scholarly journals Autophagy in Pulmonary Innate Immunity

2019 ◽  
Vol 12 (1) ◽  
pp. 21-30 ◽  
Author(s):  
Lang Rao ◽  
N. Tony Eissa
Keyword(s):  
Reactive Oxygen Species ◽  
Innate Immunity ◽  
Cell Growth ◽  
Immune Cells ◽  
Innate Immune ◽  
Inflammasome Activation ◽  
Innate Immune Cells ◽  
Oxygen Species ◽  
Intracellular Digestion ◽  
Molecular Patterns

Autophagy is a major intracellular digestion system that delivers cytoplasmic components for degradation and recycling. In this capacity, autophagy plays an important role in maintaining cellular homeostasis by mediating the degradation of cellular macromolecules and dysfunctional organelles and regeneration of nutrients for cell growth. Autophagy is important in innate immunity, as it is responsible for the clearance of various pathogens. Deficiency of intracellular autophagy can result in exaggerated activation of the inflammasome. The latter is an innate immune complex that senses diverse pathogen-associated or danger-associated molecular patterns and activates the expression of inflammatory cytokines. In autophagy-deficient cells, accumulation of damaged organelles, misfolded proteins, and reactive oxygen species contribute to inflammasome activation. The lung is continuously exposed to pathogens from the environment, rendering it vulnerable to infection. The lung innate immune cells act as a crucial initial barrier against the continuous threat from pathogens. In this review, we will summarize recent findings on the regulation of autophagy and its inter­action with innate immunity, focusing on the lung.

Role of Inflammasome Activation in Systemic Lupus Erythematosus: Are Innate Immune Cells Activated?

2020 ◽  
Author(s):  
Rodolfo Perez-Alamino ◽  
Raquel Cuchacovich ◽  
Luis R. Espinoza ◽  
Constance P. Porretta ◽  
Arnold H. Zea
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Immune Cells ◽  
Lupus Erythematosus ◽  
Innate Immune ◽  
Inflammasome Activation ◽  
Innate Immune Cells ◽  
Systemic Lupus

scholarly journals Platelets Fuel the Inflammasome Activation of Innate Immune Cells

Cell Reports ◽  
2020 ◽  
Vol 31 (6) ◽  
pp. 107615 ◽  
Author(s):  
Verena Rolfes ◽  
Lucas Secchim Ribeiro ◽  
Ibrahim Hawwari ◽  
Lisa Böttcher ◽  
Nathalia Rosero ◽  
...  
Keyword(s):  
Immune Cells ◽  
Innate Immune ◽  
Inflammasome Activation ◽  
Innate Immune Cells

scholarly journals In VitroExperimental Model of Trained Innate Immunity in Human Primary Monocytes

2016 ◽  
Vol 23 (12) ◽  
pp. 926-933 ◽  
Author(s):  
Siroon Bekkering ◽  
Bastiaan A. Blok ◽  
Leo A. B. Joosten ◽  
Niels P. Riksen ◽  
Reinout van Crevel ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Innate Immunity ◽  
Reactive Oxygen ◽  
Innate Immune ◽  
Oxygen Species ◽  
Optimal Conditions ◽  
Trained Immunity ◽  
Training Interval ◽  
Resting Time

ABSTRACTInnate immune memory, or trained immunity, has recently been described to be an important property of cells of the innate immune system. Due to the increased interest in this important new field of immunological investigation, we sought to determine the optimal conditions for anin vitroexperimental protocol of monocyte training using three of the most commonly used training stimuli from the literature: β-glucan, the bacillus Calmette-Guérin (BCG) vaccine, and oxidized low-density lipoprotein (oxLDL). We investigated and optimized a protocol of monocyte trained immunity induced by an initial training period with β-glucan, BCG, or oxLDL, followed by washing and resting of the cells and, thereafter, restimulation with secondary bacterial stimuli. The training and resting time intervals were varied to identify the optimal setting for the long-term induction of trained immunity. Trained immunity was assessed in terms of the secondary cytokine response, the production of reactive oxygen species, cell morphology, and induction of glycolysis. Monocytes primed with β-glucan, BCG, and oxLDL showed increased pro- and anti-inflammatory cytokine responses upon restimulation with nonrelated stimuli. Also, all three stimuli induced a switch to glycolysis (the Warburg effect). These effects were most pronounced when the training interval was 24 h and the resting time interval was 6 days. Training with BCG and oxLDL also led to the increased production of reactive oxygen species, whereas training with β-glucan led to the decreased production of reactive oxygen species. We describe the optimal conditions for anin vitroexperimental model with human primary monocytes for study of the induction of trained innate immunity by microbial and metabolic stimuli.

scholarly journals The cell biology of inflammation: From common traits to remarkable immunological adaptations

2020 ◽  
Vol 219 (7) ◽  
Author(s):  
Helen Weavers ◽  
Paul Martin
Keyword(s):  
Innate Immunity ◽  
Cell Division ◽  
Membrane Trafficking ◽  
Immune Cells ◽  
Cell Biology ◽  
Foreign Bodies ◽  
Cell Types ◽  
Innate Immune ◽  
Innate Immune Cells ◽  
Starting Point

Tissue damage triggers a rapid and robust inflammatory response in order to clear and repair a wound. Remarkably, many of the cell biology features that underlie the ability of leukocytes to home in to sites of injury and to fight infection—most of which are topics of intensive current research—were originally observed in various weird and wonderful translucent organisms over a century ago by Elie Metchnikoff, the “father of innate immunity,” who is credited with discovering phagocytes in 1882. In this review, we use Metchnikoff’s seminal lectures as a starting point to discuss the tremendous variety of cell biology features that underpin the function of these multitasking immune cells. Some of these are shared by other cell types (including aspects of motility, membrane trafficking, cell division, and death), but others are more unique features of innate immune cells, enabling them to fulfill their specialized functions, such as encapsulation of invading pathogens, cell–cell fusion in response to foreign bodies, and their self-sacrifice as occurs during NETosis.

scholarly journals The Role of Syk/CARD9-Coupled C-Type Lectin Receptors in Immunity toMycobacterium tuberculosisInfections

2010 ◽  
Vol 2010 ◽  
pp. 1-9 ◽  
Author(s):  
Mohlopheni Jackson Marakalala ◽  
Lisa M. Graham ◽  
Gordon D. Brown
Keyword(s):  
Immune Response ◽  
Pattern Recognition ◽  
Mycobacterium Tuberculosis ◽  
Immune Cells ◽  
Innate Immune ◽  
Innate Immune Cells ◽  
Lectin Receptors ◽  
Molecular Patterns

There is increasing interest in understanding the mechanisms underlying the interactions that occur betweenMycobacterium tuberculosisand host innate immune cells. These cells express pattern recognition receptors (PRRs) which recognise mycobacterial pathogen-associated molecular patterns (PAMPs) and which can influence the host immune response to the infection. Although many of the PRRs appear to be redundant in the control ofM. tuberculosisinfectionin vivo, recent discoveries have revealed a key, nonredundant, role of the Syk/CARD9 signalling pathway in antimycobacterial immunity. Here we review these discoveries, as well as recent data investigating the role of the Syk/CARD9-coupled PRRs that have been implicated in mycobacterial recognition, including Dectin-1 and Mincle.

scholarly journals Stress Hyperglycemia, Insulin Treatment, and Innate Immune Cells

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Fangming Xiu ◽  
Mile Stanojcic ◽  
Li Diao ◽  
Marc G. Jeschke
Keyword(s):  
Insulin Resistance ◽  
Innate Immunity ◽  
Immune System ◽  
Critical Illness ◽  
Immune Cells ◽  
Innate Immune System ◽  
Insulin Treatment ◽  
Innate Immune ◽  
Morbidity And Mortality ◽  
Innate Immune Cells

Hyperglycemia (HG) and insulin resistance are the hallmarks of a profoundly altered metabolism in critical illness resulting from the release of cortisol, catecholamines, and cytokines, as well as glucagon and growth hormone. Recent studies have proposed a fundamental role of the immune system towards the development of insulin resistance in traumatic patients. A comprehensive review of published literatures on the effects of hyperglycemia and insulin on innate immunity in critical illness was conducted. This review explored the interaction between the innate immune system and trauma-induced hypermetabolism, while providing greater insight into unraveling the relationship between innate immune cells and hyperglycemia. Critical illness substantially disturbs glucose metabolism resulting in a state of hyperglycemia. Alterations in glucose and insulin regulation affect the immune function of cellular components comprising the innate immunity system. Innate immune system dysfunction via hyperglycemia is associated with a higher morbidity and mortality in critical illness. Along with others, we hypothesize that reduction in morbidity and mortality observed in patients receiving insulin treatment is partially due to its effect on the attenuation of the immune response. However, there still remains substantial controversy regarding moderate versus intensive insulin treatment. Future studies need to determine the integrated effects of HG and insulin on the regulation of innate immunity in order to provide more effective insulin treatment regimen for these patients.

Uric acid-mediated inflammasome activation in IL-6 primed innate immune cells is regulated by baricitinib

2020 ◽  
Vol 31 (1) ◽  
pp. 270-275 ◽  
Author(s):  
Jumpei Temmoku ◽  
Yuya Fujita ◽  
Naoki Matsuoka ◽  
Takeshi Urano ◽  
Makiko Yashiro Furuya ◽  
...  
Keyword(s):  
Uric Acid ◽  
Immune Cells ◽  
Innate Immune ◽  
Inflammasome Activation ◽  
Innate Immune Cells

Role of Inflammasome Activation in Systemic Lupus Erythematosus: Are Innate Immune Cells Activated?

2021 ◽  
Vol 17 (4) ◽  
pp. 187-191
Author(s):  
Rodolfo Perez-Alamino ◽  
Raquel Cuchacovich ◽  
Luis R. Espinoza ◽  
Constance P. Porretta ◽  
Arnold H. Zea
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Immune Cells ◽  
Lupus Erythematosus ◽  
Innate Immune ◽  
Inflammasome Activation ◽  
Innate Immune Cells ◽  
Systemic Lupus

Latest Advances in Small Molecule TLR 7/8 Agonist Drug Research

2019 ◽  
Vol 19 (24) ◽  
pp. 2228-2238 ◽  
Author(s):  
David C. McGowan
Keyword(s):  
Immune Response ◽  
Innate Immunity ◽  
Small Molecule ◽  
Immune Cells ◽  
Drug Research ◽  
Innate Immune ◽  
Innate Immune Cells ◽  
Small Molecule Activation ◽  
Evolutionarily Conserved ◽  
Recent Developments

Toll-like receptors (TLRs) 7 and 8 play an important role in the activation of innate immune cells in mammals. These evolutionarily conserved receptors serve as important sentinels in response to infection. Activation of TLRs 7 and 8 triggers induction of a Th1 type innate immune response. The emergence of new structural and small molecule information generated in the last decade has contributed enormously to our understanding of this highly sophisticated process of innate immunity signaling. This review will focus on recent developments in the small molecule activation of TLR 7 and 8.

scholarly journals Trained Immunity and Cardiometabolic Disease

2020 ◽  
Author(s):  
Ioannis Mitroulis ◽  
George Hajishengallis ◽  
Triantafyllos Chavakis
Keyword(s):  
Innate Immunity ◽  
Progenitor Cells ◽  
Immune Cells ◽  
Innate Immune ◽  
Hematopoietic Progenitor Cells ◽  
Immune Memory ◽  
Cardiometabolic Disease ◽  
Innate Immune Cells ◽  
Hematopoietic Progenitor ◽  
Functional Changes

Until recently, immunologic memory was considered an exclusive characteristic of adaptive immunity. However, recent advances suggest that the innate arm of the immune system can also mount a type of nonspecific memory responses. Innate immune cells can elicit a robust response to subsequent inflammatory challenges after initial activation by certain stimuli, such as fungal-derived agents or vaccines. This type of memory, termed trained innate immunity (also named innate immune memory), is associated with epigenetic and metabolic alterations. Hematopoietic progenitor cells, which are the cells responsible for the generation of mature myeloid cells at steady-state and during inflammation, have a critical contribution to the induction of innate immune memory. Inflammation-triggered alterations in cellular metabolism, the epigenome and transcriptome of hematopoietic progenitor cells in the bone marrow promote long-lasting functional changes, resulting in increased myelopoiesis and consequent generation of trained innate immune cells. In the present brief review, we focus on the involvement of hematopoietic progenitors in the process of trained innate immunity and its possible role in cardiometabolic disease.

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