scholarly journals Interactions between Host Immunity and Skin-Colonizing Staphylococci: No Two Siblings Are Alike

2019 ◽  
Vol 20 (3) ◽  
pp. 718 ◽  
Author(s):  
Young Joon Park ◽  
Chae Won Kim ◽  
Heung Kyu Lee
Keyword(s):  
Immune Response ◽  
Immune Cells ◽  
Skin Diseases ◽  
Inflammatory Responses ◽  
Bacterial Species ◽  
Host Immunity ◽  
The Body ◽  
Skin Microbiome ◽  
Staphylococcus Epidermis ◽  
Skin Commensals

As the outermost layer of the body, the skin harbors innumerable and varied microorganisms. These microorganisms interact with the host, and these interactions contribute to host immunity. One of the most abundant genera of skin commensals is Staphylococcus. Bacteria belonging to this genus are some of the most influential commensals that reside on the skin. For example, colonization by Staphylococcus aureus, a well-known pathogen, increases inflammatory responses within the skin. Conversely, colonization by Staphylococcus epidermis, a coagulase-negative staphylococcal species that are prevalent throughout the skin, can be innocuous or beneficial. Thus, manipulating the abundance of these two bacterial species likely alters the skin microbiome and modulates the cutaneous immune response, with potential implications for various inflammation-associated skin diseases. Importantly, before researchers can begin manipulating the skin microbiome to prevent and treat disease, they must first fully understand how these two species can modulate the cutaneous immune response. In this review, we discuss the nature of the interactions between these two bacterial species and immune cells within the skin, discussing their immunogenicity within the context of skin disorders.

scholarly journals Dual-Wavelength Photosensitive Nano-in-Micro Scaffold Regulates Innate and Adaptive Immune Responses for Osteogenesis

2020 ◽  
Vol 13 (1) ◽  
Author(s):  
Qin Zhao ◽  
Miusi Shi ◽  
Chengcheng Yin ◽  
Zifan Zhao ◽  
Jinglun Zhang ◽  
...  
Keyword(s):  
Immune Response ◽  
Immune Responses ◽  
Immune Cells ◽  
Inflammatory Responses ◽  
Macrophage Polarization ◽  
T Cell Response ◽  
Dual Wavelength ◽  
M2 Macrophage ◽  
Adaptive Immune Responses ◽  
Adaptive Immune

AbstractThe immune response of a biomaterial determines its osteoinductive effect. Although the mechanisms by which some immune cells promote regeneration have been revealed, the biomaterial-induced immune response is a dynamic process involving multiple cells. Currently, it is challenging to accurately regulate the innate and adaptive immune responses to promote osteoinduction in biomaterials. Herein, we investigated the roles of macrophages and dendritic cells (DCs) during the osteoinduction of biphasic calcium phosphate (BCP) scaffolds. We found that osteoinductive BCP directed M2 macrophage polarization and inhibited DC maturation, resulting in low T cell response and efficient osteogenesis. Accordingly, a dual-targeting nano-in-micro scaffold (BCP loaded with gold nanocage, BCP-GNC) was designed to regulate the immune responses of macrophages and DCs. Through a dual-wavelength photosensitive switch, BCP-GNC releases interleukin-4 in the early stage of osteoinduction to target M2 macrophages and then releases dexamethasone in the later stage to target immature DCs, creating a desirable inflammatory environment for osteogenesis. This study demonstrates that biomaterials developed to have specific regulatory capacities for immune cells can be used to control the early inflammatory responses of implanted materials and induce osteogenesis.

scholarly journals The Surface-Associated Exopolysaccharide of Bifidobacterium longum 35624 Plays an Essential Role in Dampening Host Proinflammatory Responses and Repressing Local TH17 Responses

2016 ◽  
Vol 82 (24) ◽  
pp. 7185-7196 ◽  
Author(s):  
Elisa Schiavi ◽  
Marita Gleinser ◽  
Evelyn Molloy ◽  
David Groeger ◽  
Remo Frei ◽  
...  
Keyword(s):  
Immune Response ◽  
Immune Cells ◽  
Essential Role ◽  
Inflammatory Responses ◽  
Bifidobacterium Longum ◽  
Molecular Characteristics ◽  
Interleukin 17 ◽  
Content Type ◽  
Exopolysaccharide Production

ABSTRACTThe immune-modulating properties of certain bifidobacterial strains, such asBifidobacterium longumsubsp.longum35624 (B. longum35624), have been well described, although the strain-specific molecular characteristics associated with such immune-regulatory activity are not well defined. It has previously been demonstrated thatB. longum35624 produces a cell surface exopolysaccharide (sEPS), and in this study, we investigated the role played by this exopolysaccharide in influencing the host immune response.B. longum35624 induced relatively low levels of cytokine secretion from human dendritic cells, whereas an isogenic exopolysaccharide-negative mutant derivative (termed sEPSneg) induced vastly more cytokines, including interleukin-17 (IL-17), and this response was reversed when exopolysaccharide production was restored in sEPSnegby genetic complementation. Administration ofB. longum35624 to mice of the T cell transfer colitis model prevented disease symptoms, whereas sEPSnegdid not protect against the development of colitis, with associated enhanced recruitment of IL-17+lymphocytes to the gut. Moreover, intranasal administration of sEPSnegalso resulted in enhanced recruitment of IL-17+lymphocytes to the murine lung. These data demonstrate that the particular exopolysaccharide produced byB. longum35624 plays an essential role in dampening proinflammatory host responses to the strain and that loss of exopolysaccharide production results in the induction of local TH17 responses.IMPORTANCEParticular gut commensals, such asB. longum35624, are known to contribute positively to the development of mucosal immune cells, resulting in protection from inflammatory diseases. However, the molecular basis and mechanisms for these commensal-host interactions are poorly described. In this report, an exopolysaccharide was shown to be decisive in influencing the immune response to the bacterium. We generated an isogenic mutant unable to produce exopolysaccharide and observed that this mutation caused a dramatic change in the response of human immune cellsin vitro. In addition, the use of mouse models confirmed that lack of exopolysaccharide production induces inflammatory responses to the bacterium. These results implicate the surface-associated exopolysaccharide of theB. longum35624 cell envelope in the prevention of aberrant inflammatory responses.

scholarly journals Principals of innate and adaptive immunity. Immunity to microbes & fundamental concepts in immunology

2021 ◽  
Vol 10 (3) ◽  
pp. 188-197
Author(s):  
Andrew Kiboneka
Keyword(s):  
Immune Response ◽  
Immune Cells ◽  
Chemokine Receptors ◽  
The Body ◽  
Innate Immune ◽  
Lymphoid Cells ◽  
Biologically Active ◽  
Surface Receptors ◽  
Bacterial Surfaces ◽  
Cellular Immune

Microorganisms such as bacteria that penetrate the epithelial surfaces of the body for the first time are met immediately by cells and molecules that can mount an innate immune response. Phagocytic macrophages conduct the defense against bacteria by means of surface receptors that are able to recognize and bind common constituents of many bacterial surfaces. Bacterial molecules binding to these receptors trigger the macrophage to engulf the bacterium and also induce the secretion of biologically active molecules. Activated macrophages secrete cytokines, which are defined as proteins released by cells that affect the behavior of other cells that bear receptors for them. They also release proteins known as chemokines that attract cells with chemokine receptors such as neutrophils and monocytes from the bloodstream. Macrophages in response to bacterial constituents initiate the process known as inflammation. Antigen-presenting cells (APCs) are a heterogeneous group of immune cells that mediate the cellular immune response by processing and presenting antigens for recognition by certain lymphocytes such as T cells. Classical APCs include dendritic cells, macrophages, Langerhans cells and B cells. Innate lymphoid cells (ILCs) are immune cells that belong to the lymphoid lineage but do not express antigen-specific receptors. These cells have important functions in innate immune responses to infectious microorganisms and in the regulation of homeostasis and inflammation.

scholarly journals Features of the Skin Microbiota in Common Inflammatory Skin Diseases

Life ◽  
2021 ◽  
Vol 11 (9) ◽  
pp. 962
Author(s):  
Iva Ferček ◽  
Liborija Lugović-Mihić ◽  
Arjana Tambić-Andrašević ◽  
Diana Ćesić ◽  
Ana Gverić Grginić ◽  
...  
Keyword(s):  
Skin Diseases ◽  
Seborrheic Dermatitis ◽  
Bacterial Species ◽  
Clinical Manifestations ◽  
Skin Microbiome ◽  
Bacterial Strains ◽  
Skin Microbiota ◽  
Inflammatory Skin Diseases ◽  
Bacterial Microbiome ◽  
Inflammatory Skin

Many relatively common chronic inflammatory skin diseases manifest on the face (seborrheic dermatitis, rosacea, acne, perioral/periorificial dermatitis, periocular dermatitis, etc.), thereby significantly impairing patient appearance and quality of life. Given the yet unexplained pathogenesis and numerous factors involved, these diseases often present therapeutic challenges. The term “microbiome” comprises the totality of microorganisms (microbiota), their genomes, and environmental factors in a particular environment. Changes in human skin microbiota composition and/or functionality are believed to trigger immune dysregulation, and consequently an inflammatory response, thereby playing a potentially significant role in the clinical manifestations and treatment of these diseases. Although cultivation methods have traditionally been used in studies of bacterial microbiome species, a large number of bacterial strains cannot be grown in the laboratory. Since standard culture-dependent methods detect fewer than 1% of all bacterial species, a metagenomic approach could be used to detect bacteria that cannot be cultivated. The skin microbiome exhibits spatial distribution associated with the microenvironment (sebaceous, moist, and dry areas). However, although disturbance of the skin microbiome can lead to a number of pathological conditions and diseases, it is still not clear whether skin diseases result from change in the microbiome or cause such a change. Thus far, the skin microbiome has been studied in atopic dermatitis, seborrheic dermatitis, psoriasis, acne, and rosacea. Studies on the possible association between changes in the microbiome and their association with skin diseases have improved the understanding of disease development, diagnostics, and therapeutics. The identification of the bacterial markers associated with particular inflammatory skin diseases would significantly accelerate the diagnostics and reduce treatment costs. Microbiota research and determination could facilitate the identification of potential causes of skin diseases that cannot be detected by simpler methods, thereby contributing to the design and development of more effective therapies.

The War Against SARS-CoV-2: The Immune Giant Collapsing Under Its Own Rampaging Cytokine Storm

2021 ◽  
Author(s):  
Xanya Sofra
Keyword(s):  
Skeletal Muscle ◽  
Immune Response ◽  
Immune Cells ◽  
Preventive Intervention ◽  
Inflammatory Marker ◽  
The Body ◽  
Alternative Methods ◽  
Cytokine Storm ◽  
Protective Function ◽  
Age Related

We examined SARS-CoV-2 (Covid-19) available treatments and prophylactic methods that included interventions associated with inhibiting the ‘type II transmembrane serine protease’ (TMPRSS2) to limit the fusion between the Covid-19 Spike proteins and ACE2 receptors, or newly developed therapeutics like Remdesivir that interferes with the viral RNA replication. We explored the dilemma of ACE2 receptors that have a protective function against high blood pressure associated disorders, yet, they serve as the viral points of entry, elevating the probability of infection. Human tissues’ analysis reveals a higher ACE2 expression in adipose tissue, placing obesity-related conditions in the eye of the pandemic storm. It primarily exposes males due to the surge of ACE2 receptors in the testes along with other tissues. Males manifest a relatively higher positive ACE2 correlation with certain immune cells in the lungs, thyroid, adrenals, liver and colon, while females evidence higher ACE2 correlations with immune cells in the heart. The remaining tissues’ ACE2/immunity expressions are equivalent in both sexes, indicating that despite its preference for males, the threat of Covid-19 can easily target females. Recent reports indicate that Covid-19 is empowered by hindering the critical process of viral recognition during the adaptive immune response leading to the “cytokine storm,” the aggravated immune response that indiscriminately perseveres, rampaging the host’s vital organs. Sedentary lifestyle, age-related hormonal imbalance, and adiposity induced inflammation predispose the body to the immune collapse following Covid-19 invasion, spotlighting the detrimental aftermath of metabolic dysfunction, and excess food consumption, provoked by elevated cortisol and dysregulated appetite hormones. ACE2 expression is suppressed in the skeletal muscle, rendering fitness and weight management an effective Covid-19 preventive intervention, along with social distancing, hygiene, and facial coverings. Physical activity, or exercise alternative methods have recently demonstrated statistically significant reductions of the inflammatory marker C-Reactive Protein (CRP), triglycerides, visceral fat, cortisol and the orexigenic hormone ghrelin, juxtaposed by optimal increases of IGF-1, skeletal muscle mass, Free T3, HDL, and the anorexic hormone leptin.

scholarly journals Hypoxia/HIF Modulates Immune Responses

Biomedicines ◽  
2021 ◽  
Vol 9 (3) ◽  
pp. 260
Author(s):  
Yuling Chen ◽  
Timo Gaber
Keyword(s):  
Immune Response ◽  
Cancer Progression ◽  
Immune Cells ◽  
Cell Function ◽  
Immune Cell ◽  
Adaptive Immune Response ◽  
Oxygen Availability ◽  
The Body ◽  
Low Oxygen ◽  
Adaptive Immune

Oxygen availability varies throughout the human body in health and disease. Under physiological conditions, oxygen availability drops from the lungs over the blood stream towards the different tissues into the cells and the mitochondrial cavities leading to physiological low oxygen conditions or physiological hypoxia in all organs including primary lymphoid organs. Moreover, immune cells travel throughout the body searching for damaged cells and foreign antigens facing a variety of oxygen levels. Consequently, physiological hypoxia impacts immune cell function finally controlling innate and adaptive immune response mainly by transcriptional regulation via hypoxia-inducible factors (HIFs). Under pathophysiological conditions such as found in inflammation, injury, infection, ischemia and cancer, severe hypoxia can alter immune cells leading to dysfunctional immune response finally leading to tissue damage, cancer progression and autoimmunity. Here we summarize the effects of physiological and pathophysiological hypoxia on innate and adaptive immune activity, we provide an overview on the control of immune response by cellular hypoxia-induced pathways with focus on the role of HIFs and discuss the opportunity to target hypoxia-sensitive pathways for the treatment of cancer and autoimmunity.

scholarly journals The Threshold Effect: Lipopolysaccharide-Induced Inflammatory Responses in Primary Macrophages Are Differentially Regulated in an iRhom2-Dependent Manner

2021 ◽  
Vol 10 ◽  
Author(s):  
Joseph Skurski ◽  
Garima Dixit ◽  
Carl P. Blobel ◽  
Priya D. Issuree ◽  
Thorsten Maretzky
Keyword(s):  
Immune Response ◽  
Innate Immune Response ◽  
Immune Cells ◽  
Regulatory Mechanism ◽  
Inflammatory Responses ◽  
Genetic Model ◽  
Innate Immune ◽  
High Dose ◽  
Dependent Manner ◽  
Low Levels

A well-controlled innate immune response is characterized by a rapid yet self-limiting inflammatory response. Although much is known about the range of inflammatory stimuli capable of triggering an innate immune response, the mechanisms which govern the degree of inflammation induced by inflammatory insults and the mechanisms in place to reset or maintain homeostasis are poorly understood. Tumor necrosis factor (TNF) is a potent early response pro-inflammatory cytokine produced by immune cells following a broad range of insults spanning autoimmunity and metabolic diseases to pathogenic infections. Previous studies have shown that a disintegrin and metalloproteinase (ADAM) 17 controls the release of soluble TNF and epidermal growth factor receptor signaling. Utilizing a genetic model of ADAM17 deficiency through the deletion of its regulator, the inactive rhomboid 2 (iRhom2), we show that loss of ADAM17 activity in innate immune cells leads to decreased expression of various cytokines in response to low levels of pathogen-associated molecular pattern (PAMP) stimulation but not at high-dose stimulation. In addition, TNF receptor (TNFR) 1/2-deficient bone marrow-derived macrophages yielded significantly reduced TNF expression following low levels of PAMP stimulation, suggesting that signaling through the TNFRs in immune cells drives a feed-forward regulatory mechanism wherein low levels of TNF allow sustained enhancement of TNF expression in an iRhom2/ADAM17-dependent manner. Thus, we demonstrate that inflammatory expression of TNF and IL1β is differentially regulated following high or low doses of PAMP stimulation, invoking the activation of a previously unknown regulatory mechanism of inflammation.

scholarly journals Fibrinolytic Serine Proteases, Therapeutic Serpins and Inflammation: Fire Dancers and Firestorms

2021 ◽  
Vol 8 ◽  
Author(s):  
Jordan R. Yaron ◽  
Liqiang Zhang ◽  
Qiuyun Guo ◽  
Shelley E. Haydel ◽  
Alexandra R. Lucas
Keyword(s):  
Immune Response ◽  
Serine Protease ◽  
Serine Proteases ◽  
Immune Cell ◽  
Inflammatory Responses ◽  
Tissue Injury ◽  
The Body ◽  
Vascular Tree ◽  
Regulatory Pathways ◽  
Endothelial Cell Surface

The making and breaking of clots orchestrated by the thrombotic and thrombolytic serine protease cascades are critical determinants of morbidity and mortality during infection and with vascular or tissue injury. Both the clot forming (thrombotic) and the clot dissolving (thrombolytic or fibrinolytic) cascades are composed of a highly sensitive and complex relationship of sequentially activated serine proteases and their regulatory inhibitors in the circulating blood. The proteases and inhibitors interact continuously throughout all branches of the cardiovascular system in the human body, representing one of the most abundant groups of proteins in the blood. There is an intricate interaction of the coagulation cascades with endothelial cell surface receptors lining the vascular tree, circulating immune cells, platelets and connective tissue encasing the arterial layers. Beyond their role in control of bleeding and clotting, the thrombotic and thrombolytic cascades initiate immune cell responses, representing a front line, “off-the-shelf” system for inducing inflammatory responses. These hemostatic pathways are one of the first response systems after injury with the fibrinolytic cascade being one of the earliest to evolve in primordial immune responses. An equally important contributor and parallel ancient component of these thrombotic and thrombolytic serine protease cascades are theserineproteaseinhibitors, termedserpins. Serpins are metastable suicide inhibitors with ubiquitous roles in coagulation and fibrinolysis as well as multiple central regulatory pathways throughout the body. Serpins are now known to also modulate the immune response, either via control of thrombotic and thrombolytic cascades or via direct effects on cellular phenotypes, among many other functions. Here we review the co-evolution of the thrombolytic cascade and the immune response in disease and in treatment. We will focus on the relevance of these recent advances in the context of the ongoing COVID-19 pandemic. SARS-CoV-2 is a “respiratory” coronavirus that causes extensive cardiovascular pathogenesis, with microthrombi throughout the vascular tree, resulting in severe and potentially fatal coagulopathies.

scholarly journals Involvement of lipids in immune system regulation: A mini-review

2021 ◽  
Vol 12 (1) ◽  
pp. 68-78
Author(s):  
Kurnia Putri Utami ◽  
Widya Wasityastuti ◽  
Marsetyawan HNE Soesatyo
Keyword(s):  
Fatty Acids ◽  
Immune System ◽  
Immune Cells ◽  
Inflammatory Responses ◽  
Nk Cell ◽  
The Body ◽  
Literature Study ◽  
Immune System Regulation ◽  
Complex Lipids ◽  
Published Research

An immune system recognizes and responds to antigens entering the body. Maintaining these roles, components of the immune system need energy obtained from nutrients such as carbohydrates, proteins, and lipids. This study reviews and discusses roles of lipids, particularly fatty acids, in regulations of the immune system. This study was conducted by conducting a literature study on published research articles written in English. The articles were obtained from PubMed and Google Scholar by using search keywords: lipid, fatty acids, immune, regulation, inflammation, and response. Lipids are a group of biomolecule compounds composed of carbon, oxygen, and hydrogen, and they are classified into simple, compound and complex lipids. Fatty acids are compound lipids that act as a main fuel for metabolism, an essential component for all membranes, and a gene regulator. Fatty acids have a modulating effect on immune cells, such as: acting as a host defence, activating the immune system, interacting with nuclear transcription factors, playing roles in inflammatory responses, promoting apoptosis, as well as influencing lymphocyte proliferation, cytokine production, and Natural Killer (NK) cell activities. However, the modulation of the immune system by lipids is influenced by various factors such as concentration and types of fatty acids, types of immune cells, and species. This study is suggested to provide an overview of beneficial roles of lipids in maintaining immunity.

scholarly journals Regulation of Immune Cells by Eicosanoid Receptors

2007 ◽  
Vol 7 ◽  
pp. 1307-1328 ◽  
Author(s):  
Nancy D. Kim ◽  
Andrew D. Luster
Keyword(s):  
Immune Response ◽  
Immune Cells ◽  
Inflammatory Responses ◽  
Cell Types ◽  
Lipid Mediators ◽  
Specific Receptor ◽  
Inflammatory Conditions ◽  
Specific Effects ◽  
Key Players

Eicosanoids are potent, bioactive, lipid mediators that regulate important components of the immune response, including defense against infection, ischemia, and injury, as well as instigating and perpetuating autoimmune and inflammatory conditions. Although these lipids have numerous effects on diverse cell types and organs, a greater understanding of their specific effects on key players of the immune system has been gained in recent years through the characterization of individual eicosanoid receptors, the identification and development of specific receptor agonists and inhibitors, and the generation of mice genetically deficient in various eicosanoid receptors. In this review, we will focus on the receptors for prostaglandin D2, DP1and DP2/CRTH2; the receptors for leukotriene B4, BLT1and BLT2; and the receptors for the cysteinyl leukotrienes, CysLT1and CysLT2, by examining their specific effects on leukocyte subpopulations, and how they may act in concert towards the development of immune and inflammatory responses.

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