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1.
Leukocyte Trafficking via Lymphatic Vessels in Atherosclerosis.
Yeo, KP, Lim, HY, Angeli, V
Cells. 2021;(6)
Abstract
In recent years, lymphatic vessels have received increasing attention and our understanding of their development and functional roles in health and diseases has greatly improved. It has become clear that lymphatic vessels are critically involved in acute and chronic inflammation and its resolution by supporting the transport of immune cells, fluid, and macromolecules. As we will discuss in this review, the involvement of lymphatic vessels has been uncovered in atherosclerosis, a chronic inflammatory disease of medium- and large-sized arteries causing deadly cardiovascular complications worldwide. The progression of atherosclerosis is associated with morphological and functional alterations in lymphatic vessels draining the diseased artery. These defects in the lymphatic vasculature impact the inflammatory response in atherosclerosis by affecting immune cell trafficking, lymphoid neogenesis, and clearance of macromolecules in the arterial wall. Based on these new findings, we propose that targeting lymphatic function could be considered in conjunction with existing drugs as a treatment option for atherosclerosis.
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Selenocompounds and Sepsis: Redox Bypass Hypothesis for Early Diagnosis and Treatment: Part A-Early Acute Phase of Sepsis: An Extraordinary Redox Situation (Leukocyte/Endothelium Interaction Leading to Endothelial Damage).
Forceville, X, Van Antwerpen, P, Preiser, JC
Antioxidants & redox signaling. 2021;(2):113-138
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Abstract
Significance: Sepsis is a health disaster. In sepsis, an initial, beneficial local immune response against infection evolves rapidly into a generalized, dysregulated response or a state of chaos, leading to multiple organ failure. Use of life-sustaining supportive therapies creates an unnatural condition, enabling the complex cascades of the sepsis response to develop in patients who would otherwise die. Multiple attempts to control sepsis at an early stage have been unsuccessful. Recent Advances: Major events in early sepsis include activation and binding of leukocytes and endothelial cells in the microcirculation, damage of the endothelial surface layer (ESL), and a decrease in the plasma concentration of the antioxidant enzyme, selenoprotein-P. These events induce an increase in intracellular redox potential and lymphocyte apoptosis, whereas apoptosis is delayed in monocytes and neutrophils. They also induce endothelial mitochondrial and cell damage. Critical Issues: Neutrophil production increases dramatically, and aggressive immature forms are released. Leukocyte cross talk with other leukocytes and with damaged endothelial cells amplifies the inflammatory response. The release of large quantities of reactive oxygen, halogen, and nitrogen species as a result of the leukocyte respiratory burst, endothelial mitochondrial damage, and ischemia/reperfusion processes, along with the marked decrease in selenoprotein-P concentrations, leads to peroxynitrite damage of the ESL, reducing flow and damaging the endothelial barrier. Future Directions: Endothelial barrier damage by activated leukocytes is a time-sensitive event in sepsis, occurring within hours and representing the first step toward organ failure and death. Reducing or stopping this event is necessary before irreversible damage occurs.
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Sustaining efficient immune functions with regular physical exercise in the COVID-19 era and beyond.
Furtado, GE, Letieri, RV, Caldo-Silva, A, Sardão, VA, Teixeira, AM, de Barros, MP, Vieira, RP, Bachi, ALL
European journal of clinical investigation. 2021;(5):e13485
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Abstract
The new coronavirus (SARS-CoV-2) appearance in Wuhan, China, did rise the new virus disease (COVID-19), which spread globally in a short time, leading the World Health Organization to declare a new global pandemic. To contain and mitigate the spread of SARS-CoV-2, specific public health procedures were implemented in virtually all countries, with a significant impact on society, making it difficult to keep the regular practice of physical activity. It is widely accepted that an active lifestyle contributes to the improvement of general health and preservation of cardiovascular, respiratory, osteo-muscular and immune system capacities. The positive effects of regular physical activity on the immune system have emerged as a pivotal trigger of general health, underlying the beneficial effects of physical activity on multiple physiological systems. Accordingly, recent studies have already pointed out the negative impact of physical inactivity caused by the social isolation imposed by the public sanitary authorities due to COVID-19. Nevertheless, there are still no current narrative reviews evaluating the real impact of COVID-19 on active lifestyle or even discussing the possible beneficial effects of exercise-promoted immune upgrade against the severity or progression of COVID-19. Based on the consensus in the scientific literature, in this review, we discuss how an exercise adherence could adequately improve immune responses in times of the 'COVID-19 Era and beyond'.
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COVID-19 and hydatidiform mole.
Abbas, AM, Ahmed, L, Salem, AS, Elsamman, SH, Refai, A, Fathy, SK, Ahmed, OA, Shalotut, AS, AbdelWahab, RA
American journal of reproductive immunology (New York, N.Y. : 1989). 2020;(5):e13310
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Abstract
The emergence of coronavirus disease 2019 (COVID-19) as a pandemic threatens the entire world resulting in severe consequences for people's health. Pregnant patients with COVID-19 had immune dysregulation that could result in abnormal pregnancy outcomes such as hydatidiform mole (HM), recurrent pregnancy loss, and early-onset preeclampsia. In this article, we tried to summarize the possible association between COVID-19 and the HM's development by reviewing the role of NOD-Like Receptor (NLR) Family Pyrin Domain Containing 7 (NLRP7), cytokines, zinc, and leukocytes in the pathogenesis of HM.
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Circulating Leukocyte Alterations and the Development/Progression of Diabetic Retinopathy in Type 1 Diabetic Patients - A Pilot Study.
Obasanmi, G, Lois, N, Armstrong, D, Lavery, NJ, Hombrebueno, JR, Lynch, A, Wright, DM, Chen, M, Xu, H
Current eye research. 2020;(9):1144-1154
Abstract
BACKGROUND/AIMS: The aim of this study was to investigate the relationship between alterations in circulating leukocytes and the initiation and progression of DR in people with type 1 diabetes (T1D). METHODS Forty-one patients with T1D [13 mild non-proliferative DR (mNPDR), 14 active proliferative DR (aPDR) and 14 inactive PDR (iPDR)], and 13 age- and gender-matched healthy controls were recruited prospectively. Circulating leukocytes, including CD4+ and CD8+ T-cells, CD14+CD16-, CD14-CD16+ and CD14+CD16+ monocytes; CD16+HLA-DR- neutrophils, CD19+ B-cells and CD56+ natural killer cells and their cell surface adhesion molecules and chemokine receptors (HLA-DR, CD62L, CCR2, CCR5, CD66a, CD157 and CD305) were examined by flow cytometry. RESULTS In DR patients, compared to healthy controls, increased proportions of neutrophils (p = .0152); reduced proportions of lymphocytes (p = .0002), HLA-DR+ leukocytes (p = .0406) and non-classical monocytes (p = .0204); and reduced expression of CD66a (p = .0048) and CD157 (p = .0007) on CD4+ T cells were observed. Compared to healthy controls, CD19+ B cells were reduced at the mNPDR but not aPDR patients. Total lymphocytes, CD4+ T cells and CD8+ T cells progressively decreased whereas neutrophils, the neutrophil/lymphocyte ratio and the neutrophil/CD4+ ratio progressively increased from early to late stages of DR, reaching statistical significance at the aPDR stage. Longer diabetes duration was associated with a reduced proportion of CD8+ T cells (p = .002) and increased neutrophil/CD8+ ratio (p = .033). CONCLUSIONS In this pilot study, DR is associated with increased innate cellular immunity especially neutrophils and reduced adaptive cellular immunity particularly lymphocytes. Impaired B-cell immunity may play a role in the initiation of DR; whereas impaired T-cell immunity with increased neutrophil response may contribute to progression of DR from non-proliferative to proliferative stages in T1D patients. Large multicenter studies are needed to further understand the immune dysregulation in DR initiation and progression.
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Immunomodulatory effects of probiotics: Can they be used to treat allergies and autoimmune diseases?
Dargahi, N, Johnson, J, Donkor, O, Vasiljevic, T, Apostolopoulos, V
Maturitas. 2019;:25-38
Abstract
As a person ages, physiological, immunological and gut microbiome changes collectively result in an array of chronic conditions. According to the 'hygiene hypothesis' the increasing prevalence of immune-mediated disorders may be related to intestinal dysbiosis, leading to immune dysfunction and associated conditions such as eczema, asthma, allergies and autoimmune diseases. Beneficial probiotic bacteria can be utilized by increasing their abundance within the gastrointestinal lumen, which in turn will modulate immune cells, such as, T helper (Th)-1, Th2, Th17, regulatory T (Treg) cells and B cells, which have direct relevance to human health and the pathogenesis of immune disorders. Here, we describe the cross-talk between probiotics and the gastrointestinal immune system, and their effects in relation to inflammatory bowel disease, multiple sclerosis, allergies and atopic dermatitis.
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Characterization in humans of in vitro leucocyte maximal telomerase activity capacity and association with stress.
de Punder, K, Heim, C, Przesdzing, I, Wadhwa, PD, Entringer, S
Philosophical transactions of the Royal Society of London. Series B, Biological sciences. 2018;(1741)
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The goal of this study was to develop and validate a measure of maximal telomerase activity capacity (mTAC) for use in human studies of telomere biology, and to determine its association with measures of stress and stress responsivity. The study was conducted in a population of 28 healthy young women and men who were assessed serially across two separate days, at multiple time points, and in response to a standardized laboratory stressor. Venous blood was collected at each of these multiple assessments, and an in vitro mitogen challenge (phytohaemagglutinin supplemented with interleukin-2) was used to stimulate telomerase activity in leucocytes. After first establishing the optimal post-stimulation time course to characterize mTAC, we determined the within-subject stability and the between-subject variability of mTAC. The major findings of our study are as follows: (i) the optimal time point to quantify human leucocyte mTAC appears to be at 72 h after mitogen stimulation; (ii) mTAC exhibits substantial within-subject stability (correlations were in the range of r 0.68-0.82) and between-subject variability, with a high intra-class coefficient (0.70), indicating greater between-subject relative to within-subject variability; (iii) mTAC is not influenced by situational factors including time of day, cortisol, acute stress exposure and immune cell distribution in the pre-stimulation blood sample; and (iv) a significant proportion of the between-subject variability in mTAC is associated with measures of stress and stress responsivity (mTAC is lower in subjects reporting higher levels of perceived (chronic) stress and exhibiting higher psychophysiological stress reactivity). Based collectively on these findings, it appears that mTAC, as proposed and operationalized, empirically meets the key criteria to represent a potentially useful individual difference measure of telomerase activity capacity of human leucocytes.This article is part of the theme issue 'Understanding diversity in telomere dynamics'.
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Inflammation and the Intestinal Barrier: Leukocyte-Epithelial Cell Interactions, Cell Junction Remodeling, and Mucosal Repair.
Luissint, AC, Parkos, CA, Nusrat, A
Gastroenterology. 2016;(4):616-32
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The intestinal tract is lined by a single layer of columnar epithelial cells that forms a dynamic, permeable barrier allowing for selective absorption of nutrients, while restricting access to pathogens and food-borne antigens. Precise regulation of epithelial barrier function is therefore required for maintaining mucosal homeostasis and depends, in part, on barrier-forming elements within the epithelium and a balance between pro- and anti-inflammatory factors in the mucosa. Pathologic states, such as inflammatory bowel disease, are associated with a leaky epithelial barrier, resulting in excessive exposure to microbial antigens, recruitment of leukocytes, release of soluble mediators, and ultimately mucosal damage. An inflammatory microenvironment affects epithelial barrier properties and mucosal homeostasis by altering the structure and function of epithelial intercellular junctions through direct and indirect mechanisms. We review our current understanding of complex interactions between the intestinal epithelium and immune cells, with a focus on pathologic mucosal inflammation and mechanisms of epithelial repair. We discuss leukocyte-epithelial interactions, as well as inflammatory mediators that affect the epithelial barrier and mucosal repair. Increased knowledge of communication networks between the epithelium and immune system will lead to tissue-specific strategies for treating pathologic intestinal inflammation.
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Molecular Imaging of Inflammation: Current Status.
Hammoud, DA
Journal of nuclear medicine : official publication, Society of Nuclear Medicine. 2016;(8):1161-5
Abstract
The ability to image inflammation in vivo can improve our understanding of the pathophysiology underlying various disease etiologies, including cancer, atherosclerosis, and neurodegeneration. A great wealth of preclinical and translational research has been and is currently being developed to decipher the involvement of the immune system in disease pathophysiology, quantify the course of a disease, and visualize the potential detrimental effects of excessive inflammation. Down the road, the ultimate goal is to have clinical noninvasive in vivo imaging biomarkers of inflammation that will help diagnose disease, establish prognosis, and gauge response to preventative and therapeutic strategies.
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Peripheral blood leucocyte subclasses as potential biomarkers of adipose tissue inflammation and obesity subphenotypes in humans.
Pecht, T, Gutman-Tirosh, A, Bashan, N, Rudich, A
Obesity reviews : an official journal of the International Association for the Study of Obesity. 2014;(4):322-37
Abstract
While obesity is clearly accepted as a major risk factor for cardio-metabolic morbidity, it is also apparent that some obese patients largely escape this association, forming a unique obese subphenotype(s). Current approaches to define such subphenotypes include clinical biomarkers that largely reflect already manifested comorbidities, such as markers of dyslipidaemia, hyperglycaemia and impaired regulation of vascular tone, and anthropometric or imaging-based assessment of adipose tissue distribution. Low-grade inflammation, evident both systemically and within adipose tissue (particularly intra-abdominal fat depots), seems to characterize the more cardio-metabolically morbid forms of obesity. Indeed, several systemic inflammatory markers (C-reactive protein), adipokines (retinol-binding protein 4, adiponectin) and cytokines have been shown to correlate in humans with adipose tissue inflammation and with obesity-associated health risks. Circulating leucocytes constitute a diverse group of cells that form a major arm of the immune system. They are both major sources of cytokines and likely also of infiltrating adipose tissue immune cells in obesity. In the present review, we summarize currently available literature on 'classical' blood white cell classes and on more specific leucocyte subclasses present in the circulation in human obesity. We critically raise the possibility that leucocytes may constitute clinically available markers for the more morbidity-associated obesity subphenotype(s), and when available, for intra-abdominal adipose tissue inflammation.