Commensal fungi, a force to be reckoned with.

Fungal symbionts play a key role in maintaining host homeostasis. In a recent issue of Nature, Liao et al. show that Kazachstania pintolopesii, a symbiotic fungus in mice, is shielded from the host immune system during homeostasis but induces type 2 immunity during mucus fluctuations.

facilitates tumor-derived CCL5 to recruit dendritic cell and suppress colorectal tumorigenesis.

Gut microbes play a crucial role in regulating the tumor microenvironment (TME) of colorectal cancer (CRC). Nevertheless, the deep mechanism between the microbiota-TME interaction has not been well explored. In this study, we for the first time discovered that () effectively suppressed tumor growth both in the AOM/DSS-induced CRC model and the spontaneous adenoma model.

Adhesin RadD: the secret weapon of .

can promote colorectal cancer (CRC) development through a variety of virulence proteins. Zhang et al. recently identified an adhesin RadD, for adhesion to CRC.

The role of microbial indole metabolites in tumor.

The gut microbiota can produce a variety of microbial-derived metabolites to influence tumor development. Tryptophan, an essential amino acid in the human body, can be converted by microorganisms via the indole pathway to indole metabolites such as Indole-3-Lactic Acid (ILA), Indole-3-Propionic Acid (IPA), Indole Acetic Acid (IAA) and Indole-3-Aldehyde (IAld). Recent studies have shown that indole metabolites play key roles in tumor progression, and they can be used as adjuvant regimens for tumor immunotherapy or chemotherapy.

Environmental pollutants and bad bugs work hand in glove.

'Bad bacteria' could alter the toxicokinetics of environmental pollutants, thereby exacerbating chemically induced tumorigenesis. Recently, Roje et al. reported that specific gut microbiota can metabolize nitrosamine compounds to a toxic oxidation product, aggravating bladder cancer development and progression.

Microbial metabolite enhances immunotherapy efficacy by modulating T cell stemness in pan-cancer.

The immune checkpoint blockade (ICB) response in human cancers is closely linked to the gut microbiota. Here, we report that the abundance of commensal Lactobacillus johnsonii is positively correlated with the responsiveness of ICB. Supplementation with Lactobacillus johnsonii or tryptophan-derived metabolite indole-3-propionic acid (IPA) enhances the efficacy of CD8 T cell-mediated αPD-1 immunotherapy.

L-arginine metabolism ameliorates age-related cognitive impairment by Amuc_1100-mediated gut homeostasis maintaining.

Aging-induced cognitive impairment is associated with a loss of metabolic homeostasis and plasticity. An emerging idea is that targeting key metabolites is sufficient to impact the function of other organisms. Therefore, more metabolism-targeted therapeutic intervention is needed to improve cognitive impairment.

Microbiota: A key factor affecting and regulating the efficacy of immunotherapy.

Background: Immunotherapy has made significant progress in cancer treatment; however, the responsiveness to immunotherapy varies widely among patients. Growing evidence has demonstrated the role of the gut microbiota in the efficacy of immunotherapy.

Main Body: Herein, we summarise the changes in the microbiota in different cancers under various immunotherapies.

Lactobacillus Intestinalis Primes Epithelial Cells to Suppress Colitis-Related Th17 Response by Host-Microbe Retinoic Acid Biosynthesis.

Gut microbiome is integral to the pathogenesis of ulcerative colitis. A novel probiotic Lactobacillus intestinalis (L. intestinalis) exerts a protective effect against dextran sodium sulfate-induced colitis in mice.

Heat-inactivated Bifidobacterium adolescentis ameliorates colon senescence through Paneth-like-cell-mediated stem cell activation.

Declined numbers and weakened functions of intestinal stem cells (ISCs) impair the integrity of the intestinal epithelium during aging. However, the impact of intestinal microbiota on ISCs in this process is unclear. Here, using premature aging mice (telomerase RNA component knockout, Terc), natural aging mice, and in vitro colonoid models, we explore how heat-inactivated Bifidobacterium adolescentis (B.

Bifidobacterium adolescentis orchestrates CD143 cancer-associated fibroblasts to suppress colorectal tumorigenesis by Wnt signaling-regulated GAS1.

Background: The interplay between gut microbiota and tumor microenvironment (TME) in the pathogenesis of colorectal cancer (CRC) is not well explored. Here, we elucidated the functional role of Bifidobacterium adolescentis (B.a) on CRC and investigated its possible mechanism on the manipulation of cancer-associated fibroblasts (CAFs) in CRC.

Bifidobacterium adolescentis induces Decorin macrophages via TLR2 to suppress colorectal carcinogenesis.

Background: The interplay between gut microbiota and tumor microenvironment (TME) in the pathogenesis of colorectal cancer (CRC) is largely unknown. Here, we elucidated the functional role of B. adolescentis and its possible mechanism on the manipulation of Decorin macrophages in colorectal cancer.

alleviates colitis by TLR1/2-STAT3 mediated CD206 macrophages activation.

Imbalance of gut microbiota homeostasis is related to the occurrence of ulcerative colitis (UC), and probiotics are thought to modulate immune microenvironment and repair barrier function. Here, in order to reveal the interaction between UC and gut microbiota, we screened a new probiotic strain by 16S rRNA sequencing from Dextran Sulfate Sodium (DSS)-induced colitis mice, and explored the mechanism and clinical relevance. (), as a potential anti-inflammatory bacterium was decreased colonization in colitis mice.

promotes colorectal cancer cells adhesion to endothelial cells and facilitates extravasation and metastasis by inducing ALPK1/NF-κB/ICAM1 axis.

Metastasis is the leading cause of death for colorectal cancer (CRC) patients, and the spreading tumor cells adhesion to endothelial cells is a critical step for extravasation and further distant metastasis. Previous studies have documented the important roles of gut microbiota-host interactions in the CRC malignancy, and () was reported to increase proliferation and invasive activities of CRC cells. However, the potential functions and underlying mechanisms of in the interactions between CRC cells and endothelial cells and subsequent extravasation remain unclear.

Micropeptide ASAP encoded by LINC00467 promotes colorectal cancer progression by directly modulating ATP synthase activity.

Emerging evidence has shown that open reading frames inside long noncoding RNAs (lncRNAs) could encode micropeptides. However, their roles in cellular energy metabolism and tumor progression remain largely unknown. Here, we identified a 94 amino acid-length micropeptide encoded by lncRNA LINC00467 in colorectal cancer.