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The gut microbiome is an important determinant in various diseases. Here we perform a cross-sectional study of Japanese adults and identify the Blautia genus, especially B. wexlerae , as a commensal bacterium that is inversely correlated with obesity and type 2 diabetes mellitus. Oral administration of B. wexlerae to mice induce metabolic changes and anti-inflammatory effects that decrease both high-fat diet–induced obesity and diabetes. The beneficial effects of B. wexlerae are correlated with unique amino-acid metabolism to produce S-adenosylmethionine, acetylcholine, and l -ornithine and carbohydrate metabolism resulting in the accumulation of amylopectin and production of succinate, lactate, and acetate, with simultaneous modification of the gut bacterial composition. These findings reveal unique regulatory pathways of host and microbial metabolism that may provide novel strategies in preventive and therapeutic approaches for metabolic disorders. Here, the authors inversely associate Blautia wexlerae with obesity and type 2 diabetes mellitus in humans and further show that administration of B. wexlerae to mice decrease both high-fat diet–induced obesity and diabetes via modulating gut microbial metabolism.

This study demonstrates that monoclonal antibodies can be developed to targeting specific gut bacteria prevalent in the Japanese population and the potential for creating a novel diagnostic system using these antibodies. In this study, we established specific antibodies against representative bacteria from the genera Bacteroides , Faecalibacterium , and Prevotella and showed that they could be detected using ELISA, flow cytometry, and western blot analysis. Furthermore, a technique to quantify target bacteria was developed by combining these antibodies in a sandwich ELISA, enabling the quantification of bacteria in human fecal samples. This technology serves as a foundational method for rapidly and easily measuring gut bacteria and is expected to evolve into a powerful tool for analyzing the impact of gut bacteria on health, as well as for personalized health management based on individual gut environments.

Background The human gut harbors a diverse microbiota that is crucial for maintaining health but also contributes to several diseases. Understanding how microbial communities are assembled and maintained is critical for advancing gut health. Results We identified a unique interaction between the pathobiont Fusobacterium varium and the symbiont Faecalibacterium prausnitzii , both members of the gut microbial community; their interaction is driven by metabolites and direct cell-to-cell contact. Growth of F. varium was inhibited in the presence of F. prausnitzii because of a decrease in pH and an increase in β -hydroxybutyric acid. Conversely, the growth of F. prausnitzii was promoted in the presence of F. varium , likely via direct contact. Conclusions These findings highlight the importance of metabolite-driven interactions and direct contact in shaping gut microbial communities and emphasize the potential of interactions between F. prausnitzii and F. varium in influencing gut health. FLryDwzSyUiUebEJdxwjmw Video Abstract

An 81‐year‐old man initially underwent right hepatic lobectomy for liver cancer and was pathologically diagnosed with combined hepatocellular and cholangiocarcinoma (CHC). At 13 months after resection, multiple lymph node metastases were observed. We started atezolizumab plus bevacizumab (Atez/Bev), achieving a 7.5‐month progression‐free survival. Atez/Bev might exhibit efficacy for CHC patients. Although no standard systemic chemotherapy for combined hepatocellular and cholangiocarcinoma patients has yet been established, atezolizumab plus bevacizumab, which is a combination therapy of anti‐programmed death ligand‐1 and anti‐vascular endothelial growth factor, might exhibit good therapeutic outcome.

Phosphorylation of IκB by the IκB kinase (IKK) complex is a critical step leading to IκB degradation and activation of transcription factor NF-κB 1 . The IKK complex contains two catalytic subunits, IKKα and IKKβ, the latter being indispensable for NF-κB activation by pro-inflammatory cytokines 2 , 3 , 4 , 5 , 6 , 7 . Although IKK is activated by phosphorylation of the IKKβ activation loop 8 , the physiological IKK kinases that mediate responses to extracellular stimuli remain obscure 1 , 9 . Here we describe an IKK-related kinase, named NAK (NF-κB-activating kinase), that can activate IKK through direct phosphorylation. NAK induces IκB degradation and NF-κB activity through IKKβ. Endogenous NAK is activated by phorbol ester tumour promoters and growth factors, whereas catalytically inactive NAK specifically inhibits activation of NF-κB by protein kinase C-ε (PKCε). Thus, NAK is an IKK kinase that may mediate IKK and NF-κB activation in response to growth factors that stimulate PKCε activity.