We aimed to determine the prebiotic impact of Mushroom
Bulgaria inquinans
(BI) on the host immune response and gut microbiota. Male C57BL/6 mice were fed a diet supplemented with 0, 1, or 2% BI for 4 wks. Compared to mice fed with a control diet (0% BI), mice fed with 1 or 2% BI had an increase of T cell proliferation from the spleen, but such change was not found between 1 and 2% BI treated mice. Also, BI at 2% increased the production of IL-2 of splenocytes stimulated with T-cell mitogens, but BI at 1 and 2% did not affect productions of other splenic-T cell cytokines including IL-4, IL-10, and IFN-γ. Interestingly, BI at 1 or 2% inhibited T cell proliferation of mesenteric lymph node (mLN) but this effect was not found between 1 and 2% BI treated mice. Furthermore, BI inhibited the production of IL-2 in anti-CD3/CD28-stimulated T cells from mLN in a dose-dependent manner. Meanwhile, BI at 2%, not 1% inhibited the production of IL-4, IL-10, and IFN-γ of mLN. Since BI at 2% produced a more significant effect on the immune response, we further used BI at 2% to evaluate the effect of BI on gut microbiota. Of note, BI reduced the diversity of gut microbiota and resulted in an increase of
Faecalibaculum
and
Parabacteroides
abundance and the decrease of
Allobaculum, Candidatus
_
Saccharimonas
, and
Rikenella
abundance at the genus level. Finally, the correlation was observed between specific bacteria genera and the productions of T-cell cytokines from mesenteric lymphocytes:
Rikenella
and
Candidatus_Saccharimonas
correlated positively with IL-2, IL-4, IL-10, and IFN-γ;
Bacteroides
and
Parabacteroides
correlated negatively with IL-2 and IL-4;
Faecalibaculum
correlated negatively with IFN-γ and IL-4 and
Bacteroides
and
Bifidobacterium
correlated negatively with IFN-γ. The specific role of each intestinal microbiota observed is still unclear, but BI might exert a prebiotic effect on gut microbiota by increasing the abundance of potentially beneficial bacteria (
Faecalibaculum
). This is helpful for further demonstrating the healthy-promotion mechanism of
B. inquinans
.
Aims:
Obesity is characterized as a chronic state of low-grade inflammation with progressive immune cell infiltration into adipose tissue. Adipose tissue macrophages play a critical role in the establishment of chronic inflammatory states and metabolic dysfunctions.
Inonotus
(
I
.)
sanghuang
and
its
extract polyphenols exhibit anti-carcinogenesis, anti-inflammatory, and anti-oxidant activities. However, the action of
I. sanghuang
polyphenols in obesity-related inflammation has not been reported. The aim of this study was to explore the anti-inflammatory action of polyphenols from
I. sanghuang
extract (ISE) in macrophages and the interaction between macrophages and adipocytes.
Materials and Methods:
RAW264.7 macrophages were stimulated with LPS or conditioned medium of hypertrophied 3T3-L1 adipocytes or cocultured with differentiated adipocytes in the presence of different doses of ISE. The inflammatory cytokines were evaluated by ELISA, the MAPK, NF-κB, and IL-6/STAT3 signals were determined by immunoblotting, and the migrated function of macrophages was determined by migration assay.
Results:
ISE suppressed the inflammatory mediators including NO, TNF-α, IL-6, and MCP-1 induced by either LPS or conditioned medium derived from 3T3-L1 adipocytes. ISE also decreased the production of these inflammatory mediators in cocultures of 3T3-L1 adipocytes and RAW264.7 macrophages. Furthermore, ISE blocked RAW264.7 macrophages migration toward 3T3-L1 adipocytes in cocultures. Finally, this effect of ISE might be mediated via inhibiting ERK, p38, and STAT3 activation.
Conclusions:
Our findings indicate the possibility that ISE suppresses the interaction between macrophages and adipocytes, attenuates chronic inflammation in adipose tissue and improves obesity-related insulin resistance and complication, suggesting that ISE might be a valuable medicinal food effective in improving insulin resistance and metabolic syndrome.
MLTK (mixed-lineage kinase-like mitogen-activated protein triple kinase) is a member of the mitogen-activated protein kinase family and functioned as a mitogen activated kinase kinase kinase. MLTKα, one of the alternatively spliced forms of MLTK, could activate the c-Jun N-terminal kinase pathway, which involved in cellular stress responses and apoptosis. But the role of MLTKα in neural apoptosis was still unclear. Here, we performed a transient global cerebral ischemia model (TGCI) in adult rats and detected the dynamic changes of MLTKα in hippocampal CA1 neurons and brain cortex. We found the MLTKα expression was increased shortly after TGCI and peaked after 8 h. In spatial distribution, MLTKα was widely located in neurons rather than astrocytes and microglia. Moreover, there was a concomitant up-regulation of active caspase-3. Taken together, we hypothesized the up-regulation of MLTKα played an essential role in the apoptosis of hippocampal CA1 neurons.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.