QI-TRAINING (QIGONG) ENHANCED IMMUNE FUNCTIONS: WHAT IS THE UNDERLYING MECHANISM?

Background:: The Coronavirus Disease 2019 (COVID-19) is becoming the major health issue in recent human history with thousands of deaths and millions of cases worldwide. Newer research and old experience with other corona-viruses highlighted a probable underlying mechanism of disturbance of the renin-angiotensin system (RAS) that is associ-ated with intrinsic effects of SARS-CoV-2 infection Objective:: In this review, we aimed to describe the intimate connections between the RAS components, the immune system and COVID-19 pathophysiology. Methods:: This non-systematic review article summarizes recent evidence on the relationship between COVID-19 and the RAS. Results:: Several studies have indicated that the downregulation of membrane-bound ACE2 may exert a key role for the impairment of immune functions and for COVID-19 patients’ outcome. The downregulation may occur by distinct mecha-nisms, particularly: (1) the shedding process induced by SARS-CoV-2 fusion pathway, which reduces the amount of mem-brane-bound ACE2, stimulating more shedding by the high levels of Angiotensin II; (2) the endocytosis of ACE2 receptor with the virus itself and (3) by the interferon inhibition caused by SARS-CoV-2 effects on immune system, which leads to reduction of ACE2 receptor expression. Conclusion:: Recent research provides evidence of a reduction of the components of the alternative RAS axis, including ACE2 and Angiotensin-(1-7). In contrast, increased levels of Angiotensin II can activate the AT1 receptor in several organs. Consequently, increased inflammation, thrombosis and angiogenesis occur in patients infected with SARS-COV-2. Atten-tion should be paid to the interactions of the RAS and COVID-19, mainly in the context of novel vaccines and proposed medications.

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Probiotics ingestion prevents HDAC11-induced DEC205+ dendritic cell dysfunction in night shift nurses

Scientific Reports ◽

10.1038/s41598-019-54558-4 ◽

2019 ◽

Vol 9 (1) ◽

Cited By ~ 4

Author(s):

Hui Yang ◽

Jing Yang ◽

Hui Cheng ◽

Huili Cao ◽

Shan Tang ◽

...

Keyword(s):

Dendritic Cell ◽

Negative Impact ◽

Night Shift ◽

Underlying Mechanism ◽

Immune Functions ◽

Cell Dysfunction ◽

Shift Rotation ◽

Regulatory Effects ◽

Regulatory Functions

AbstractIt is known that the day-night shift-rotation has a negative impact on the immune system. The underlying mechanism remains to be further investigated. Probiotics have regulatory effects on immune functions. This study aims to investigate the role of probiotic ingestion in preventing the DEC205+ dendritic cell (decDC) dysfunction in day-night shift-engaging nurses. In this study, blood samples were collected from day-night shift-rotating nurses who took or did not take yogurt (containing C. Butyricum) during the night shift (NS). decDC functions were evaluated with pertinent immunological approaches. We observed that the immune tolerogenic functions and interleukin (IL)-10 expression were impaired in decDCs of nurses after NS. HDAC11 was detected in decDCs that was markedly up regulated after NS. The HDAC11 levels were negatively correlated with the immune tolerogenic functions in decDCs. Ingestion of probiotic-containing yogurt during NS efficiently suppressed Bmal1 and HDAC11 levels as well as up regulated the immune regulatory functions in decDCs. In conclusion, NS has a negative impact on decDC immune tolerogenic functions, which can be prevented by ingesting probiotics-containing yogurt during NS.

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Abstract 12529: Low Dose Oral Cyclophosphamide Therapy Reduces Atherosclerosis Progression and Promotes Plaque Stability in a Murine Model of Atherosclerosis

Circulation ◽

10.1161/circ.130.suppl_2.12529 ◽

2014 ◽

Vol 130 (suppl_2) ◽

Author(s):

Yayoi Sato-Okabayashi ◽

Chiemi Nishida ◽

Daida Hiroyuki ◽

Shinya Munakata ◽

Hiroshi Shimazu ◽

...

Keyword(s):

Disease Progression ◽

Murine Model ◽

High Fat Diet ◽

Low Dose ◽

Oral Treatment ◽

Underlying Mechanism ◽

Matrix Metalloproteinase 2 ◽

Immune Functions ◽

High Fat ◽

Plaque Stability

Introduction: Atherosclerosis is a chronic inflammatory disease and the primary cause of heart disease and stroke in Western countries. The cytotoxic drug cyclophosphamide (CPA) can modulate immune functions. Extended survival of patients with severe atherosclerosis has been reported after CPA treatment, but the underlying mechanism is still poorly understood. The objective of this study was to examine the antiatherosclerotic effects of CPA and the underlying mechanism in a murine model of atherosclerosis. Hypothesis: CPA treatment can alter inflammatory processes pivotal for the development of atherosclerosis, therefore limiting disease progression. Method: Apolipoprotein E deficient (ApoE-/-) mice fed a high fat diet received CPA resuspended in drinking water (37.5 g/kg /day p.o.) or water for 12 weeks, respectively. In an interventional protocol, mice fed a high fat diet received the same dose of CPA or water from week 14 to 18, respectively. Mice were sacrificed at week 12, 14 and 18, and aorta, peripheral blood cells, spleen cells and peritoneal cells of treated mice were analysed using histological methods and FACS analysis. Result: In a preventive protocol, continuous oral administration of low-dose CPA prevented disease initiation in ApoE-/- mice fed with a high fat diet. Encouraged by these data we treated mice with pre-established atherosclerosis for 4 weeks with CPA, in an interventional protocol. CPA treatment delayed disease progression in mice with advanced atherosclerosis and reduced the macrophage infiltration in plaques. Importantly, improved plaque stability with a thicker fibrous cap, and an increase in collagen deposition and decreased matrix metalloproteinase-2 and -9 expression, and a reduction of classical inflammatory macrophage (M1) numbers was observed. In addition, CPA treatment reduced the numbers of IFN-γ-producing TH1, but not TH2 lymphocytes in vivo. Conclution: Our data demonstrate that oral treatment with CPA inhibits atherosclerosis initiation and progression in ApoE-/- mouse model, through pleiotropic immunomodulatory effects on lymphoid and myeloid cells. Thus, CPA may be a valuable drug for treating advanced atherosclerosis.

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Insight into the mechanism by which metoclopramide improves immune functions after trauma-hemorrhage

AJP Cell Physiology ◽

10.1152/ajpcell.2000.279.1.c72 ◽

2000 ◽

Vol 279 (1) ◽

pp. C72-C80 ◽

Cited By ~ 26

Author(s):

Markus W. Knöferl ◽

Martin K. Angele ◽

Alfred Ayala ◽

William G. Cioffi ◽

Kirby I. Bland ◽

...

Keyword(s):

Underlying Mechanism ◽

Sham Operation ◽

Dependent Manner ◽

Splenocyte Proliferation ◽

Immune Functions ◽

Beneficial Effects ◽

Plasma Prl ◽

Tissue Trauma ◽

Dose Dependent

Although studies have shown that prolactin (Prl) and metoclopramide (Mcp) administration restores the depressed cell-mediated immune functions after hemorrhage, the underlying mechanism responsible for the immunostimulatory effects of Mcp remains unknown. We hypothesized that Mcp improves immune responses by upregulating the secretion of Prl. To test this hypothesis, male C3H/HeN mice were subjected to sham operation or laparotomy (i.e., soft tissue trauma) and hemorrhagic shock (Hem; 35 ± 5 mmHg for 90 min) and then resuscitated. Plasma Prl levels were determined 30 min after Mcp (1 μg/g body wt sc at end of Hem) or vehicle (Veh) treatment in sham and Hem mice. The results indicate that plasma Prl levels increased significantly in Mcp-treated mice (sham-Veh 249.9 ± 5.3, Hem-Veh 229.9 ± 7.6, Hem-Mcp 596.9 ± 73.1 ng/ml, one-way ANOVA, P < 0.05 vs. Veh). To determine whether Mcp produces its salutary effects directly or indirectly via increased Prl secretion, splenocyte proliferation and splenocyte interleukin (IL)-2 and IL-3 release from untreated sham or Hem mice were determined in the presence of increasing concentrations of mouse Prl or Mcp. The addition of Mcp had no effect on splenocyte immune functions in vitro. However, the addition of Prl restored the hemorrhage-induced depressed splenocyte proliferation as well as splenocyte IL-2 and IL-3 release in vitro in a dose-dependent manner. Thus the beneficial effects of Mcp on immune functions after Hem appear to be mediated by Prl. Because Mcp increases plasma levels of the immunoenhancing hormone Prl, this agent should be considered a useful adjunct for the treatment of immunodepression in trauma victims.

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Face Inversion Effect Emerges Under Critical Configural Discrepancy

Swiss Journal of Psychology ◽

10.1024/1421-0185/a000018 ◽

2010 ◽

Vol 69 (3) ◽

pp. 161-167 ◽

Cited By ~ 3

Author(s):

Jisien Yang ◽

Adrian Schwaninger

Keyword(s):

Face Recognition ◽

Face Processing ◽

Underlying Mechanism ◽

Inversion Effect ◽

Configural Processing ◽

Major Contributor ◽

Face Inversion Effect ◽

Configural Information ◽

Face Inversion ◽

The Face

Configural processing has been considered the major contributor to the face inversion effect (FIE) in face recognition. However, most researchers have only obtained the FIE with one specific ratio of configural alteration. It remains unclear whether the ratio of configural alteration itself can mediate the occurrence of the FIE. We aimed to clarify this issue by manipulating the configural information parametrically using six different ratios, ranging from 4% to 24%. Participants were asked to judge whether a pair of faces were entirely identical or different. The paired faces that were to be compared were presented either simultaneously (Experiment 1) or sequentially (Experiment 2). Both experiments revealed that the FIE was observed only when the ratio of configural alteration was in the intermediate range. These results indicate that even though the FIE has been frequently adopted as an index to examine the underlying mechanism of face processing, the emergence of the FIE is not robust with any configural alteration but dependent on the ratio of configural alteration.

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Learned Placebo Effects in the Immune System

Zeitschrift für Psychologie ◽

10.1027/2151-2604/a000184 ◽

2014 ◽

Vol 222 (3) ◽

pp. 148-153 ◽

Cited By ~ 2

Author(s):

Sabine Vits ◽

Manfred Schedlowski

Keyword(s):

Nervous System ◽

Immune System ◽

Associative Learning ◽

Placebo Response ◽

Immunosuppressive Drug ◽

Immune Functions ◽

Placebo Effects ◽

New Therapeutic Approaches ◽

Biological Variables ◽

Experimental Approaches

Associative learning processes are one of the major neuropsychological mechanisms steering the placebo response in different physiological systems and end organ functions. Learned placebo effects on immune functions are based on the bidirectional communication between the central nervous system (CNS) and the peripheral immune system. Based on this “hardware,” experimental evidence in animals and humans showed that humoral and cellular immune functions can be affected by behavioral conditioning processes. We will first highlight and summarize data documenting the variety of experimental approaches conditioning protocols employed, affecting different immunological functions by associative learning. Taking a well-established paradigm employing a conditioned taste aversion model in rats with the immunosuppressive drug cyclosporine A (CsA) as an unconditioned stimulus (US) as an example, we will then summarize the efferent and afferent communication pathways as well as central processes activated during a learned immunosuppression. In addition, the potential clinical relevance of learned placebo effects on the outcome of immune-related diseases has been demonstrated in a number of different clinical conditions in rodents. More importantly, the learned immunosuppression is not restricted to experimental animals but can be also induced in humans. These data so far show that (i) behavioral conditioned immunosuppression is not limited to a single event but can be reproduced over time, (ii) immunosuppression cannot be induced by mere expectation, (iii) psychological and biological variables can be identified as predictors for this learned immunosuppression. Together with experimental approaches employing a placebo-controlled dose reduction these data provide a basis for new therapeutic approaches to the treatment of diseases where a suppression of immune functions is required via modulation of nervous system-immune system communication by learned placebo effects.

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