lipopolysaccharide binding
Recently Published Documents


TOTAL DOCUMENTS

542
(FIVE YEARS 56)

H-INDEX

62
(FIVE YEARS 3)

2021 ◽  
pp. 1-24
Author(s):  
Kyoko Hasebe ◽  
Mohammadreza Mohebbi ◽  
Laura Gray ◽  
Adam J. Walker ◽  
Chiara C. Bortolasci ◽  
...  

Abstract Objective: This study aimed to explore effects of adjunctive minocycline treatment on inflammatory and neurogenesis markers in major depressive disorder (MDD). Methods: Serum samples were collected from a randomised, placebo-controlled 12-week clinical trial of minocycline (200mg/day, added to treatment as usual) for adults (n=71) experiencing MDD to determine changes in interleukin-6 (IL-6), lipopolysaccharide binding protein (LBP) and brain derived neurotrophic factor (BDNF). General Estimate Equation modelling explored moderation effects of baseline markers and exploratory analyses investigated associations between markers and clinical outcomes. Results: There was no difference between adjunctive minocycline or placebo groups at baseline or week 12 in the levels of IL-6 (week 12; placebo 2.06±1.35 pg/ml; minocycline 1.77±0.79 pg/ml; p=0.317), LBP (week 12; placebo 3.74±0.95 µg/ml; minocycline 3.93±1.33 µg/ml; p=0.525) or BDNF (week 12; placebo 24.28±6.69 ng/ml; minocycline 26.56±5.45 ng/ml; p=0.161). Higher IL-6 levels at baseline were a predictor of greater clinical improvement. Exploratory analyses suggested that the change in IL-6 levels were significantly associated with anxiety symptoms (HAMA; p=0.021) and quality of life (Q-LES-Q-SF; p=0.023) scale scores. No other clinical outcomes were shown to have this mediation effect, nor did the other markers (LBP or BDNF) moderate clinical outcomes. Conclusion: There were no overall changes in IL-6, LBP or BDNF following adjunctive minocycline treatment. Exploratory analyses suggest a potential role of IL-6 on mediating anxiety symptoms with MDD. Future trials may consider enrichment of recruitment by identifying several markers or a panel of factors to better represent an inflammatory phenotype in MDD with larger sample size.


Biomedicines ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 29
Author(s):  
Chien-Sung Tsai ◽  
Mei-Hua Hu ◽  
Yung-Chi Hsu ◽  
Go-Shine Huang

The role of platelet TLR4 in transfusion reactions remains unclear. This study analyzed platelet TLR4 and certain damage-associated molecular patterns (DAMPs) and evaluated how ABO compatibility affected TLR4 expression after a simulated ex vivo transfusion. A blood bank was the source of donor red blood cells. Blood from patients undergoing cardiac surgery was processed to generate a washed platelet suspension to which the donor blood was added in concentrations 1, 5, and 10% (v/v). Blood-mixing experiments were performed on four groups: a 0.9% saline control group (n = 31); a matched-blood-type mixing group (group M, n = 20); an uncross-matched ABO-specific mixing group (group S, n = 20); and an ABO-incompatible blood mixing group (group I, n = 20). TLR4 expression in the platelets was determined after blood mixing. We evaluated levels of TLR4-binding DAMPs (HMGB1, S100A8, S100A9, and SAA), lipopolysaccharide-binding protein, and endpoint proteins in the TLR4 signaling pathway. In the M, S, and I groups, 1, 5, and 10% blood mixtures significantly increased TLR4 expression (all p < 0.001) in a concentration-dependent manner. Groups M, S, and I were not discovered to have significantly differing TLR4 expression (p = 0.148). HMGB1, S100A8, and S100A9 levels were elevated in response to blood mixing, but SAA, lipopolysaccharide-binding protein, TNF-α, IL-1β, and IL-6 levels were not. Blood mixing may elicit innate immune responses by upregulating platelet TLR4 and DAMPs unassociated with ABO compatibility, suggesting that innate immunity through TLR4-mediated signaling may induce transfusion reactions.


Author(s):  
Aisha Q. Atwater ◽  
Lilly Cheng Immergluck ◽  
Alec J. Davidson ◽  
Oscar Castanon-Cervantes

The disruption of inflammatory responses is a potential mechanism behind the harmful effects of shift work and is associated with increased risk of hypertension, stroke, obesity, diabetes, and cancer. These responses are linked to the proliferation of leukocytes in shift workers, suggesting a systemic signal as a potential mediator. The purpose of this study was to assess the relationship between systemic inflammation, leukocyte counts, and systemic endotoxemia in samples from a diverse cohort of day workers and shift workers. Participants (normothermic and normotensive) were healthy volunteers, non-smoking, and drug- and medication-free. The following outcomes were measured: C-reactive protein, TNF-α, IL-6, IL-1β, IL-10, leukocyte counts (monocytes, lymphocytes, and neutrophils), and lipopolysaccharide-binding protein (LBP). Risk factors that increase systemic inflammation, such as blood pressure, sleep loss, and cortisol, were also assessed. The results indicated that shift workers slept significantly less than day workers and had significantly increased concentrations of all of the cytokines measured as well as plasma cortisol. Regression models found that after controlling for covariates, shift-work exposure predicted the significant increase observed in IL-10, leukocyte counts, and LBP. Our results suggest that acute increases in low-grade systemic endotoxemia are unresolved during chronic shift-work exposure. This ongoing immune challenge may underlie the disrupted inflammatory responses characteristic of shift-work-related pathologies. Systemic endotoxemia may represent a novel target to investigate the early effects of exposure to shift-work schedules.


2021 ◽  
Vol 5 (12) ◽  
pp. 972-982
Author(s):  
Oliver Kumpf ◽  
Kathleen Gürtler ◽  
Saubashya Sur ◽  
Monalisa Parvin ◽  
Lena-Karoline Zerbe ◽  
...  

2021 ◽  
Author(s):  
Hanieh Irani ◽  
Banafsheh Khodami ◽  
Behnaz Abiri ◽  
Atoosa Saidpour

Abstract Background: Food addiction, the desire to eat compulsively and excessively palatable foods, is one of the behavioral factors that plays an important role in pathogenesis of obesity. Food addiction, like drug addiction, changes the dopaminergic system in rewards region of brain, but at lower levels. There are evidence suggesting brain-derived neurotrophic factor (BDNF) is synthesized in dopaminergic pathways in the reward regions of the brain and is involved in regulating food intake and body weight. BDNF is also associated with eating disorders in humans and hyperphagia in mice. On the other hand, it has been shown that the intestinal microbiome is effective in eating behavior through the production of neuronal and hormonal mediators, including BDNF. Intestinal microbiome changes greatly under the influence of diet. It has been shown that a time-restricted feeding (TRF) has been able to maintain fluctuations in the intestinal microbiome in response to the body's circadian rhythm. Furthermore, increased pathogens in the gut are associated with increased release of polysaccharides from the bacterial wall, resulting in increased levels of lipopolysaccharide binding protein (LBP). This study will aim to evaluate the effect of TRF on anthropometric measures, body composition, eating behavior, stress level, BDNF and LBP levels in over weight and obese women with food addiction.Methods/design: we will carry on a randomized clinical trial for 8 weeks to evaluate the effect of a TRF on anthropometric measures, body composition, eating behavior, stress level, BDNF and LBP levels in obese and overweight women with food addiction.Discussion: Given the effect of BDNF on regulating eating behavior and body weight and the effect of dietary restrictions on BDNF and the gut microbiome, the TRF diet could possibly be a new way to successfully manage weight through modifying BDNF in people with eating disorders, including food addiction.Trial Registration: Iranian Registry of Clinical Trials. IRCT20131228015968N7. Registered on 2020-10-25.


2021 ◽  
Vol 127 (5) ◽  
pp. S39
Author(s):  
V. Beloglazov ◽  
I. Yatskov ◽  
A. Nikolaeva ◽  
E. Lavrenchuk ◽  
L. DuBuske

Therapy ◽  
2021 ◽  
Vol 7_2021 ◽  
pp. 64-70
Author(s):  
Levitan B.N. Levitan ◽  
Kasyanova T.R. Kasyanova ◽  
Voloshina O.A. Voloshina ◽  
Martynova A.D. Martynova ◽  
◽  
...  

mSystems ◽  
2021 ◽  
Vol 6 (3) ◽  
Author(s):  
Abigail J. S. Armstrong ◽  
Kevin Quinn ◽  
Jennifer Fouquier ◽  
Sam X. Li ◽  
Jennifer M. Schneider ◽  
...  

ABSTRACT Poor metabolic health, characterized by insulin resistance and dyslipidemia, is higher in people living with HIV and has been linked with inflammation, antiretroviral therapy (ART) drugs, and ART-associated lipodystrophy (LD). Metabolic disease is associated with gut microbiome composition outside the context of HIV but has not been deeply explored in HIV infection or in high-risk men who have sex with men (HR-MSM), who have a highly altered gut microbiome composition. Furthermore, the contribution of increased bacterial translocation and associated systemic inflammation that has been described in HIV-positive and HR-MSM individuals has not been explored. We used a multiomic approach to explore relationships between impaired metabolic health, defined using fasting blood markers, gut microbes, immune phenotypes, and diet. Our cohort included ART-treated HIV-positive MSM with or without LD, untreated HIV-positive MSM, and HR-MSM. For HIV-positive MSM on ART, we further explored associations with the plasma metabolome. We found that elevated plasma lipopolysaccharide binding protein (LBP) was the most important predictor of impaired metabolic health and network analysis showed that LBP formed a hub joining correlated microbial and immune predictors of metabolic disease. Taken together, our results suggest the role of inflammatory processes linked with bacterial translocation and interaction with the gut microbiome in metabolic disease among HIV-positive and -negative MSM. IMPORTANCE The gut microbiome in people living with HIV (PLWH) is of interest since chronic infection often results in long-term comorbidities. Metabolic disease is prevalent in PLWH even in well-controlled infection and has been linked with the gut microbiome in previous studies, but little attention has been given to PLWH. Furthermore, integrated analyses that consider gut microbiome, together with diet, systemic immune activation, metabolites, and demographics, have been lacking. In a systems-level analysis of predictors of metabolic disease in PLWH and men who are at high risk of acquiring HIV, we found that increased lipopolysaccharide-binding protein, an inflammatory marker indicative of compromised intestinal barrier function, was associated with worse metabolic health. We also found impaired metabolic health associated with specific dietary components, gut microbes, and host and microbial metabolites. This study lays the framework for mechanistic studies aimed at targeting the microbiome to prevent or treat metabolic endotoxemia in HIV-infected individuals.


Sign in / Sign up

Export Citation Format

Share Document