Abstract Upon implantation of a biomaterial, mesenchymal stem cells (MSCs) and macrophages contribute to the wound healing response and the regeneration cascade. Although biomaterial properties are known to direct MSC differentiation and macrophage polarization, the role of biomaterial cues, specifically stiffness, in directing the crosstalk between the two cell types is still poorly understood. This study aimed to elucidate the role of substrate stiffness in modulating the immunomodulatory properties of MSCs and to shed light on their complex interactions with macrophages when presented with diverse biomaterial stiffness cues, a situation analogous to the implant environment where multiple cell types interact with an implanted biomaterial to determine regenerative outcomes. We show that MSCs do not play an immunomodulatory role in the absence of an inflammatory stimulus. Using collagen-coated polyacrylamide gels of varying stiffness values, we demonstrate that the immunomodulatory capability of MSCs in the presence of an inflammatory stimulus is not dependent on the stiffness of the underlying substrate. Moreover, using paracrine and direct contact culture models, we show that a bidirectional crosstalk between MSCs and macrophages is necessary for promoting anti-inflammatory responses and positive immunomodulation, which is dependent on the stiffness of the underlying substrate. We finally show that direct cell–cell contact is not essential for this effect, with paracrine interactions promoting immunomodulatory interactions between MSCs and macrophages. Together, these results demonstrate that biophysical cues such as stiffness that are presented by biomaterials can be tuned to promote positive interactions between MSCs and macrophages which can in turn direct the downstream regenerative response.

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