scholarly journals Perinatal Nutritional and Metabolic Pathways: Early Origins of Chronic Lung Diseases

2021 ◽  
Vol 8 ◽  
Author(s):  
Celien Kuiper-Makris ◽  
Jaco Selle ◽  
Eva Nüsken ◽  
Jörg Dötsch ◽  
Miguel A. Alejandre Alcazar
Keyword(s):  
Lung Diseases ◽  
Maternal Obesity ◽  
Current Knowledge ◽  
Oxygen Toxicity ◽  
Experimental Models ◽  
Nutrient Sensing ◽  
Matrix Remodeling ◽  
Comprehensive Overview ◽  
Chronic Lung Diseases ◽  
The Impact

Lung development is not completed at birth, but expands beyond infancy, rendering the lung highly susceptible to injury. Exposure to various influences during a critical window of organ growth can interfere with the finely-tuned process of development and induce pathological processes with aberrant alveolarization and long-term structural and functional sequelae. This concept of developmental origins of chronic disease has been coined as perinatal programming. Some adverse perinatal factors, including prematurity along with respiratory support, are well-recognized to induce bronchopulmonary dysplasia (BPD), a neonatal chronic lung disease that is characterized by arrest of alveolar and microvascular formation as well as lung matrix remodeling. While the pathogenesis of various experimental models focus on oxygen toxicity, mechanical ventilation and inflammation, the role of nutrition before and after birth remain poorly investigated. There is accumulating clinical and experimental evidence that intrauterine growth restriction (IUGR) as a consequence of limited nutritive supply due to placental insufficiency or maternal malnutrition is a major risk factor for BPD and impaired lung function later in life. In contrast, a surplus of nutrition with perinatal maternal obesity, accelerated postnatal weight gain and early childhood obesity is associated with wheezing and adverse clinical course of chronic lung diseases, such as asthma. While the link between perinatal nutrition and lung health has been described, the underlying mechanisms remain poorly understood. There are initial data showing that inflammatory and nutrient sensing processes are involved in programming of alveolarization, pulmonary angiogenesis, and composition of extracellular matrix. Here, we provide a comprehensive overview of the current knowledge regarding the impact of perinatal metabolism and nutrition on the lung and beyond the cardiopulmonary system as well as possible mechanisms determining the individual susceptibility to CLD early in life. We aim to emphasize the importance of unraveling the mechanisms of perinatal metabolic programming to develop novel preventive and therapeutic avenues.

The Oxford Handbook of Hope

2017 ◽  
Keyword(s):  
Current Knowledge ◽  
Physical And Mental Health ◽  
Comprehensive Overview ◽  
Future Directions ◽  
Theoretical Perspectives ◽  
The Many ◽  
The Impact ◽  
Made In

The Oxford Handbook of Hope provides a comprehensive overview of current knowledge regarding the science and practice of hope. Hope has long been a topic of interest to philosophers and the general public, but it was only in recent decades that hope became a focus of psychological science. Rick Snyder defined hope as a cognitive trait that helps individuals to identify and pursue goals and consists of two components: pathways, the perceived capacity to identify strategies necessary to achieve goals, and agency, the willpower or motivation to pursue those pathways to achieve goals. Hope has become one of most robust and promising topics in the burgeoning field of positive psychology. This book reviews the progress that has been made in the past 25 years regarding the origins and influence of hope. Topics covered include current theoretical perspectives on how best to define hope and how it is distinct from related constructs, current best practices for measuring and quantifying hope, interventions and strategies for promoting hope across different settings and the lifespan, the impact that hope has on many dimensions and domains of physical and mental health, and the many ways and contexts in which hope promotes resilience and positive functioning. Experts in the field both review what is currently known about the role of hope in different domains and identify topics and questions that can help to guide the next decade of research. The handbook concludes with a collaborative vision on the future directions of the science of hope.

Structural diversity in echinocandin biosynthesis: the impact of oxidation steps and approaches toward an evolutionary explanation

2017 ◽  
Vol 72 (1-2) ◽  
pp. 1-20 ◽  
Author(s):  
Wolfgang Hüttel
Keyword(s):  
Secondary Metabolism ◽  
Current Knowledge ◽  
Structural Diversity ◽  
Special Focus ◽  
Oxidation Reactions ◽  
Metabolic Diversity ◽  
Comprehensive Overview ◽  
Single Organism ◽  
The Impact ◽  
Best Fit

AbstractEchinocandins are an important group of cyclic non-ribosomal peptides with strong antifungal activity produced by filamentous fungi from Aspergillaceae and Leotiomycetes. Their structure is characterized by numerous hydroxylated non-proteinogenic amino acids. Biosynthetic clusters discovered in the last years contain up to six oxygenases, all of which are involved in amino acid modifications. Especially, variations in the oxidation pattern induced by these enzymes account for a remarkable structural diversity among the echinocandins. This review provides an overview of the current knowledge of echinocandin biosynthesis with a special focus on diversity-inducing oxidation steps. The emergence of metabolic diversity is further discussed on the basis of a comprehensive overview of the structurally characterized echinocandins, their producer strains and biosynthetic clusters. For the pneumocandins, echinocandins produced byGlarea lozoyensis, the formation of metabolic diversity in a single organism is analyzed. It is compared to two common models for the evolution of secondary metabolism: the ‘target-based’ approach and the ‘diversity-based’ model. Whereas the early phase of pneumocandin biosynthesis supports the target-based model, the diversity-inducing late steps and most oxidation reactions best fit the diversity-based approach. Moreover, two types of diversity-inducing steps can be distinguished. Although incomplete hydroxylation is a common phenomenon in echinocandin production and secondary metabolite biosynthesis in general, the incorporation of diverse hydroxyprolines at position 6 is apparently a unique feature of pneumocandin biosynthesis, which stands in stark contrast to the strict selectivity found in echinocandin biosynthesis by Aspergillaceae. The example of echinocandin biosynthesis shows that the existing models for the evolution of secondary metabolism can be well applied to parts of the pathway; however, thus far, there is no comprehensive theory that could explain the entire biosynthesis.

scholarly journals Impact of Housing Environment on the Immune System in Chickens: A Review

Animals ◽  
2020 ◽  
Vol 10 (7) ◽  
pp. 1138 ◽  
Author(s):  
Tanja Hofmann ◽  
Sonja S. Schmucker ◽  
Werner Bessei ◽  
Michael Grashorn ◽  
Volker Stefanski
Keyword(s):  
Immune System ◽  
Allostatic Load ◽  
Current Knowledge ◽  
Future Research ◽  
Poultry Production ◽  
Negative Consequences ◽  
Comprehensive Overview ◽  
Housing Environment ◽  
Wide Range ◽  
The Impact

During their lifespan, chickens are confronted with a wide range of acute and chronic stressors in their housing environment that may threaten their welfare and health by modulating the immune system. Especially chronic stressful conditions can exceed the individual’s allostatic load, with negative consequences for immunity. A fully functional immune system is mandatory for health and welfare and, consequently, also for high productivity and safe animal products. This review provides a comprehensive overview of the impact of housing form, light regime as well as aerial ammonia and hydrogen sulfide concentrations on the immune system in chickens. Certain housing conditions are clearly associated with immunological alterations which potentially impair the success of vaccinations or affect disease susceptibility. Such poor conditions counteract sustainable poultry production. This review also outlines current knowledge gaps and provides recommendations for future research.

THE IMPACT OF CHRONIC LUNG DISEASES ON THE QUALITY OF LIFE OF PATIENTS MEASURED BOTH BY DISEASE SPECIFIC AND GENERIC INSTRUMENTS

CHEST Journal ◽  
2005 ◽  
Vol 128 (4) ◽  
pp. 393S
Author(s):  
Siu Pui Lam ◽  
Pui Shan Lam ◽  
Wai Woon Ho ◽  
Ho Pui So
Keyword(s):  
Quality Of Life ◽  
Lung Diseases ◽  
Chronic Lung Diseases ◽  
The Impact ◽  
Disease Specific

scholarly journals Gut Microbiota, in the Halfway between Nutrition and Lung Function

Nutrients ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 1716
Author(s):  
Christophe Espírito Santo ◽  
Catarina Caseiro ◽  
Maria João Martins ◽  
Rosário Monteiro ◽  
Inês Brandão
Keyword(s):  
Lung Function ◽  
Gut Microbiota ◽  
Intestinal Microbiota ◽  
Lung Diseases ◽  
Dietary Habits ◽  
Metabolic Diseases ◽  
Current Knowledge ◽  
Intestinal Barrier ◽  
Community Interest ◽  
The Impact

The gut microbiota is often mentioned as a “forgotten organ” or “metabolic organ”, given its profound impact on host physiology, metabolism, immune function and nutrition. A healthy diet is undoubtedly a major contributor for promoting a “good” microbial community that turns out to be crucial for a fine-tuned symbiotic relationship with the host. Both microbial-derived components and produced metabolites elicit the activation of downstream cascades capable to modulate both local and systemic immune responses. A balance between host and gut microbiota is crucial to keep a healthy intestinal barrier and an optimal immune homeostasis, thus contributing to prevent disease occurrence. How dietary habits can impact gut microbiota and, ultimately, host immunity in health and disease has been the subject of intense study, especially with regard to metabolic diseases. Only recently, these links have started to be explored in relation to lung diseases. The objective of this review is to address the current knowledge on how diet affects gut microbiota and how it acts on lung function. As the immune system seems to be the key player in the cross-talk between diet, gut microbiota and the lungs, involved immune interactions are discussed. There are key nutrients that, when present in our diet, help in gut homeostasis and lead to a healthier lifestyle, even ameliorating chronic diseases. Thus, with this review we hope to incite the scientific community interest to use diet as a valuable non-pharmacological addition to lung diseases management. First, we talk about the intestinal microbiota and interactions through the intestinal barrier for a better understanding of the following sections, which are the main focus of this article: the way diet impacts the intestinal microbiota and the immune interactions of the gut–lung axis that can explain the impact of diet, a key modifiable factor influencing the gut microbiota in several lung diseases.

Vascular endothelial growth factor in the lung

2006 ◽  
Vol 290 (2) ◽  
pp. L209-L221 ◽  
Author(s):  
Norbert F. Voelkel ◽  
R. William Vandivier ◽  
Rubin M. Tuder
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Lung Diseases ◽  
Cell Function ◽  
Adult Life ◽  
Vascular Endothelial ◽  
Comprehensive Overview ◽  
Endothelial Cell Function ◽  
Chronic Lung Diseases ◽  
Endothelial Growth Factor

Vascular endothelial growth factor (VEGF) is a pluripotent growth and permeability factor that has a broad impact on endothelial cell function. The lung tissue is very rich in this protein; many different lung cells produce VEGF and also respond to VEGF. VEGF is critical for the development of the lung and serves as a maintenance factor during adult life. In addition to the physiological functions of this protein, there is increasing evidence that VEGF also plays a role in several acute and chronic lung diseases, such as acute lung injury, severe pulmonary hypertension, and emphysema. Here we provide a comprehensive overview of the rapidly expanding literature.

Apigenin Alleviates Oxidative Stress-Induced Cellular Senescence via Modulation of the SIRT1-NAD+-CD38 Axis

2021 ◽  
pp. 1-16
Author(s):  
Bing Si Li ◽  
Ri Zhe Zhu ◽  
Seok-Hee Lim ◽  
Jae Ho Seo ◽  
Byung-Min Choi
Keyword(s):  
Oxidative Stress ◽  
Cellular Senescence ◽  
Lung Diseases ◽  
Molecular Mechanisms ◽  
Driving Mechanism ◽  
Dependent Manner ◽  
Aging Effects ◽  
Chronic Lung Diseases ◽  
Age Related ◽  
The Impact

Oxidative stress-induced cellular senescence is now regarded as an important driving mechanism in chronic lung diseases-particularly chronic obstructive pulmonary disease (COPD). 4′,5,7-trihydroxyflavone (Apigenin) is a natural flavonoid product abundantly present in fruits, vegetables, and Chinese medicinal herbs. It has been known that apigenin has anti-oxidant, anti-inflammatory and liver-protecting effects. The efficacy of apigenin for lung aging, however, has not been reported. In this study, we selected the hydrogen peroxide (H2O[Formula: see text]- or doxorubicin (DOXO)-induced senescence model in WI-38 human embryonic lung fibroblast cells to determine the potential anti-aging effects of apigenin in vitro and associated molecular mechanisms. We found that apigenin reduced senescence-associated [Formula: see text]-galactosidase (SA-[Formula: see text]-gal) activity and promoted cell growth, concomitant with a decrease in levels of Acetyl (ac)-p53, p21[Formula: see text], and p16[Formula: see text] and an increase in phospho (p)-Rb. Apigenin also increased the activation ratio of silent information regulator 1 (SIRT1), nicotinamide adenine dinucleotide (NAD[Formula: see text], and NAD[Formula: see text]/NADH and inhibited cluster of differentiation 38 (CD38) activity in a concentration-dependent manner. SIRT1 inhibition by SIRT1 siRNA abolished the anti-aging effect of apigenin. In addition, CD38 inhibition by CD38 siRNA or apigenin increased the SIRT1 level and reduced H2O2-induced senescence. Our findings suggest that apigenin is a promising phytochemical for reducing the impact of senescent cells in age-related lung diseases such as COPD.

scholarly journals Shared epithelial pathways to lung repair and disease

2017 ◽  
Vol 26 (144) ◽  
pp. 170048 ◽  
Author(s):  
Magda Spella ◽  
Ioannis Lilis ◽  
Georgios T. Stathopoulos
Keyword(s):  
Epithelial Cells ◽  
Lung Diseases ◽  
Current Knowledge ◽  
Cell Types ◽  
Lung Epithelial Cells ◽  
Chronic Obstructive ◽  
Lung Repair ◽  
Chronic Lung Diseases ◽  
Lung Epithelial ◽  
Lung Regeneration

Chronic lung diseases present tremendous health burdens and share a common pathobiology of dysfunctional epithelial repair. Lung adenocarcinoma, the leading cancer killer worldwide, is caused mainly by chemical carcinogens of tobacco smoke that induce mutations in pulmonary epithelial cells leading to uncontrolled epithelial proliferation. Lung epithelial cells that possess the capacity for self-renewal and regeneration of other lung cell types are believed to underlie the pathobiology of chronic obstructive, fibrotic and neoplastic lung disorders. However, the understanding of lung epithelial progenitor cell hierarchy and turnover is incomplete and a comprehensive model of the cellular and transcriptional events that underlie lung regeneration and carcinogenesis is missing. The mapping of these processes is extremely important, since their modulation would potentially allow effective cure and/or prevention of chronic lung diseases. In this review we describe current knowledge on cellular and molecular pathways at play during lung repair and carcinogenesis and summarise the critical lung cell populations with regenerative and cancerous potential.

scholarly journals The impact of long-term azithromycin on antibiotic resistance in HIV-associated chronic lung disease

2021 ◽  
pp. 00491-2021
Author(s):  
Regina E. Abotsi ◽  
Mark P. Nicol ◽  
Grace McHugh ◽  
Victoria Simms ◽  
Andrea M. Rehman ◽  
...  
Keyword(s):  
Antibiotic Resistance ◽  
Lung Diseases ◽  
Treatment Needs ◽  
Post Intervention ◽  
Exact Test ◽  
Chronic Lung Diseases ◽  
Selection For ◽  
The Impact ◽  
To Receive

Selection for resistance to azithromycin (AZM) and other antibiotics such as tetracyclines and lincosamides remains a concern with long-term AZM use for treatment of chronic lung diseases (CLD). We investigated the impact of 48 weeks of AZM on the carriage and antibiotic resistance of common respiratory bacteria among children with HIV-associated CLD.Nasopharyngeal (NP) swabs and sputa were collected at baseline, 48 and 72 weeks from participants with HIV-associated CLD randomised to receive weekly AZM or placebo for 48 weeks and followed post-intervention until 72 weeks. The primary outcomes were prevalence and antibiotic resistance of Streptococcus pneumoniae (SP), Staphylococcus aureus (SA), Haemophilus influenzae (HI), and Moraxella catarrhalis (MC) at these timepoints. Mixed-effects logistic regression and Fisher's exact test were used to compare carriage and resistance respectively.Of 347 (174 AZM, 173 placebo) participants (median age 15 years [IQR=13–18], females 49%),NP carriage was significantly lower in the AZM (n=159) compared to placebo (n=153) arm for SP (18% versus 41%, p<0.001), HI (7% versus 16%, p=0.01), and MC (4% versus 11%, p=0.02); SP resistance to AZM (62% [18/29] versus 13%[8/63], p<0.0001) or tetracycline (60%[18/29] versus 21%[13/63], p<0.0001) were higher in the AZM arm. Carriage of SA resistant to AZM (91% [31/34] versus 3% [1/31], p<0.0001), tetracycline (35% [12/34] versus 13% [4/31], p=0.05) and clindamycin (79% [27/34] versus 3% [1/31], p<0.0001) was also significantly higher in the AZM arm and persisted at 72 weeks. Similar findings were observed for sputa.The persistence of antibiotic resistance and its clinical relevance for future infectious episodes requiring treatment needs further investigation.

scholarly journals A Review of The Role of The Microbiome on Immune Responses and Its Association With Cystic Fibrosis

2021 ◽  
Vol 3 (2) ◽  
pp. 75-88
Author(s):  
Mahtab Ghorban Movahed ◽  
◽  
Ahya Abdi Ali ◽  
Keyword(s):  
Cystic Fibrosis ◽  
Immune Responses ◽  
Lung Diseases ◽  
Complex Disease ◽  
Pulmonary Complications ◽  
Host Susceptibility ◽  
Chronic Obstructive ◽  
Chronic Lung Diseases ◽  
The Impact

In recent years, the microbiome has been recognized as a key regulator of immune responses. Evidence suggests that changes in the microbiome can lead to chronic disease and even exacerbation of the disease. Impairment of innate immunity resulting from microbial incompatibility may worsen host susceptibility to infection and exacerbate chronic lung diseases. Specific microbes play a key role in improving immune responses and microbial incompatibility is involved in chronic lung diseases such as asthma, chronic obstructive pulmonary disease, and Cystic Fibrosis (CF). CF is an extremely complex disease that results from a gene mutation. Lack of expression of Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) has late complications. Incompatibility in lung microbiota is associated with chronic lung diseases, but it is not determined whether this incompatibility can cause health problems or ineffective regulation of immune response create the disease and its progression. In the CF, due to the deficiency of the immune system, many opportunistic microorganisms, including Pseudomonas. aeruginosa or Staphylococcus aureus are colonized in the patient’s lung and due to an immunodeficiency causedby a defect in the system CFTR, lungs are unable to clear the bacteria that leads to severe pulmonary complications and respiratory and digestive problems in such patients. Therefore, in these patients, the microbiome contributes to dysfunctional immune responses and disease exacerbations. This review summarizes the impact of the microbiome on host immune responses and its relationship with CF to explore the role of the microbiome in causing CF.

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