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Frontiers in Immunology 2021
Topics: Animals; Autoimmunity; Disease Susceptibility; Humans; Scleroderma, Systemic
PubMed: 33828566
DOI: 10.3389/fimmu.2021.663381 -
The Journals of Gerontology. Series B,... Feb 2020Personality, especially the dimensions of neuroticism and conscientiousness, has prospectively predicted the risk of incident Alzheimer's disease (AD). Such a... (Review)
Review
Personality, especially the dimensions of neuroticism and conscientiousness, has prospectively predicted the risk of incident Alzheimer's disease (AD). Such a relationship could be explained by personality and AD risk having a common cause such as a gene; by personality creating a predisposition for AD through health behavior or inflammation; by personality exerting a pathoplastic effect on the cognitive consequences of neuropathology; or by AD and personality change existing on a disease spectrum that begins up to decades before diagnosis. Using the 5-dimensional taxonomy of personality, the present review describes how these models might arise, the evidence for each, and how they might be distinguished from one another empirically. At present, the evidence is sparse but tends to suggest predisposition and/or pathoplastic relationships. Future studies using noninvasive assessment of neuropathology are needed to distinguish these 2 possibilities.
Topics: Aged; Alzheimer Disease; Disease Susceptibility; Genetic Predisposition to Disease; Humans; Personality
PubMed: 29846724
DOI: 10.1093/geronb/gby063 -
International Journal of Molecular... Sep 2021Thalassemia, a chronic disease with chronic anemia, is caused by mutations in the β-globin gene, leading to reduced levels or complete deficiency of β-globin chain... (Review)
Review
Thalassemia, a chronic disease with chronic anemia, is caused by mutations in the β-globin gene, leading to reduced levels or complete deficiency of β-globin chain synthesis. Patients with β-thalassemia display variable clinical severity which ranges from asymptomatic features to severe transfusion-dependent anemia and complications in multiple organs. They not only are at increased risk of blood-borne infections resulting from multiple transfusions, but they also show enhanced susceptibility to infections as a consequence of coexistent immune deficiency. Enhanced susceptibility to infections in β-thalassemia patients is associated with the interplay of several complex biological processes. β-thalassemia-related abnormalities of the innate immune system include decreased levels of complement, properdin, and lysozyme, reduced absorption and phagocytic ability of polymorphonuclear neutrophils, disturbed chemotaxis, and altered intracellular metabolism processes. According to available literature data, immunological abnormalities observed in patients with thalassemia can be caused by both the disease itself as well as therapies. The most important factors promoting such alterations involve iron overload, phenotypical and functional abnormalities of immune system cells resulting from chronic inflammation oxidative stress, multiple blood transfusion, iron chelation therapy, and splenectomy. Unravelling the mechanisms underlying immune deficiency in β-thalassemia patients may enable the designing of appropriate therapies for this group of patients.
Topics: Adaptive Immunity; Biomarkers; Disease Susceptibility; Genetic Predisposition to Disease; Humans; Immune System; Immunity, Innate; beta-Thalassemia
PubMed: 34575839
DOI: 10.3390/ijms22189677 -
Molecular Medicine (Cambridge, Mass.) Jan 2022Biofilm is a community of bacteria embedded in an extracellular matrix, which can colonize different human cells and tissues and subvert the host immune reactions by... (Review)
Review
BACKGROUND
Biofilm is a community of bacteria embedded in an extracellular matrix, which can colonize different human cells and tissues and subvert the host immune reactions by preventing immune detection and polarizing the immune reactions towards an anti-inflammatory state, promoting the persistence of biofilm-embedded bacteria in the host.
MAIN BODY OF THE MANUSCRIPT
It is now well established that the function of immune cells is ultimately mediated by cellular metabolism. The immune cells are stimulated to regulate their immune functions upon sensing danger signals. Recent studies have determined that immune cells often display distinct metabolic alterations that impair their immune responses when triggered. Such metabolic reprogramming and its physiological implications are well established in cancer situations. In bacterial infections, immuno-metabolic evaluations have primarily focused on macrophages and neutrophils in the planktonic growth mode.
CONCLUSION
Based on differences in inflammatory reactions of macrophages and neutrophils in planktonic- versus biofilm-associated bacterial infections, studies must also consider the metabolic functions of immune cells against biofilm infections. The profound characterization of the metabolic and immune cell reactions could offer exciting novel targets for antibiofilm therapy.
Topics: Animals; Biofilms; Biomarkers; Disease Management; Disease Susceptibility; Energy Metabolism; Host-Pathogen Interactions; Humans; Immune System; Infections; Neoplasms; Organ Specificity
PubMed: 35093033
DOI: 10.1186/s10020-022-00435-2 -
Frontiers in Immunology 2021
Topics: Animals; Disease Susceptibility; Host-Parasite Interactions; Humans; Nerve Tissue; Organ Specificity; Parasites; Tropism
PubMed: 34659274
DOI: 10.3389/fimmu.2021.775666 -
Frontiers in Immunology 2021
Topics: Animals; Disease Susceptibility; Host-Pathogen Interactions; Humans; Immunity; Skin Diseases, Infectious; Skin Physiological Phenomena
PubMed: 35095901
DOI: 10.3389/fimmu.2021.810059 -
Blood Nov 1946
Topics: Disease Susceptibility; Hemorrhagic Disorders; von Willebrand Diseases
PubMed: 21002320
DOI: No ID Found -
Journal of Neuroinflammation Jan 2017Epilepsy is a common and debilitating consequence of traumatic brain injury (TBI). Seizures contribute to progressive neurodegeneration and poor functional and... (Review)
Review
BACKGROUND
Epilepsy is a common and debilitating consequence of traumatic brain injury (TBI). Seizures contribute to progressive neurodegeneration and poor functional and psychosocial outcomes for TBI survivors, and epilepsy after TBI is often resistant to existing anti-epileptic drugs. The development of post-traumatic epilepsy (PTE) occurs in a complex neurobiological environment characterized by ongoing TBI-induced secondary injury processes. Neuroinflammation is an important secondary injury process, though how it contributes to epileptogenesis, and the development of chronic, spontaneous seizure activity, remains poorly understood. A mechanistic understanding of how inflammation contributes to the development of epilepsy (epileptogenesis) after TBI is important to facilitate the identification of novel therapeutic strategies to reduce or prevent seizures. BODY: We reviewed previous clinical and pre-clinical data to evaluate the hypothesis that inflammation contributes to seizures and epilepsy after TBI. Increasing evidence indicates that neuroinflammation is a common consequence of epileptic seizure activity, and also contributes to epileptogenesis as well as seizure initiation (ictogenesis) and perpetuation. Three key signaling factors implicated in both seizure activity and TBI-induced secondary pathogenesis are highlighted in this review: high-mobility group box protein-1 interacting with toll-like receptors, interleukin-1β interacting with its receptors, and transforming growth factor-β signaling from extravascular albumin. Lastly, we consider age-dependent differences in seizure susceptibility and neuroinflammation as mechanisms which may contribute to a heightened vulnerability to epileptogenesis in young brain-injured patients.
CONCLUSION
Several inflammatory mediators exhibit epileptogenic and ictogenic properties, acting on glia and neurons both directly and indirectly influence neuronal excitability. Further research is required to establish causality between inflammatory signaling cascades and the development of epilepsy post-TBI, and to evaluate the therapeutic potential of pharmaceuticals targeting inflammatory pathways to prevent or mitigate the development of PTE.
Topics: Animals; Brain Injuries, Traumatic; Disease Susceptibility; Epilepsy; Humans; Inflammation; Seizures; Signal Transduction
PubMed: 28086980
DOI: 10.1186/s12974-016-0786-1 -
Journal of Animal Science Jun 2022Biological sex is a major host factor influencing risk for infectious disease-associated mortality, and chronic inflammatory and metabolic diseases. Research in human... (Review)
Review
Biological sex is a major host factor influencing risk for infectious disease-associated mortality, and chronic inflammatory and metabolic diseases. Research in human and rodent models -has revealed sex differences that exist across organ systems during health and disease that may contribute to sex biases in disease risk. Despite the robust and growing literature on the role of sex as a risk factor in human disease, comparatively little attention has been focused on investigating the role of biological sex in disease susceptibility in agriculturally important animal populations such as the pig. To date, comparisons between sexes have focused on carcass composition, growth rate, and feed efficiency in pigs. However, there is a large gap in the literature regarding the effects of biological sex on other integral aspects of health and disease. The objective of this review is to highlight the available literature reporting sex differences in pig health and biology with an emphasis on sex differences in mortality, immunity, and gastrointestinal (GI) physiology and to address biological sex as a significant biological variable in disease risk and research study design. A basic overview of the biology of sex differences including the major hormonal and genetic/chromosomal mechanisms of sexual differentiation and the developmental periods in which sex differences emerge will be covered. This review will also discuss how production-relevant management and environmental factors (e.g., wean age, castration, stress, and nutrition) interact with biological sex to shape host immune and GI development and function. Perceived gaps in knowledge and areas of future research will also be discussed.
Topics: Animals; Disease Susceptibility; Female; Male; Orchiectomy; Research Design; Risk Factors; Sex Characteristics; Sex Factors; Swine; Swine Diseases
PubMed: 35708590
DOI: 10.1093/jas/skac146 -
Neuropsychopharmacology : Official... Jan 2016A swiftly growing volume of literature, comprising both human and animal studies and employing both observational and experimental designs, has documented striking... (Review)
Review
A swiftly growing volume of literature, comprising both human and animal studies and employing both observational and experimental designs, has documented striking individual differences in neurobiological sensitivities to environmental circumstances within subgroups of study samples. This differential susceptibility to social and physical environments operates bidirectionally, in both adverse and beneficial contexts, and results in a minority subpopulation with remarkably poor or unusually positive trajectories of health and development, contingent upon the character of environmental conditions. Differences in contextual susceptibility appear to emerge in early development, as the interactive and adaptive product of genetic and environmental attributes. This paper surveys what is currently known of the mechanisms or mediators of differential susceptibility, at the levels of temperament and behavior, physiological systems, brain circuitry and neuronal function, and genetic and epigenetic variation. It concludes with the assertion that differential susceptibility is inherently grounded within processes of biological moderation, the complexities of which are at present only partially understood.
Topics: Animals; Brain; Disease Susceptibility; Humans; Individuality; Risk Factors; Social Environment; Stress, Psychological; Temperament
PubMed: 26391599
DOI: 10.1038/npp.2015.294