Contribution of Macrophages in Sepsis-induced Pulmonary Apoptosis and Acute Lung Injury PDF Download

Author: Osama Kishta
Publisher:
ISBN:
Category :
Languages : en
Pages : 96

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Author: Habib Moshref Razavi
Publisher:
ISBN:
Category :
Languages : en
Pages : 448

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Author: E. Abraham
Publisher: Springer Science & Business Media
ISBN: 9783540301585
Category : Medical
Languages : en
Pages : 476

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There have been tremendous advances in understanding the cellular mechanisms involved in sepsis and contributing to the development of multiple organ dysfunction and mortality in this setting. The chapters in this book provide up-to-date insights into important pathways that are initiated by sepsis.

Author: Hector R. Wong
Publisher: Springer Science & Business Media
ISBN: 1461514274
Category : Medical
Languages : en
Pages : 329

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Book Description
Acute lung injury (ALI) impacts patient care in every ICU in the world. Our collective understanding of this condition has grown immensely over the past decade but morbidity and mortality remain unacceptably high. To enhance the understanding of clinicians and researchers, this book addresses the pathophysiology of acute lung injury from a molecular and cellular standpoint; includes animal models of acute lung injury and points to potential therapeutic advances based on scientific findings. It is a concise compendium of the multiple pathways, mechanisms and molecules involved in the pathophysiology of acute lung injury and is intended to help caregivers understand the process and thus care for patients more effectively.

Author: Xiaobing Fu
Publisher: Springer
ISBN: 981133353X
Category : Medical
Languages : en
Pages : 389

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Book Description
This book discusses recent progress in organ damage and tissue repair following severe trauma and sepsis. In part 1, it introduces the theory and clinical practice in organ damage. In part 2, it covers all the subjects of sepsis, ranging from mechanism, inflammation, and infection to the lung injury and neonatal sepsis. In part 3, it discusses 4 new advances techniques in tissue repair. There are 20 chapters contributed by experts in each area. This book is a valuable reference for scientists and clinicians to know the new knowledge and technology in severe trauma and sepsis, which will benefit their work in research and clinic through multidisciplinary collaboration.

Author: Michael Sean Valentine
Publisher:
ISBN:
Category :
Languages : en
Pages : 164

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Book Description
Patients with severe lung pathologies, such as Acute Respiratory Distress Syndrome (ARDS), often require mechanical ventilation as a clinical intervention; however, this procedure frequently exacerbates the original pulmonary issue and produces an exaggerated inflammatory response that potentially leads to sepsis, multisystem organ failure, and mortality. This acute lung injury (ALI) condition has been termed Ventilator-Induced Lung Injury (VILI). Alveolar overdistension, cyclic atelectasis, and biotrauma are the primary injury mechanisms in VILI that lead to the loss of alveolar barrier integrity and pulmonary inflammation. Stress and strains during mechanical ventilation are believed to initiate alveolar epithelial mechanotransduction signaling mechanisms that contribute to injury and repair responses and lead to the direct activation of resident lung and recruited macrophages. These types of cells, alveolar and interstitial macrophages, have various polarization states, such as M1 and M2, which are believed to play significant roles in tissue homeostasis and inflammatory regulation. Epidemiology studies have also suggested that age influences lung function and is a predictive factor in the severity of VILI; however, the mechanisms of aging that influence the progression or increased susceptibility of VILI in the elderly are still unknown. Aging also critically impacts immune system function and may increase inflammation in healthy individuals, which is known as inflammaging. Disruption to Endoplasmic Reticulum (ER) homeostasis results in a condition known as ER stress that leads to disruption of cellular homeostasis, apoptosis, and inflammation. ER stress is increased with aging and other pathological stimuli. We hypothesized that age and mechanical stretch increase alveolar epithelial cells' pro-inflammatory responses that are mediated by ER stress. Furthermore, we hypothesized that inhibition of this upstream mechanism with 4PBA, an ER stress reducer, alleviates subsequent inflammation and monocyte recruitment. Type II alveolar epithelial cells (ATII) were harvested from C57Bl6/J mice 2 months (young) and 20 months (old) of age. The cells were cyclically stretched at 15% change in surface area for up to 24 hours. Prior to stretch, groups were administered 4PBA or vehicle as a control. Mechanical stretch and age upregulated ER stress and proinflammatory signaling expression in ATIIs. Age increases susceptibility to stretch-induced ER stress and downstream inflammatory gene expression in a primary ATII epithelial cell model. Administration of 4PBA attenuated the increased ER stress and proinflammatory responses from stretch and/or age and significantly reduced monocyte migration to ATII conditioned media. Recent studies also suggest a critical, protective role for the bioactive sphingolipid mediator sphingosine-1-phosphate (S1P) signaling in several lung pathologies and macrophage differentiation and function. It is unknown whether aging alters S1P signaling that appears involved in lung inflammation, injury, and apoptosis. We postulated that aging and injurious mechanical ventilation synergistically impair macrophage polarization in the lung that is associated with dysfunctional S1P signaling and produces amplified alveolar barrier damage and diminished pulmonary function. Young (2-3mo) and old (20-25mo) C57BL/6 mice were mechanically ventilated for 2 hours using pressure-controlled mechanical ventilation (PCMV). We assessed tissue mechanics, lung injury/repair responses, macrophage polarization, and S1P/S1PL lung activity. PCMV exacerbated lung injury in old mice. CD80 and CD206, classical and alternative macrophage markers, were both elevated in old alveolar and interstitial macrophages that also further increased due to PCMV. S1P lung levels were elevated in the young ventilated mice compared to the control group, which was not observed with the old mice. S1P lyase expression increased in the young and old ventilated mice and the old nonventilated group. 2-Acetyl-4- tetrahydroxybutyl Imidazole (THI) administration reduced indications of ALI in both young and old mice and altered macrophage polarization. The structural and cellular implications in injury responses of an aging lung more accurately represent clinical conditions and warrant further study at a cellular level. We found that aging significantly impacts alveolar epithelial and lung macrophage signaling and polarization; moreover, these aging disparities may result from elevated ER stress and/or a loss of protective S1P signaling in response to mechanical stretch that further contribute to the age-associated susceptibility and alveolar barrier dysfunction. Furthermore, administration of 4PBA, an ER stress inhibitor, and THI, an S1PL inhibitor, attenuated ER stress and S1PL activity, respectively, as well as several indications of ALI.

Author: Augustine M.K. Choi
Publisher: CRC Press
ISBN: 1420088416
Category : Medical
Languages : en
Pages : 478

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Book Description
The only available text to focus primarily on Acute Respiratory Distress Syndrome (ARDS).Thoroughly revised content and ten new chapters provide pulmonologists with the latest developments and applications of pharmacological and mechanical therapies needed to treat the debilitating and difficult condition of ARDS.Highlights include:the definition,

Author: Nicholas S. Ward
Publisher: Humana Press
ISBN: 3319484702
Category : Medical
Languages : en
Pages : 271

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Book Description
This book is designed to provide a comprehensive and state-of-the-art resource for clinicians who care for patients with sepsis and research scientist alike, . Patients with severe sepsis requiring ICU admission have very high rates of ICU and overall hospital mortality, with estimates ranging from 18 to 50%. Risk factors for death from sepsis include underlying illness, increased age, and multi-system organ failure. This is compounded by the significant variation in the management of early severe sepsis. Care of these patients and clinical conditions can be quite complex, and materials are collected from the most current, evidence-based resources. Book sections have been structured to review the overall definitions and epidemiology of sepsis as well as current insights into the pathophysiology of sepsis. This review summarizes the evidence for the international consensus guidelines for the identification and management of sepsis. The latter part of this book reviews emerging concepts and approaches in the diagnosis and management of sepsis that may significantly reduce mortality in the future. Sepsis: Pathophysiology, Definitions and the Challenge of Bedside Management represents a collaboration between authors drawn from a variety of disciplines and contributions from basic scientists and highly recognized clinical opinion leaders with expertise in clinical trials.​

Author: Heiko Mühl
Publisher: Frontiers E-books
ISBN: 2889190730
Category :
Languages : en
Pages : 139

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Book Description
Macrophages were initially identified as a key element in the innate host response to infection and injury due to their phagocytic clearance and elimination of pathogenic and non-pathogenic entities. However, as macrophage research advanced it became clear that not only are these cells amenable to the acquisition of multiple plastic phenotypes during inflammatory responses to different pathogens, they also play a paramount role in the termination of inflammation and acquired immune responses. In addition, macrophages profoundly affect host physiology when they migrate to distant sites and differentiate to specialized cells, like foam cells, osteoclasts, adipose tissue- and tumor -associated macrophages and other macrophage-derived cell types. These processes are affected by the inflammation-resolution axis and can result in health threats, such as atherosclerosis, bone loss, obesity, fibrosis and cancer. This Research Topic issue will cover a wide range of topics in macrophage biology: 1. Macrophages in immune responses to pathogens 2. Macrophages in the termination of acute and acquired immunity. 3. The role of macrophages and their descendents in inflammation-associated pathologies. 4. Macrophage polarization and differentiation. Particular focus will be given to the modulation of macrophage phenotype and function following their encounter with apoptotic cells and the signaling cascades that govern these changes.

Author: Didier Dreyfuss
Publisher: CRC Press
ISBN: 1420019260
Category : Medical
Languages : en
Pages : 776

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Book Description
This reference surveys current best practices in the prevention and management of ventilator-induced lung injury (VILI) and spans the many pathways and mechanisms of VILI including cell injury and repair, the modulation of alveolar-capillary barrier properties, and lung and systemic inflammatory consequences of injurous mechanical ventilation. Cons