Background: Gutmicrobiota dysbiosis, endotoxemia, and systemic inflammation are major factors contributing to disease pathophysiology in patients with critical illness. The present study aimed to assess the effects of synbiotic supplementation on serum endotoxin and inflammationof adult patients with critical illness.
Methods: This double-anonymized, randomized controlled trial was conducted at the intensive care unit (ICU) of Imam Reza Hospital in Mashhad, Iran. In the intervention group, 20 patients received synbiotic capsules (containing a combination of Lactobacillus, Bifidobacterium, Streptococcus, and fructooligosaccharides) twice per day for a maximum of 14 days. In the control group, 18 patients received placebo capsules. The serum levels of endotoxin and C-reactive protein and the neutrophil to lymphocyte ratio (NLR) were measured before and after the intervention. In addition, clinical outcomes and Acute Physiology and Chronic Health Evaluation and Sequential Organ Failure Assessment scores were recorded.
Results: Basic characteristics were similar in the intervention and control groups. The NLR and serum endotoxin levels (median [IQR]) significantly declined in the synbiotic group (7.83 [4.58-12.57] to 6.01 [4.25-9.38]; P = .04; and 11.98 [10.64-12.65] to 10.58 [9.41-12.34]; P = .03, respectively). However, no significant changes were observed in the mentioned parameters in the placebo group. The clinical outcomes were also similar in the study groups, such as the length of hospital/ICU stay and hospital/28-day mortality rate.
Conclusion: Although synbiotic supplementation (500 mg twice daily for 14 days) could reduce serum endotoxin and inflammatory markers, it had no effects on the clinical outcomes of the patients.
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http://dx.doi.org/10.1002/ncp.10758 | DOI Listing |
Alzheimers Dement
December 2024
University of Kentucky, Lexington, KY, USA.
Background: Aging microglia accumulate lipid droplets (LDs), secrete pro-inflammatory cytokines, and are defective in phagocytosis. The E4 allele of Apolipoprotein E (APOE) is the strongest genetic risk factor for late-onset Alzheimer's disease (LOAD) and is associated with increased neuroinflammation and LD accumulation. Here, we aimed to determine if the effects of aging and the E4 allele are synergistic in causing the accumulation of LDs seen in LOAD.
View Article and Find Full Text PDFSci Rep
January 2025
Department of Gastroenterology, Fifth Affiliated Hospital, Zhengzhou University, Zhengzhou, China.
The deregulation of immune responses is what causes food allergy (FA) to occur. FA's cause is still unknown. The goal of this study is to investigate the mechanism how the impaired production of IL-10 occurs in peripheral naive B cells of patients with FA.
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January 2025
Occupational and Environmental Epidemiology Branch, Division of Cancer Epidemiology & Genetics, National Cancer Institute, Rockville, Maryland, USA
Background: Occupational exposure to endotoxin has been associated with reduced lung cancer risk. The mechanisms underlying this association are unclear, though immunological alterations likely play a role. Farmers who perform certain tasks (eg, raising hogs) can be highly exposed to endotoxin.
View Article and Find Full Text PDFFront Biosci (Landmark Ed)
December 2024
Department of Critical Care Medicine, The First Affiliated Hospital of Chongqing Medical University, 400016 Chongqing, China.
Background: Acute lung injury (ALI) significantly impacts the survival rates in intensive care units (ICU). Releasing a lot of pro-inflammatory mediators during the progression of the disease is a core feature of ALI, which may lead to uncontrolled inflammation and further damages the tissues and organs of patients. This study explores the potential therapeutic mechanisms of Dexmedetomidine (Dex) in ALI.
View Article and Find Full Text PDFCan J Gastroenterol Hepatol
December 2024
Department of Infectious Diseases, Songjiang Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Aims: Carboxylesterase (Ces)1f is implicated in protection against hepatic inflammation, but it is unclear whether the enzyme has an influence in polarization of Kupffer cells (KCs), the innate immune cells mediating hepatic inflammatory injury including acute liver failure (ALF). In the present study, we aim to explore KC polarization induced by Ces1f in mice with lipopolysaccharide/D-galactosamine (LPS/D-GalN)-induced ALF. We adopted a novel delivery system, β-1,3-D-glucan-encapsulated Endoporter-siRNA particles, to specifically target KC Ces1f knockdown via tail vein injection in mice.
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