COMPARATIVE IMMUNOLOGY MICROBIOLOGY AND INFECTIOUS DISEASES
·
2021
·
IF 2.268
Yafei Chen,Zuoyi Jiang,Zhihai Lei,Jihui Ping,Juan Su
Gut-lung axis injury is a common finding in patients with respiratory diseases as well as in animal model of influenza virus infection. Influenza virus damages the intestinal microecology while affecting the lungs. Rifaximin, a non-absorbable derivative of rifamycin, is an effective antibiotic that acts by inhibiting bacterial RNA synthesis. This study aimed to determine whether rifaximin-perturbation of the intestinal microbiome leads to protective effects against influenza infection, via the gut-lung axis. Our results showed that influenza virus infection caused inflammation of and damage to the lungs. The expression of tight junction proteins in the lung and colon of H1N1 infected mice decreased significantly, attesting that the barrier structure of the lung and colon was damaged. Due to this perturbation in the gut-lung axis, the intestinal microbiota became imbalanced as Escherichia coli bacteria replicated opportunistically, causing intestinal injury. When influenza infection was treated with rifamixin, qPCR results from the gut showed significant increases in Lactobacillus and Bifidobacterium populations, while Escherichia coli populations markedly decreased. Furthermore, pathology sections and western blotting results illustrated that rifaximin treatment strengthened the physical barriers of the lung-gut axis through increased expression of tight junction protein in the colon and lungs. These results indicated that rifaximin ameliorated lung and intestine injury induced by influenza virus infection. The mechanisms identified were the regulation of gut flora balance and intestinal and lung permeability, which might be related to the regulation of the gut-lung axis. Rifaximin might be useful as a co-treatment drug for the prevention of influenza virus infection.
研究领域:
微生物学
·
免疫学
·
呼吸系统疾病
·
药理学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Frontiers in Immunology
·
2017
·
IF 6.429
Ren Wenkai,Yin Jie,Xiao Hao,Chen Shuai,Liu Gang,Tan Bie,Li Nengzhang,Peng Yuanyi,Li Tiejun,Zeng Benhua,Li Wenxia,Wei Hong,Yin Zhinan,Wu Guoyao,Hardwidge Philip R.,Yin Yulong
Intestinal microbiota has critical importance in pathogenesis of intestinal infection; however, the role of intestinal microbiota in intestinal immunity during enterotoxigenic Escherichia coli (ETEC) infection is poorly understood. The present study tested the hypothesis that the intestinal microbiota is associated with intestinal interleukin-17 (IL-17) expression in response to ETEC infection. Here, we found ETEC infection induced expression of intestinal IL-17 and dysbiosis of intestinal microbiota, increasing abundance of γ-aminobutyric acid (GABA)-producing Lactococcus lactis subsp. lactis. Antibiotics treatment in mice lowered the expression of intestinal IL-17 during ETEC infection, while GABA or L. lactis subsp. lactis administration restored the expression of intestinal IL-17. L. lactis subsp. lactis administration also promoted expression of intestinal IL-17 in germ-free mice during ETEC infection. GABA enhanced intestinal IL-17 expression in the context of ETEC infection through activating mechanistic target of rapamycin complex 1 (mTORC1)-ribosomal protein S6 kinase 1 (S6K1) signaling. GABA–mTORC1 signaling also affected intestinal IL-17 expression in response to Citrobacter rodentium infection and in drug-induced model of intestinal inflammation. These findings highlight the importance of intestinal GABA signaling in intestinal IL-17 expression during intestinal infection and indicate the potential of intestinal microbiota-GABA signaling in IL-17-associated intestinal diseases.
研究领域:
微生物学
·
免疫学
·
病理学
·
分子生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
MOLECULES
·
2021
·Vol. 26
·期 21
·6604
·
IF 4.412
Ruige Cao,Xing Wu,Hui Guo,Xin Pan,Rong Huang,Gangqiang Wang,Jikai Liu
Naringin is a kind of multi-source food additive which has been explored broadly for its various biological activities and therapeutic potential. In the present study, the protective effect and mechanism of naringin on dextran sulfate sodium (DSS)-induced ulcerative colitis (UC) in mice were investigated. The results showed that naringin significantly alleviated DSS-induced colitis symptoms, including disease activity index (DAI), colon length shortening, and colon pathological damage. The tissue and serum secretion of inflammatory cytokines, as well as the oxidative stress, were decreased accordingly upon naringin intervention. Naringin also decreased the proteins involved in inflammation and increased the expression of tight junction (TJ) proteins. Moreover, naringin increased the relative abundance ofFirmicutes/Bacteroidesand reduced the content ofProteobacteriato improve the intestinal flora disorder caused by DSS, which promotes the intestinal health of mice. It was concluded that naringin can significantly ameliorate the pathogenic symptoms of UC through inhibiting inflammatory response and regulating intestinal microbiota, which might be a promising natural therapeutic agent for the dietary treatment of UC and the improvement of intestinal symbiosis.Keywords:ulcerative colitis;naringin;intestinal microbiota;inflammation
研究领域:
药理学
·
免疫学
·
胃肠病学
·
微生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
PHARMACOLOGICAL RESEARCH
·
2022
·
IF 10.334
Suhang Guo,Yi Peng,Yan Lou,Lijuan Cao,Junqing Liu,Nengming Lin,Sheng Cai,Yu Kang,Su Zeng,Lushan Yu
Colorectal cancer (CRC) is the third most commonly diagnosed cancer and the second leading cause of cancer-related deaths in the world. The downregulation of farnesoid X receptor (FXR) is frequently founded in CRC patients. The current study found that the decreased expression of FXR in colorectal cancer leads to disorders of bile acids (BAs) metabolism. The altered BAs profile shaped distinct intestinal flora and positively regulated secretory immunoglobulin A (sIgA). The dual regulation of BAs and sIgA enhanced adhesion and biofilm formation of enterotoxigenic Bacteroides fragilis (ETBF), which has a colorectal tumorigenesis effect. The abundance of ETBF increased significantly in intestinal mucosa of colitis-associated cancer (CAC) mice, and finally promoted the development of colorectal cancer. This study suggests that downregulation of FXR in CRC results in BAs dysregulation, and BAs have strong effects on sIgA and gut flora. The elevated BAs concentration and altered gut microbiome are risk factors for CRC.
研究领域:
肿瘤学
·
胃肠病学
·
微生物学
·
免疫学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Nutrients
·
2025
·Vol. 17
·期 18
·2988
·
IF 5
Hedong Jiang,Gonglong Li,Liuming Xie,Nanhai Zhang,Yi Huang,Xinli Liang,Fanghua Guo,Qieying Jiang,Zhenggen Liao
Background: Curcumin (Cur) and tryptophan (Trp) both show promise for treating ulcerative colitis (UC) alone, but their combination has not been explored. This study investigated the therapeutic advantage of the combination (Cur–Trp) for DSS-induced ulcerative colitis in mice.Methods: We established a mouse model of ulcerative colitis induced by dextran sulfate sodium (DSS). The mice were treated with Cur, Trp, or Cur–Trp, and to evaluate the therapeutic effects, we assessed clinical signs such as body weight, disease activity index (DAI), and colon length. We also examined intestinal barrier function through indicators including histopathological changes, inflammatory factors, oxidative stress levels, mucin secretion, and tight junction protein expression. Additionally, we analyzed the composition of gut microbiota and the content of its metabolites like short-chain fatty acids (SCFAs).Results: The Cur–Trp group produced the most significant improvement, exceeding that of Cur or Trp group. This was evidenced by a significant recovery of this sign, including slower weight loss, reduced colon shortening, and de-creased disease activity index. Compared with the model group, the weight loss of mice in the Cur–Trp group was reduced from 17.15% to 9.73%, which was better than that in the cur group (11.33%) and the Trp group (11.59%). The DAI decreased from the model group (3.6) to the Cur–Trp group (2.4), while the DAI in the Cur group and the Trp group only decreased to 2.9 and 2.8, respectively. The colon length in the Cur–Trp group (6.52 cm) was larger than that in the cur group (6.31 cm), the Trp group (6.23 cm) and the model group (5.5 cm). The Cur–Trp intervention effectively restored intestinal barrier function, as shown by reducing colon tissue dam-age, modulating inflammatory factors, restoring oxidative balance, increasing mucin secretion, and upregulating tight junction protein expression. Further studies showed that the combination uniquely modulated the gut microbiome, increased the Firmicutes/Bacteroidetes (F/B) ratio, decreased the genus of pro-inflammatory bacteria, and in-creased beneficial bacteria, while increasing SCFA levels to alleviate DSS-induced ulcerative colitis.Conclusions: Cur–Trp has shown great potential in alleviating colitis and promoting intestinal barrier function, suggesting that the combination of Cur and Trp has the potential to be developed as a therapeutic functional food or dietary supplement for UC. However, more studies are needed to validate this finding. Future research should focus on elucidating the precise molecular mechanisms, optimizing dosage and clinical trials in chronic models and humans to provide more targeted treatment options.
研究领域:
药理学
·
胃肠病学
·
营养科学
·
微生物组研究
✓ 已验证
产品关联
DOI
PubMed
高影响因子
INFLAMMOPHARMACOLOGY
·
2025
·
IF 5.3
Xu Wenxiu,Wang Hongbo,Sun Zhenyu,Zhang Hui,Zhang Zhijun,Sun Xiangrong,Gu Jiayu,Gong Yanling
Limonene, a monoterpene naturally abundant in various Citrus fruits, is widely used as a fragrance component and dietary supplement. Ulcerative colitis (UC), a representative inflammatory bowel disease, is characterized by an arising incidence and considerable impact on human health. Although several reports have demonstrated the beneficial effects of limonene on UC, detailed mechanisms remain incompletely understood. In this study, we employed a dextran sulfate sodium (DSS)-induced UC murine model and a lipopolysaccharide (LPS)-stimulated Caco-2 cell model to explore the mechanisms of limonene on UC. The results revealed that limonene significantly decreased disease activity index (DAI) score and alleviated pathological damage in UC mice, exhibiting therapeutic potential for UC. Limonene significantly inhibited interleukin-6 (IL-6), interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α) and malondialdehyde (MDA) while increased superoxide dismutase (SOD) in both DSS-induced UC mice and LPS-induced Caco-2 cells. Furthermore, limonene significantly increased expressions of Zonula occludens-1 (ZO-1), occludin, and claudin-1, thereby enhancing intestinal barrier integrity. Limonene mitigated UC-associated dysbiosis by shifting the gut microbial composition toward that of healthy controls. Specifically, it modulated the microbiota at the phylum, family, genus and species levels, increasing the abundance of anti-inflammatory bacteria while decreasing inflammatory related taxa. Collectively, our in vivo and in vitro results demonstrate that limonene alleviates UC involving in anti-inflammation, anti-oxidation, restoration of intestinal barrier integrity and regulation of the gut microbiota. Future studies are warranted to explore whether gut microbial metabolites contribute to the protective effects of limonene in UC. Graphical abstract
研究领域:
消化病学
·
免疫学
·
分子生物学
·
药理学
·
微生物组学
·
氧化应激
·
肠道屏障功能
·
天然产物药理
✓ 已验证
产品关联
DOI
PubMed
高影响因子
CARBOHYDRATE POLYMERS
·
2025
·
IF 12.5
Jin-Yang Shi,Yong-Jian Wang,Qian-Wen Bao,Ya-Min Qin,Pei-Pei Li,Qiao-Qiao Wu,Cheng-Kai Xia,De-Ling Wu,Song-Zi Xie
Polygonatum cyrtonema polysaccharides (PCP) exhibit ameliorative effects on colitis. However, whether the protective effects of PCP depend on the gut microbiota and how PCP regulates intestinal immune responses to alleviate colitis remain unclear. Therefore, this study investigated the effect of PCP against colitis focusing on the regulation of intestinal immune response. The PCP structure was reclassified as fructan. PCP treatment significantly reduced the symptoms of colitis. PCP restored IgA, ZO-1, Occludin, and MUC2 expression to enhance intestinal barrier function. Oral PCP administration markedly inhibited excessive inflammation-mediated immune response by modulating inflammatory cytokines secretion and Th17/Tregs cell balance and restored gut microbial composition. Interestingly, PCP still had a significant ameliorating effect on intestinal inflammation in colitis mice with gut microbial depletion by antibiotics. In the Caco-2/RAW264.7 co-culture inflammation model, PCP treatment improved the intestinal epithelial barrier function by regulating the inflammatory immune response through signal transduction pathways. Overall, these findings suggested that the alleviating effects of PCP on colitis are independent of gut microbiota, and that PCP can directly modulate the inflammatory immune response and intestinal barrier function, which in turn regulates gut microbiota. These findings will provide new insights into the action mechanism of natural polysaccharides in relieving colitis.
研究领域:
免疫学
·
胃肠病学
·
药理学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Nutrients
·
2024
·Vol. 16
·期 13
·2052
·
IF 4.8
Haidong Wang,Ji Qiu,Minyao Zhou,Yanqiu Luo,Xinyu Li,Minqi Wang
In this study, we investigated the effect of monobutyrin (MB) on the gut microbiota and intestinal health of weaned mice. MB was administered via gavage to 21-day-old weaned mice. Samples of small intestinal and ileal contents were collected on day 1, day 7, and day 21 post-administration. Seven days of MB administration enhanced the mucin layer and morphological structure of the intestine and the integrity of the intestinal brush border. Both MB and sodium butyrate (SB) accelerated tight junction development. Compared to SB, MB modulated intestinal T cells in a distinct manner. MB increased the ratio of Treg cells in the small intestine upon the cessation of weaning. After 21 days of MB administration, enhancement of the villus structure of the ileum was observed. MB increased the proportion of Th17 cells in the ileum. MB facilitated the transition of the small intestinal microbiota toward an adult microbial community structure and enhanced the complexity of the microbial community structure. An increase in Th17 cells enhanced intestinal barrier function. The regulatory effect of MB on Th17 cells may occur through the intestinal microbiota. Therefore, MB can potentially be used to promote intestinal barrier function, especially for weaning animals, with promising application prospects.
研究领域:
微生物学
·
免疫学
·
营养学
·
动物科学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
ONCOGENE
·
2022
·Vol. 42
·期 7
·530-540
·
IF 8.756
Shi Feiyu,Liu Gaixia,Lin Yufeng,Guo Cosmos liutao,Han Jing,Chu Eagle S. H.,Shi Chengxin,Li Yaguang,Zhang Haowei,Hu Chenhao,Liu Ruihan,He Shuixiang,Guo Gang,Chen Yinnan,Zhang Xiang,Coker Olabisi Oluwabukola,Wong Sunny Hei,Yu Jun,She Junjun
Appendectomy impacts the homeostasis of gut microbiome in patients. We aimed to study the role of appendectomy in colorectal cancer (CRC) risk through causing gut microbial dysbiosis. Population-based longitudinal study (cohort 1, n = 129,155) showed a 73.0% increase in CRC risk among appendectomy cases throughout 20 years follow-up (Adjusted sub-distribution hazard ratio (SHR) 1.73, 95% CI 1.49–2.01, P < 0.001). Shotgun metagenomic sequencing was performed on fecal samples from cohort 2 ( n = 314). Gut microbial dysbiosis in appendectomy subjects was observed with significant enrichment of 7 CRC-promoting bacteria ( Bacteroides vulgatus, Bacteroides fragilis, Veillonella dispar, Prevotella ruminicola, Prevotella fucsa, Prevotella dentalis, Prevotella denticola ) and depletion of 5 beneficial commensals ( Blautia sp YL58, Enterococcus hirae, Lachnospiraceae bacterium Choco86, Collinsella aerofaciens, Blautia sp SC05B48 ). Microbial network analysis showed increased correlation strengths among enriched bacteria and their enriched oncogenic pathways in appendectomy subjects compared to controls. Of which, B. fragilis was the centrality in the network of the enriched bacteria. We further confirmed that appendectomy promoted colorectal tumorigenesis in mice by causing gut microbial dysbiosis and impaired intestinal barrier function. Collectively, this study revealed appendectomy-induced microbial dysbiosis characterized by enriched CRC-promoting bacteria and depleted beneficial commensals, signifying that the gut microbiome may play a crucial role in CRC development induced by appendectomy.
研究领域:
肿瘤学
·
微生物学
·
胃肠病学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Microorganisms
·
2020
·Vol. 8
·期 2
·211
·
IF 4.152
Yehao Liu,Yuhui Li,Yuhong Xia,Kaiyong Liu,Lingling Ren,Yanli Ji
Cadmium (Cd), widely present in food and drinking water at low doses, can cause health risks. However, the mechanistic effects of long-term Cd exposure at low dose through dietary intake is poorly studied. The aim of this study is to elucidate whether the dysbiosis of gut microbiota caused by Cd at an environmental low dose can aggravate the injury of mice liver, and the possible mechanism is investigated. In order to explore the potential underlying mechanism, the analyses of the variation of gut microbiota composition, intestinal permeability, and hepatic transcriptome were conducted. Our results showed that gut microbiota was disturbed. The rise of intestinal permeability induced by the dysbiosis of gut microbiota resulted in more Cd ions accumulating in mice liver, but it could be restored partly through depleting gut microbiota by antibiotics cocktail. Transcriptomic analyses indicated that 162 genes were significantly differentially expressed including 59 up-regulated and 103 down-regulated in Cd treatment. These genes were involved in several important pathways. Our findings provide a better understanding about the health risks of cadmium in the environment.Keywords:transcriptome analyses;gut microbiota;cadmium;intestinal permeability
研究领域:
环境健康
·
微生物学
·
分子生物学
·
毒理学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Gut Microbes
·
2025
·
IF 11
Xinwei Li,Xia Xiao,Shengnan Wang,Biyu Wu,Yixuan Zhou,Pan Deng
Polyamines are important gut microbial metabolites known to affect host physiology, yet the mechanisms behind their microbial production remain incompletely understood. In this study, we developed a stable isotope-resolved metabolomic (SIRM) approach to track polyamine biosynthesis in the gut microbiome. Viable microbial cells were extracted from fresh human and mouse feces and incubated anaerobically with [U-13C]-labeled inulin (tracer). Liquid chromatography-high resolution mass spectrometry analysis revealed distinct 13C enrichment profiles for spermidine (SPD) and putrescine (PUT), indicating that the arginine-agmatine-SPD pathway contributes to SPD biosynthesis in addition to the well-known spermidine synthase pathway (PUT aminopropylation). Species differences were observed in the 13C enrichments of polyamines and related metabolites between the human and mouse microbiome. By analyzing the fecal metabolomics and metatranscriptomic data from an inflammatory bowel disease (IBD) cohort, we found significantly higher polyamine levels in IBD patients compared to healthy controls. Further investigations using single-strain SIRM and in silico analyses identified Bacteroides spp. as key contributors to polyamine biosynthesis, harboring essential genes for this process and potentially driving the upregulation of polyamines in IBD. Taken together, this study expands our understanding of polyamine biosynthesis in the gut microbiome and will facilitate the development of precision therapies to target polyamine-associated diseases.
研究领域:
微生物学
·
代谢组学
·
医学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Journal of Functional Foods
·
2025
·
IF 4
Zhaoxi Deng,Yanfei Ma,Kangwei Hou,Jinyan Dai,Yifan Zhong,Yingying Mao,Jinzhi Zhang,Haifeng Wang
Quorum sensing (QS) is an essential pathway for bacterial communication through autoinducers (AIs). The luxS gene involved in QS has been proven to regulate different behavior of Lactobacillus rhamnosus GG (LGG), whereas it is unclear whether the AI-2/LuxS system have beneficial effects the host by regulating LGG. Our aim was to investigate whether luxS mutation affects the ability of LGG to maintain intestinal microbiota homeostasis, intestinal barrier integrity and inflammatory immune responses in mice infected with Escherichia coli ( E. coli ). This study showed that both wild-type (WT) and luxS mutant (ΔluxS) of LGG can alleviate changes in the microbiota caused by E. coli by down-regulating the relative abundance of Parasturtella . Supplementation with WT and ΔluxS increased the CD4 + /CD8 + ratio in spleen, improved goblet cell numbers and enhanced Muc 2 secretion. Moreover, WT and ΔluxS decreases proinflammatory mediator levels by inhibiting MAPK and NF-κB signal transduction.
研究领域:
微生物学
·
免疫学
·
分子生物学
✓ 已验证
产品关联
DOI
高影响因子
危险品化学品经营许可证（带存储）