Huanlong Qin’s research while affiliated with Tongji University and other places

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Publications (247)


Fecal microbiota transplantation: transitioning from chaos and controversial realm to scientific precision era
  • Literature Review

January 2025

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14 Reads

Science Bulletin

Xinjun Wang

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Huanlong Qin

Figure 1. Schematic illustration of NanoFMT.
Figure 2. Preparation of single-cell nanocapsules of the gut microbiota. EcN, PA, SC, and microbiota were coated by co-incubation with 0.1% (w/v) silk fibroin while shaking at 35 rpm for 10 min before being resuspended in 0.1 M K + phosphate buffer with vigorous vortexing for 10 min. Silk fibroin coated cells were centrifuged, washed, resuspended in 5 mg/mL phosphatidylcholine, and incubated with vigorous shaking for 10 min. The final coated cells were named NanoEcN, NanoPA, NanoSC, and NanoMicrobiota. (A-C) Size distribution of microbes and their nanoderivatives. (D-E) Zeta potentials of microbes and their nanoderivatives. (G) Representative TEM images of microbes and their nanoderivatives. Scale bar: 500 nm (EcN, NanoEcN, PA, and NanoPA) or 2 μm (SC and NanoSC). (H) Typical confocal images of microbes and their nanoderivatives. The green and red channels indicate silk fibroin labeled with FITC and phosphatidylcholine labeled with rhodamine B, respectively. Scale bar: 10 μm or 25 μm (NanoSC). (I) Flow cytometric analysis of microbes and their nanoderivatives.
Figure 3. Impact of nanocapsules on resistance to environmental assaults, intestinal adhesion, and anti-inflammation. (A-D) Growth curves of nanocapsule-coated EcN, PA, SC, and microbiota at 37 ℃ and 200 rpm. (E-H) The survived number of nanocapsule-coated EcN, PA, SC, and microbiota after exposure to SGF (pH 2.5) supplemented with pepsin
Figure 4. Nanocapsule-mediated intestinal colonization in SPF mice and gut microbiota distribution in germ-free mice. (A) Experimental design for evaluating in vivo resistance of NanoEcN against insults within the GI tract in SPF Balb/c mice. Mice were randomly divided into 2 groups (n = 6) and fed 2 × 10 7 CFU/mouse EcN or NanoEcN via oral gavage. (B) Typical images captured using IVIS after 4 h post-administration. (C) Quantification of fluorescence intensities in mice. Error bars represent standard error of mean. (D) Representative fluorescent images of the GI tract. (E) Quantification of fluorescence intensities of the GI tract. (F-H) Bacterial count of EcN in small intestine (F), cecum (G) and
Figure 5. Therapeutic effect of NanoFMT in an STm-induced colitis mouse model. (A) Experimental design for the treatment of STm-induced colitis in mice. Mice were treated with 100 μl of streptomycin solution (200 mg/mL) prior to infection by oral inoculation with 1 × 10 9 CFU of Salmonella. Mice were randomly divided into 3 groups (n = 5) and treated with PBS, FMT (2 × 10 7 CFU/mouse/day), and NanoFMT (2 × 10 7 CFU/mouse/day) on days 2 and 4 post-infection. All mice were sacrificed for sampling on day 6

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Single-cell nanocapsules of gut microbiota facilitate fecal microbiota transplantation
  • Article
  • Full-text available

January 2025

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6 Reads

Theranostics

Rationale: Fecal microbiota transplantation (FMT) is advantageous for treating intractable diseases via the microbiota-gut-organ axis. However, invasive administration of gut microbiota via nasal feeding tubes limits the widespread application of FMT. Here, we attempted to develop a novel strategy to deliver gut microbiota using nanocapsules. Methods: Single-cell nanocapsules were fabricated within 1 h by layer-by-layer assembly of silk fibroin and phosphatidylcholine to generate a protective nanoshell on the cell surface of complicated microbiota. The physical properties of the microbiota nanocapsules were analyzed. The protective effects of nanocapsules on the gastrointestinal tract were analyzed both in vitro and in vivo. The efficacy of FMT assisted by single-cell nanocapsules (NanoFMT) was evaluated using the inflammatory response, gut microbiota balance, and histopathological analysis in animal model. Results: The nanocapsules achieved a good coating ratio for a single type of microbe and complex microbiota, resulting in a remarkable increase in the survival rate of microbes in the gastrointestinal tract. NanoFMT improved the diversity and abundance of the gut microbiota better than common FMT in germ-free mice. Moreover, NanoFMT alleviated intestinal inflammation and positively reversed the microbiota balance in a mouse model of colitis compared with common FMT, assisted by the inherent anti-inflammatory effects of silk fibroin and phosphatidylcholine. Conclusions: Considering its rapid preparation, convenient delivery, and perfect therapeutic effect, we anticipate that NanoFMT may be a promising clinical candidate for next-generation FMT treatment.

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The E3 ligase NEDD4L prevents colorectal cancer liver metastasis via degradation of PRMT5 to inhibit the AKT/mTOR signaling pathway

October 2024

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14 Reads

Colorectal cancer is the second most common cause of cancer mortality worldwide, and liver metastasis is the major cause of death in patients with colorectal cancer. Dysfunctional E3 ligase activity has recently been shown to be associated with colorectal cancer. However, the key E3 ligase affecting colorectal cancer liver metastasis remains unknown. Therefore, we used an shRNA library targeting 156 E3 ubiquitin ligases to perform an in vivo loss-of-function screen of a human colorectal cancer cell line in a mouse model of colorectal cancer liver metastasis. The screen revealed that NEDD4L knockdown promoted colorectal cancer liver metastasis. Moreover, overexpression of NEDD4L prevented colorectal cancer liver metastasis. Mechanistic studies revealed that NEDD4L bound to the PPNAY motif in PRMT5 and ubiquitinated PRMT5 to promote its degradation. PRMT5 degradation attenuated the methylation of an arginine residue in AKT1 to inhibit the AKT/mTOR signaling pathway, consequently decreasing colorectal cancer cell proliferation. We are the first to show that PRMT5 is a substrate protein of the E3 ligase NEDD4L and reveals not only the metastasis-inhibiting function of NEDD4L but also a novel mechanism by which NEDD4L suppresses colorectal cancer liver metastasis. These findings may provide a new preventive strategy for liver metastasis.


Author Correction: Profiling Fusobacterium infection at high taxonomic resolution reveals lineage-specific correlations in colorectal cancer

October 2024

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26 Reads






Gastrointestinal Dysmotility Predisposes to Colitis through Regulation of Gut Microbial Composition and Linoleic Acid Metabolism

March 2024

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108 Reads

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4 Citations

Disrupted gastrointestinal (GI) motility is highly prevalent in patients with inflammatory bowel disease (IBD), but its potential causative role remains unknown. Herein, the role and the mechanism of impaired GI motility in colitis pathogenesis are investigated. Increased colonic mucosal inflammation is found in patients with chronic constipation (CC). Mice with GI dysmotility induced by genetic mutation or chemical insult exhibit increased susceptibility to colitis, dependent on the gut microbiota. GI dysmotility markedly decreases the abundance of Lactobacillus animlalis and increases the abundance of Akkermansia muciniphila. The reduction in L. animlalis, leads to the accumulation of linoleic acid due to compromised conversion to conjugated linoleic acid. The accumulation of linoleic acid inhibits Treg cell differentiation and increases colitis susceptibility via inducing macrophage infiltration and proinflammatory cytokine expression in macrophage. Lactobacillus and A. muciniphila abnormalities are also observed in CC and IBD patients, and mice receiving fecal microbiota from CC patients displayed an increased susceptibility to colitis. These findings suggest that GI dysmotility predisposes host to colitis development by modulating the composition of microbiota and facilitating linoleic acid accumulation. Targeted modulation of microbiota and linoleic acid metabolism may be promising to protect patients with motility disorder from intestinal inflammation.


Citations (77)


... In addition to affecting chemotherapy response, F. nucleatum also plays a role in modulating the response to immunotherapy [2]. F. nucleatum promotes an immunosuppressive milieu by interacting with both tumor cells and immune cells, hindering the effectiveness of immunotherapies such as checkpoint inhibitors (e.g., PD-1/PD-L1 inhibitors), CAR T-cell therapies, and other immune modulators [96][97][98][99][100]. As mentioned earlier, F. nucleatum's role in immune modulation is multifaceted. ...

Reference:

Unraveling the Role of Fusobacterium nucleatum in Colorectal Cancer: Molecular Mechanisms and Pathogenic Insights
Fusobacterium nucleatum facilitates anti-PD-1 therapy in microsatellite stable colorectal cancer

Cancer Cell

... This study showed that succinate supplementation upregulated the levels of 13(S)-HPODE and 5(S)-HETE in fatty acyls. 13(S)-HPODE is involved in linoleic acid metabolism and leads to a reduction in intestinal inflammation and changes in the body weight of mice (Zhang, et al., 2024). Moreover, 13(S)-HPODE is a natural activator of the cancer therapeutic target PPARg, which can effectively promote apoptosis of cancer cells in the body (Biswas, et al., 2023). ...

Gastrointestinal Dysmotility Predisposes to Colitis through Regulation of Gut Microbial Composition and Linoleic Acid Metabolism

... Given the serious threat cancer poses to human health, exploring effective cancer treatment technologies has gained significant interest. Among the many advances made in the past decade, photodynamic therapy (PDT) has emerged as a promising treatment approach due to its ability to generate cytotoxic reactive oxygen species (ROS) by photosensitizers (PSs) under light irradiation [1][2][3][4][5][6]. PDT offers advantages such as minimal invasiveness, high spatiotemporal controllability, and reduced drug resistance, making it a highly effective strategy for cancer treatment with significant clinical potential [7][8][9][10][11]. ...

NIR-II imaging-guided precise photodynamic therapy for augmenting tumor-starvation therapy by glucose metabolism reprogramming interference
  • Citing Article
  • February 2024

Science Bulletin

... Some known bacteria species with pro-tumoral properties are Fusobacterium nucleatum, Helicobacter pylori, Escherichia coli (certain strains), Salmonella Typhimurium (certain strains), and Enterococcus faecalis. [32][33][34] Fusobacterium nucleatum demonstrates a close association with colorectal cancer (CRC), and it promotes cancer by several mechanisms. The bacterial protein Fap2 interacts with the immune checkpoint receptor TIGIT on NK cells and T cells, inhibiting their antitumor activity. ...

Fusobacterium nucleatum promotes tumor progression in KRAS p.G12D-mutant colorectal cancer by binding to DHX15

... Nutritional support is a critical aspect of perioperative care for patients undergoing major surgeries, such as those for cancer. The early achievement of energy targets after major abdominal surgery has proven to be crucial for patients' quicker postoperative recovery, for example by lowering the risk of infectious complications [29]. Boelens et al. (2014) demonstrated that early postoperative enteral nutrition significantly reduces the duration of postoperative ileus, anastomotic leakage, and hospital stay length [ Figure 3]. ...

Early Enteral Nutrition versus Early Supplemental Parenteral Nutrition in Patients Undergoing Major Abdominal Surgery: A Secondary Analysis of Two Randomized Clinical Trials
  • Citing Article
  • February 2024

American Journal of Clinical Nutrition

... In this context, the gut microbiota has emerged as an invaluable source of inspiration for the development of biomimetic solutions in relevant fields such as medicine or biotechnology, among others. Biological principles derived from the gut microbiota, such as resilience, self-regulation, and microbial communication, offer innovative perspectives for the creation of advanced technologies that mimic these natural mechanisms [86][87][88]. ...

Enzyme-like biomimetic oral-agent enabling modulating gut microbiota and restoring redox homeostasis to treat inflammatory bowel disease

Bioactive Materials

... Future research should focus on enhancing outcomes for patients with ACM by modulating GM through interventions such as probiotics or dietary modifications. This strategy represents a novel therapeutic approach with significant potential for clinical applications (186,187). ...

Fecal microbiota transplantation in clinical practice: Present controversies and future prospects
  • Citing Article
  • February 2024

hLife

... G6PDH supports GPX4's antioxidant function by generating NADPH, thereby protecting cells from oxidative stress and ferroptosis. Ferroptosis plays a significant role in various diseases, including cancer, neurodegenerative diseases, and ischemia-reperfusion injury [60][61][62]. Numerous studies have proposed new therapeutic strategies targeting the mechanisms of ferroptosis, such as inhibiting transferrin receptors or promoting the expression and function of ferritin to reduce intracellular iron levels, thereby decreasing ferroptosis [63]. Using lipid peroxidase inhibitors or antioxidants can reduce the generation of lipid peroxides and protect the integrity of cell membranes [64]. ...

7-Dehydrocholesterol dictates ferroptosis sensitivity

Nature

... This interaction may explain the higher metabolic rate observed in Kv1.3 KO mice(73). Interestingly, the Kv1.3 channel C-terminus also interacts with LAMTOR1, an activator of the mTOR pathway(74). In physiological conditions, it would be interesting to explore how these interactions are balanced within the cell to ensure proper cellular function. ...

TRAF4‐Mediated LAMTOR1 Ubiquitination Promotes mTORC1 Activation and Inhibits the Inflammation‐Induced Colorectal Cancer Progression

... The resulting hypoxia can induce CAF-like features in normal fibroblasts [96], and the resulting upregulation of HIF-1α in cancer cells contributes to cancer cell survival following radiotherapy [97,98]. As radiation-induced ECM changes by CAFs also impair the permeation of possible neoadjuvant chemoand/or immunotherapies, CAFs could not only contribute to radioresistance, but also to resistance against possible adjuvant therapy [99,100]. ...

Targeting integrin α5 in fibroblasts potentiates colorectal cancer response to PD-L1 blockade by affecting extracellular-matrix deposition