Obesity and metabolic dysfunction-associated fatty liver disease (MAFLD) are prevalent metabolic disorders with substantial global health implications that are often inadequately addressed by current treatments and may have side effects.
Probiotics have emerged as promising therapeutic agents owing to their beneficial effects on gut health and metabolism. This study investigated the synergistic effects of a probiotic combination of BNR17 and ABF21069 on obesity and MAFLD in C57BL/6 mice fed a high-sucrose diet. The probiotic combination significantly reduced body weight and fat accumulation compared with the high-sucrose diet. It also alleviated elevated serum leptin levels induced by a high-sucrose diet.
Histological analysis revealed a significant reduction in white adipose tissue and fatty liver in the mice treated with the probiotic combination. Furthermore, increased expression of genes related to β-oxidation, thermogenesis, and lipolysis suggested enhanced metabolic activity. The probiotic groups, particularly the BNR17 group, showed an increase in fecal exopolysaccharides, along with a tendency toward a lower expression of intestinal sugar transport genes, indicating reduced sugar absorption. Additionally, inflammatory markers in the liver tissue exhibited lower expression in the ABF21069 group than in the HSD group. Despite each strain in the combination group having distinct characteristics and functions, their combined effect demonstrated synergy in mitigating obesity and MAFLD, likely through the modulation of fecal exopolysaccharides content and improvement in lipid metabolism. These findings underscore the potential of probiotic supplementation as a promising assistant therapy for managing obesity and MAFLD and provide valuable insights into its therapeutic mechanisms in metabolic disorders.
Colorectal cancer (CRC) is the second-highest cause of cancer-associated mortality among both men and women worldwide. One of the risk factors for CRC is obesity, which is correlated with a high-fat diet prevalent in Western dietary habits. The association between an obesogenic high-fat diet and CRC has been established for several decades; however, the mechanisms by which a high-fat diet increases the risk of CRC remain unclear. Recent studies indicate that gut microbiota strongly infuence the pathogenesis of both high-fat diet-induced obesity and CRC. The gut microbiota is composed of hundreds of bacterial species, some of which are implicated in CRC. In particular, the expansion of facultative anaerobic Enterobacteriaceae, which is considered a microbial signature of intestinal microbiota functional imbalance (dysbiosis), is associated with both high-fat diet-induced obesity and CRC. Here, we review the interaction between the gut microbiome and its metabolic byproducts in the context of colorectal cancer (CRC) during high-fat diet-induced obesity. In addition, we will cover how a high-fat diet can drive the expansion of genotoxin-producing Escherichia coli by altering intestinal epithelial cell metabolism during gut infammation conditions.
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rapid elimination. As pattern recognition receptors, Toll-like
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viruses. Here, we investigated if a 2,4-diaminoquinazolinebased
TLR7/8 agonist, (S)-3-((2-amino-8-fluoroquinazolin-
4-yl)amino)hexan-1-ol (named compound 31), could be used
as an adjuvant to enhance the serological and mucosal immunity
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the production of proinflammatory cytokines in macrophages.
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of 1 μg compound 31 together with an inactivated vaccine
(0.5 μg) to mice not only enhanced virus-specific IgG and
IgA production but also neutralized influenza A virus with
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viral infection-mediated loss of body weight and increased
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respiratory RNA viruses such as influenza viruses and potentially
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recombination. The htpsC deletion strain exhibited a
diminished ability to adhere to and invade epithelial cells from
different sources. Double immunofluorescence microscopy
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by the wild type strain was inhibited by a monoclonal
antibody against E-cadherin. In contrast, the htpsC-deficient
mutant was unaffected by the same treatment, suggesting that
E-cadherin is the host-cell receptor that interacts with HtpsC
and facilitates bacterial internalization. Based on these results,
we propose that HtpsC is involved in the process by which
S. suis 2 penetrates host epithelial cells, and that this protein
is an important virulence factor associated with cell adhesion
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In recent years, the occurrence of antibiotic-resistant pathogens
is increasing rapidly. There is growing concern as
the development of antibiotics is slower than the increase in
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morphology and migration. Wiskott-Aldrich Syndrome proteins
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polymerization by activating the Arp2/3 complex. The present
study investigated the roles of WasC, one of the 3 WASPs
in Dictyostelium, in cellular processes. Cells lacking WasC
displayed strong cell adhesion and approximately 1.5-fold
increase in F-actin levels as compared to the wild-type cells.
Loss of wasC caused defects in phagocytosis and decreased
the migration speed in chemoattractant-mediated cell migration
but did not affect directionality. WasC was localized to the
protruding region in migrating cells and, transiently and rapidly
translocated to the cell cortex in response to chemoattractant
stimulation, in an F-actin dependent manner. Our results suggest that WasC is involved in cell adhesion and
migration by regulating F-actin polymerization at the leading
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The increased strength of adhesion in wasC null cells is likely
to decrease the migration speed but not the directionality.
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J. Microbiol. 2018;56(9):673-682. Published online August 23, 2018
Obesity is a chronic disease associated with different metabolic
diseases as well as alterations in immune cell function.
It is characterized by a chronic systemic low grade inflammation.
There are several studies demonstrating the influence
of obesity on the impaired immune response to infection.
However, it is not completely clear whether the obese environment
influences the development or maintenance of the
immune response against infections. The aim of this study
was to determine how obesity induced by a high-fat diet affects
the immune response to an early oral Salmonella infection.
Four groups of mice were kept in separate cages. Two of
these designated as controls, fed with a normal diet; whereas
other two groups were fed with a high fat diet for 10 weeks.
Some mice were used for Salmonella oral infection. After 7
days of oral infection with S. Thypimurium the proportions
of spleen cell subsets expressing activation markers in normal
diet and HFD obese mice were stained with monoclonal
antibodies and analyzed by flow cytometry. Also, mRNA
levels of different cytokines were quantified by RT-PCR. It
was found that obesity affects the function of the immune
system against an early oral Salmonella infection, decreasing
NK cells, altering the expression of activation molecules as
well as cytokines mRNA levels. Interestingly, the expression
some activation molecules on T lymphocytes was reestablished
after Salmonella infection, but not the CD25 expression.
Immune alterations could lead to immunosuppression
or increased susceptibility to infections in HFD obese mice.
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