scholarly journals Modulation of Bacterial Pathogenesis by Oppressive Aging Factors: Insights into Host-Pneumococcal Interaction Strategies

2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
Pooja Shivshankar
Keyword(s):  
Cellular Senescence ◽  
Significant Risk ◽  
Significant Risk Factor ◽  
The Elderly ◽  
Receptor Expression ◽  
Chronic Obstructive ◽  
Related Phenomenon ◽  
Aged Mice ◽  
Inflammatory Status ◽  
Age Related

Streptococcus pneumonia, (Spn, the pneumococcus), is the leading cause of community-acquired pneumonia (CAP) and is responsible for 15–40% deaths in the elderly worldwide. A primed inflammatory status is a significant risk factor for the increased severity of infectious diseases among the elderly (≥65 years of age). Studies have shown that expression of host receptors that the pneumococci bind to invade the tissues are increased thereby increasing the susceptibility to pneumococcal challenge in aged mice. Cellular senescence, an age-related phenomenon that leads to cell cycle arrest may also contribute to increased inflammation in aged mice. Evidence of cellular senescence in aged lungs of humans and mice adds credits to the concept of inflammaging and enhanced bacterial ligands expression during aging. Furthermore, cell senescence has been shown to occur in age-associated lung pathologies such as idiopathic pulmonary fibrosis (IPF) and chronic obstructive pulmonary disease (COPD) that may predispose the elderly to pathogenic assaults, including S. pneumoniae. This review highlights the aspects of: chronic inflammation in the aged population; contribution of cellular senescence to age-associated inflammation and their impact on host receptor expression; and, increased susceptibility of fibrosis and emphysematous lesions-bearing lungs to microbial infections.

scholarly journals 453 - The effect of ageing in personality and emotions

2020 ◽  
Vol 32 (S1) ◽  
pp. 173-173
Author(s):  
Catarina Pedro ◽  
Mariana Duarte ◽  
Beatriz Jorge ◽  
Daniela Freitas
Keyword(s):  
Old Age ◽  
Emotional Processing ◽  
Personality Development ◽  
Early Adulthood ◽  
Significant Risk ◽  
Marked Change ◽  
Significant Risk Factor ◽  
The Elderly ◽  
Big Five Personality ◽  
Age Related

Introduction:Personality and emotions have not been studied as thoroughly as cognition in old age. Recent research suggests personality changes across the entire life span, through middle age and even into old age. Thus, the previous assumption of stability in personality traits from early adulthood has been challenged and novel approaches to the study of personality development have emerged.Objectives:The aim of this presentation is to describe the effects of the ageing process in personality and emotions.Methods:A non-systematic review of the literature was performed on PubMed, PsycINFO and Web of science using selected keywords.Results:When older adults compare their current and past selves, they usually perceive a subjective growth in personality. Descriptive research suggests that the big five personality characteristics (neuroticism, extraversion, openness, agreeableness and conscientiousness) remain generally stable over the lifespan, despite variations in life experiences. Some studies revealed age-related linear decrease in extraversion. One of the studies found that hearing impairment, already identified as a significant risk factor for social isolation, was related to this decline in extraversion. Although levels of neuroticism tends to go down over the course of adulthood, the increased vulnerabilities that accompany old age may amplify neurotic traits, increasing worries about physical health and memory, common features of depression in the elderly. Emotions, relative to more neutral knowledge and skills, increase in later years. Elderly have better control over emotions than do younger adults, they reason more flexibly about emotion-laden dilemmas and remember emotionally charged information better than neutral facts. Older people also rely more often on emotion-focused forms of coping, as opposed to active, problem-solving approaches.Conclusions:Core features of personality seem to remain relatively stable throughout adulthood and any marked change in mood or social behavior may indicate a disorder. However, more subtle reordering of personal priorities and shifts in coping styles are common with normal ageing. The richness of emotional processing in older persons runs counter to the generally declining patterns seen in many cognitive and physical skills.

scholarly journals The Biology and Pathobiology of Glutamatergic, Cholinergic, and Dopaminergic Signaling in the Aging Brain

2021 ◽  
Vol 13 ◽  
Author(s):  
Anna Gasiorowska ◽  
Malgorzata Wydrych ◽  
Patrycja Drapich ◽  
Maciej Zadrozny ◽  
Marta Steczkowska ◽  
...  
Keyword(s):  
Neurodegenerative Diseases ◽  
Experimental Studies ◽  
Significant Risk ◽  
Significant Risk Factor ◽  
The Elderly ◽  
Aging Brain ◽  
Detailed Knowledge ◽  
Age Related ◽  
Parkinson’S Diseases ◽  
The Brain

The elderly population is growing worldwide, with important health and socioeconomic implications. Clinical and experimental studies on aging have uncovered numerous changes in the brain, such as decreased neurogenesis, increased synaptic defects, greater metabolic stress, and enhanced inflammation. These changes are associated with cognitive decline and neurobehavioral deficits. Although aging is not a disease, it is a significant risk factor for functional worsening, affective impairment, disease exaggeration, dementia, and general disease susceptibility. Conversely, life events related to mental stress and trauma can also lead to accelerated age-associated disorders and dementia. Here, we review human studies and studies on mice and rats, such as those modeling human neurodegenerative diseases, that have helped elucidate (1) the dynamics and mechanisms underlying the biological and pathological aging of the main projecting systems in the brain (glutamatergic, cholinergic, and dopaminergic) and (2) the effect of defective glutamatergic, cholinergic, and dopaminergic projection on disabilities associated with aging and neurodegenerative disorders, such as Alzheimer’s and Parkinson’s diseases. Detailed knowledge of the mechanisms of age-related diseases can be an important element in the development of effective ways of treatment. In this context, we briefly analyze which adverse changes associated with neurodegenerative diseases in the cholinergic, glutaminergic and dopaminergic systems could be targeted by therapeutic strategies developed as a result of our better understanding of these damaging mechanisms.

Hip Fracture

2019 ◽  
pp. 281-293
Author(s):  
Franchesca Arias ◽  
Catherine C. Price ◽  
Jeffrey C. Gadsden
Keyword(s):  
Risk Factor ◽  
Hip Fracture ◽  
Significant Risk ◽  
Public Health Problem ◽  
Significant Risk Factor ◽  
The Elderly ◽  
Age Related ◽  
Significant Public Health ◽  
Continuous Nerve Block ◽  
Fascia Iliaca Block

This chapter discusses hip fracture, which is a significant public health problem associated with substantial morbidity and mortality. Pain with hip fracture is often severe but despite this is frequently undertreated in the elderly population. Untreated pain not only is inhumane but also is a significant risk factor for delirium in this population that is already at increased risk due to age-related cognitive decline. Hip fracture patients benefit from early intervention with regional analgesic techniques such as femoral or fascia iliaca block, as well as a scheduled regimen of nonopioid analgesics such as acetaminophen and nonsteroidal anti-inflammatory medications. While opioids are known to contribute to risk for delirium, pain itself is a much stronger risk factor, and when nonopioid options are exhausted, opioids should be carefully considered. Continuous nerve block techniques provide opportunities for extended pain relief, which is associated with improved recovery profile, greater satisfaction, and a decreased risk for complications.

Abstract 65: Restoration of Growth Differentiation Factor 11 Protects Against Stroke in Mice

Stroke ◽  
2016 ◽  
Vol 47 (suppl_1) ◽  
Author(s):  
Anjali Chauhan ◽  
Jacob Hudobenko ◽  
Anthony Patrizz ◽  
Louise D McCullough
Keyword(s):  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
The Elderly ◽  
Vehicle Group ◽  
Peripheral Tissues ◽  
Delayed Treatment ◽  
Aged Mice ◽  
Infarct Area ◽  
Age Related

Introduction: GDF 11 is a member of the transforming growth factor β superfamily. Loss of GDF11 occurs with aging and declining levels correlate with several detrimental age-associated phenotypes in both peripheral tissues and brain. Restoration of GDF11 enhances neurogenesis and cognitive function in aged mice. Brain expression of GDF11 has not been investigated after stroke. Stroke differentially affects the elderly. In this work we examined the role of GDF11 in aging, stroke and its potential utility as a neuroprotective agent. Methods: Male C57/BL6NCrl young (2-3 months) and aged (19-21) mice were used. Brain GDF11 expression was evaluated in young and aged mice by western blot. Focal ischemia was induced with a transient middle cerebral artery occlusion (MCAO). Mice were randomly assigned into two groups and were subjected to 90 min MCAO. Group 1 received vehicle (phosphate buffered saline) and group 2 was administered rGDF11 (100 ug/kg., ip) at the onset of ischemia. In additional experiments, the efficacy of delayed treatment (3 h after ischemia) with rGDF11 was tested. These mice were subjected to a 60 min MCAO. Mice were euthanized after 24 hours and 7 days respectively and brains were harvested to estimate infarct area. Results: A significant decrease in brain GDF11 levels was observed in aged mice as compared to young (p<0.05). Additionally, a significant decline in brain GDF11 expression was observed after stroke at 24 hours vs. sham groups (p<0.05). A significant decrease in cortical and hemispheric infarct area was observed in the rGDF11 group (cortical 48.73±1.05; hemisphere 49.68±3.58) as compared to vehicle group (60.54±4.88; 61.35±6.03), when GDF was administered at the time of ischemia. Delayed treatment with rGDF11 also reduced infarct at 7 days. Conclusions: Brain GDF11 levels decline with age and after stroke. Supplementation with rGDF11 ameliorates stroke induced injury in young mice at 24h and 7 days. These finding suggest potential role of GDF11 in age and stroke. Restoration of age-related loss of GDF may be a viable therapy for stroke.

scholarly journals Asthma in the Elderly: Can We Distinguish It from COPD?

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Eleni G. Tzortzaki ◽  
Athanasia Proklou ◽  
Nikolaos M. Siafakas
Keyword(s):  
Late Onset ◽  
Airflow Obstruction ◽  
Bronchial Hyperresponsiveness ◽  
The Elderly ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Age Related ◽  
Inflammatory Pattern ◽  
Common Clinical Practice ◽  
Elderly Asthmatics

Asthma in older adults affects quality of life and results in a higher hospitalization rate and mortality. In common clinical practice, asthma in the elderly is underdiagnosed and undertreated or overdiagnosed and mistreated. The age-related reduction in perception of shortness of breath and the high incidence of comorbidities make the diagnosis and management more difficult and challenging for the physicians. Chronic obstructive pulmonary disease (COPD) is usually easy to distinguish from asthma, but sometimes the distinction from late-onset asthma in older patients, particularly in cigarette smokers, is difficult and may be impossible. Both diseases are characterized by the presence of airflow obstruction but have distinct pathogenesis, inflammatory pattern, and prognosis. The distinction between Asthma and COPD based simply on spirometric parameters is difficult especially in the elderly asthmatics. The combination of lung function testing, bronchial hyperresponsiveness (BHR) and atopy status, HRCT scans, and the newly developed biological techniques, allowing the assessment of biomarker profiles, could facilitate the distinction between these diseases.

scholarly journals Macrophage LC3-associated phagocytosis is an immune defense against Streptococcus pneumoniae that diminishes with host aging

2020 ◽  
Vol 117 (52) ◽  
pp. 33561-33569
Author(s):  
Megumi Inomata ◽  
Shuying Xu ◽  
Pallavi Chandra ◽  
Simin N. Meydani ◽  
Genzou Takemura ◽  
...  
Keyword(s):  
Streptococcus Pneumoniae ◽  
Inflammatory Responses ◽  
The Elderly ◽  
Invasive Disease ◽  
Immune Defense ◽  
Bacterial Killing ◽  
Murine Bone Marrow ◽  
Aged Mice ◽  
Age Related ◽  
Old Mice

Streptococcus pneumoniae is a leading cause of pneumonia and invasive disease, particularly, in the elderly. S. pneumoniae lung infection of aged mice is associated with high bacterial burdens and detrimental inflammatory responses. Macrophages can clear microorganisms and modulate inflammation through two distinct lysosomal trafficking pathways that involve 1A/1B-light chain 3 (LC3)-marked organelles, canonical autophagy, and LC3-associated phagocytosis (LAP). The S. pneumoniae pore-forming toxin pneumolysin (PLY) triggers an autophagic response in nonphagocytic cells, but the role of LAP in macrophage defense against S. pneumoniae or in age-related susceptibility to infection is unexplored. We found that infection of murine bone-marrow-derived macrophages (BMDMs) by PLY-producing S. pneumoniae triggered Atg5- and Atg7-dependent recruitment of LC3 to S. pneumoniae-containing vesicles. The association of LC3 with S. pneumoniae-containing phagosomes required components specific for LAP, such as Rubicon and the NADPH oxidase, but not factors, such as Ulk1, FIP200, or Atg14, required specifically for canonical autophagy. In addition, S. pneumoniae was sequestered within single-membrane compartments indicative of LAP. Importantly, compared to BMDMs from young (2-mo-old) mice, BMDMs from aged (20- to 22-mo-old) mice infected with S. pneumoniae were not only deficient in LAP and bacterial killing, but also produced higher levels of proinflammatory cytokines. Inhibition of LAP enhanced S. pneumoniae survival and cytokine responses in BMDMs from young but not aged mice. Thus, LAP is an important innate immune defense employed by BMDMs to control S. pneumoniae infection and concomitant inflammation, one that diminishes with age and may contribute to age-related susceptibility to this important pathogen.

scholarly journals Age-dependent involvement of gut mast cells and histamine in post-stroke inflammation

2020 ◽  
Author(s):  
Maria Pilar Blasco ◽  
Anjali Chauhan ◽  
Pedram Honarpisheh ◽  
Hilda Ahnstedt ◽  
John d’Aigle ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Mast Cells ◽  
Receptor Expression ◽  
Mast Cell Activation ◽  
Low Grade ◽  
Gut Inflammation ◽  
Aged Mice ◽  
Post Stroke ◽  
Age Related ◽  
The Brain

Abstract Background Risk of stroke-related morbidity and mortality increases significantly with age. Aging is associated with chronic, low-grade inflammation, which is thought to contribute to the poorer outcomes after stroke seen in the elderly. Histamine (HA) is a major molecular mediator of inflammation and mast cells residing in the gut are a primary source of histamine. Methods Stroke was induced in male C57BL/6J mice at 3 months (young) and 20 months (aged) of age. Role of histamine after stroke was examined using young (Yg) and aged (Ag) mice, mice underwent MCAO surgery and were euthanized at 6h, 24h and 7 days post-ischemia; sham mice received the same surgery but no MCAO. In this work, we evaluated whether worsened outcomes after experimental stroke in aged mice was associated with age-related changes in mast cells, histamine levels, and histamine receptor expression in the gut, brain, and plasma. Results We found increased numbers of mast cells in the gut and the brain with aging. Using the middle cerebral artery occlusion (MCAO) model of ischemic stroke, we demonstrate that stroke leads to increased numbers of mast cells and histamine receptors in the gut. These gut-centric changes are associated with elevated levels of HA and other pro-inflammatory cytokines including IL-6, G-CSF, TNF-α, and IFN-γ in the peripheral circulation. Our data also shows that post-stroke gut inflammation led to a significant reduction of mucin-producing goblet cells and a loss of gut barrier integrity. Lastly, gut inflammation after stroke is associated with changes in the composition of the gut microbiota as early as 24 hours post-stroke. Conclusion An important theme emerging from our results is that acute inflammatory events following ischemic insults in the brain persist longer in the aged mice when compared to younger animals. Taken together, our findings implicate mast cell activation and histamine signaling as a part of peripheral inflammatory response after ischemic stroke, which are profound in aged animals. Interfering with histamine signaling orally might provide translational value to improve stroke outcome.

scholarly journals Age-related exacerbation of hematopoietic organ damage induced by systemic hyper-inflammation in senescence-accelerated mice

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Tomonori Harada ◽  
Isao Tsuboi ◽  
Hirotsugu Hino ◽  
Miyuki Yuda ◽  
Yoko Hirabayashi ◽  
...  
Keyword(s):  
Stromal Cells ◽  
The Elderly ◽  
Organ Damage ◽  
Hematopoietic Organ ◽  
Aged Mice ◽  
Gm Csf ◽  
Expression Of Genes ◽  
Age Related ◽  
Genes Encoding ◽  
Positive Regulators

AbstractHemophagocytic lymphohistiocytosis (HLH) is a life-threatening systemic hyper-inflammatory disorder. The mortality of HLH is higher in the elderly than in young adults. Senescence-accelerated mice (SAMP1/TA-1) exhibit characteristic accelerated aging after 30 weeks of age, and HLH-like features, including hematopoietic organ damage, are seen after lipopolysaccharide (LPS) treatment. Thus, SAMP1/TA-1 is a useful model of hematological pathophysiology in the elderly with HLH. In this study, dosing of SAMP1/TA-1 mice with LPS revealed that the suppression of myelopoiesis and B-lymphopoiesis was more severe in aged mice than in young mice. The bone marrow (BM) expression of genes encoding positive regulators of myelopoiesis (G-CSF, GM-CSF, and IL-6) and of those encoding negative regulators of B cell lymphopoiesis (TNF-α) increased in both groups, while the expression of genes encoding positive-regulators of B cell lymphopoiesis (IL-7, SDF-1, and SCF) decreased. The expression of the GM-CSF-encoding transcript was lower in aged mice than in young animals. The production of GM-CSF by cultured stromal cells after LPS treatment was also lower in aged mice than in young mice. The accumulation of the TNF-α-encoding transcript and the depletion of the IL-7-encoding transcript were prolonged in aged mice compared to young animals. LPS dosing led to a prolonged increase in the proportion of BM M1 macrophages in aged mice compared to young animals. The expression of the gene encoding p16INK4a and the proportion of β-galactosidase- and phosphorylated ribosomal protein S6-positive cells were increased in cultured stromal cells from aged mice compared to those from young animals, while the proportion of Ki67-positive cells was decreased in stromal cells from aged mice. Thus, age-related deterioration of stromal cells probably causes the suppression of hematopoiesis in aged mice. This age-related latent organ dysfunction may be exacerbated in elderly people with HLH, resulting in poor prognosis.

scholarly journals Senolytics Reduce Coronavirus-Related Mortality in Old Mice

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. 247-248
Author(s):  
Christina Camell
Keyword(s):  
Viral Infection ◽  
Cellular Senescence ◽  
Chronically Ill ◽  
The Elderly ◽  
Viral Antibodies ◽  
Age Related ◽  
Old Mice ◽  
Multiple Chronic Diseases ◽  
Pathogen Exposure ◽  
Related Mortality

Abstract The elderly and chronically ill are among groups at the highest risk for morbidity and mortality to several infections, including SARs-CoV-2. Cellular senescence contributes to inflammation, multiple chronic diseases, and age-related dysfunction, but effects on responses to viral infection are unclear. Old mice acutely infected with pathogens that included a SARS-CoV-2-related mouse β-coronavirus experienced increased senescence and inflammation with nearly 100% mortality. Targeting SCs using senolytic drugs before or after pathogen exposure significantly reduced mortality, cellular senescence, and inflammatory markers and increased anti-viral antibodies. Thus, reducing the SC burden in diseased or aged individuals should enhance resilience and reduce mortality following viral infection, including SARS-CoV-2.

Adult Cardiac Conditions

Asthma ◽  
2014 ◽  
pp. 193-203
Author(s):  
Paola Rogliani ◽  
Andrea Segreti ◽  
Mario Cazzola
Keyword(s):  
Coronary Heart Disease ◽  
Risk Factor ◽  
Heart Disease ◽  
Significant Risk ◽  
Significant Risk Factor ◽  
Systematic Evaluation ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Cardiovascular Comorbidities ◽  
Cardiac Asthma

In this chapter, the relationship between asthma and its cardiovascular comorbidities is reviewed. Asthma seems not to be a risk factor for coronary heart disease in middle-aged adults; nevertheless, some reports suggest that subjects with severe asthma, especially females, are at significant risk for ischemic heart disease. Additionally, adult-onset asthma, particularly in females, may be a significant risk factor for coronary heart disease. The physician should know how to differentiate between asthma, chronic obstructive pulmonary disease, and cardiac asthma (congestive heart failure), often a difficult proposition. A systematic evaluation, not only of the presence of comorbid conditions, is necessary to ensure that such comorbidities are adequately treated and controlled so that the effect on asthma is minimized.

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