Formation of self-assembled fibril aggregates of trypsin-controllably hydrolyzed soy protein and its regulation on stability of high internal phase Pickering emulsions.

The mechanisms of trypsin hydrolysis time on the structure of soy protein hydrolysate fibril aggregates (SPHFAs) and the stability of SPHFAs-high internal phase Pickering emulsions (HIPPEs) were investigated. SPHFAs were prepared using soy protein hydrolysate (SPH) with different trypsin hydrolysis time (0 min-120 min) to stabilize SPHFAs-HIPPEs. The results showed that moderate trypsin hydrolysis (30 min, hydrolysis degree of 2.31 %) induced SPH unfolding and increased the surface hydrophobicity of SPH, thereby promoting the formation of flexible SPHFAs with maximal thioflavin T intensity and ζ-potential. Moreover, moderate trypsin hydrolysis improved the viscoelasticity of SPHFAs-HIPPEs, and SPHFAs-HIPPEs remained stable after storage at 25 °C for 80 d and heating at 100 °C for 1 h. Excessive trypsin hydrolysis (> 30 min) decreased the stability of SPHFAs-HIPPEs. In conclusion, moderate trypsin hydrolysis promoted the formation of flexible SPHFAs with high surface charge by inducing SPH unfolding, thereby promoting the stability of SPHFAs-HIPPEs.

KDELR2 is necessary for chronic obstructive pulmonary disease airway Mucin5AC hypersecretion via an IRE1α/XBP-1s-dependent mechanism.

Airway mucus hypersecretion, a crucial pathological feature of chronic obstructive pulmonary disease (COPD), contributes to the initiation, progression, and exacerbation of this disease. As a macromolecular mucin, the secretory behaviour of Mucin5AC (MUC5AC) is highly dependent on a series of modifying and folding processes that occur in the endoplasmic reticulum (ER). In this study, we focused on the ER quality control protein KDEL receptor (KDELR) and demonstrated that KDELR2 and MUC5AC were colocalized in the airway epithelium of COPD patients and COPD model rats. In addition, knockdown of KDELR2 markedly reduced the expression of MUC5AC both in vivo and in vitro and knockdown of ATF6 further decreased the levels of KDELR2. Furthermore, pretreatment with 4µ8C, an IRE1α inhibitor, led to a partial reduction in the expression of KDELR2 and MUC5AC both in vivo and in vitro, which indicated the involvement of IRE1α/XBP-1s in the upstream signalling cascade. Our study revealed that KDELR2 plays a crucial role in airway MUC5AC hypersecretion in COPD, which might be dependent on ATF6 and IRE1α/XBP-1s upstream signalling.

A genome-wide association study of neonatal metabolites.

Genetic factors significantly influence the concentration of metabolites in adults. Nevertheless, the genetic influence on neonatal metabolites remains uncertain. To bridge this gap, we employed genotype imputation techniques on large-scale low-pass genome data obtained from non-invasive prenatal testing. Subsequently, we conducted association studies on a total of 75 metabolic components in neonates. The study identified 19 previously reported associations and 11 novel associations between single-nucleotide polymorphisms and metabolic components. These associations were initially found in the discovery cohort (8,744 participants) and subsequently confirmed in a replication cohort (19,041 participants). The average heritability of metabolic components was estimated to be 76.2%, with a range of 69%-78.8%. These findings offer valuable insights into the genetic architecture of neonatal metabolism.

Effect of ultrasonic pretreatment on the emulsion rheological properties and interface protein structure of epigallocatechin-3-gallate and rice bran protein complex.

The effect of ultrasonic pretreatment on the emulsion rheological properties and the structural characteristics of interface-adsorbed protein (IAP) and interface-unabsorbed protein (IUP) of rice bran protein and epigallocatechin-3-gallate complex (RBP-EGCG) were studied. Compared to RBP-EGCG without ultrasonic pretreatment, appropriate ultrasonic pretreatment (ultrasonic power was 425 W) enhanced the IAP trypsin sensitivity (from 3.20 to 3.73), increased the IUP surface hydrophobicity (from 12.59 to 20.87), and decreased the ζ-potential (from -24.93 mV to -36.88 mV) and particle size (from 567.30 nm to 273.13 nm) of IUP, thereby increasing the viscosity and viscoelasticity of emulsion. Compared to appropriate ultrasonic pretreatment, high-power ultrasonic pretreatment (ultrasonic power was 500 W) attenuated the IAP trypsin sensitivity, and increased the ζ-potential and particle size of IUP, thereby decreasing the viscosity and viscoelasticity of emulsion. Overall, ultrasonic pretreatment changed the EGCG-RBP emulsion viscoelasticity by regulating spatial structural characteristics and flexibility of interface protein.

Cloning and Functional Study of AmGDSL1 in Agropyron mongolicum.

Agropyron mongolicum Keng is a diploid perennial grass of triticeae in gramineae. It has strong drought resistance and developed roots that can effectively fix the soil and prevent soil erosion. GDSL lipase or esterases/lipase has a variety of functions, mainly focusing on plant abiotic stress response. In this study, a GDSL gene from A. mongolicum, designated as AmGDSL1, was successfully cloned and isolated. The subcellular localization of the AmGDSL1 gene (pCAMBIA1302-AmGDSL1-EGFP) results showed that the AmGDSL1 protein of A. mongolicum was only localized in the cytoplasm. When transferred into tobacco (Nicotiana benthamiana), the heterologous expression of AmGDSL1 led to enhanced drought tolerance. Under drought stress, AmGDSL1 overexpressing plants showed fewer wilting leaves, longer roots, and larger root surface area. These overexpression lines possessed higher superoxide dismutase (SOD), peroxidase (POD), catalase (CAT), and proline (PRO) activities. At the same time, the malondialdehyde (MDA) content was lower than that in wild-type (WT) tobacco. These findings shed light on the molecular mechanisms involved in the GDSL gene's role in drought resistance, contributing to the discovery and utilization of drought-resistant genes in A. mongolicum for enhancing crop drought resistance.

Natural protein-polysaccharide-phenol complex particles from rice bran as novel food-grade Pickering emulsion stabilizers.

To develop novel food-grade Pickering emulsion stabilizers, insoluble rice bran protein-polysaccharide-phenol natural complex (IRBPPP) was prepared into Pickering emulsion stabilizers after different mechanical pretreatments (shear, high-pressure homogenization, ultrasonic, and combined mechanical pretreatment). With the increase in mechanical pretreatment types, the covalent binding of proteins and polysaccharides in IRBPPP gradually enhanced, the breakage efficiency of IRBPPP gradually increased (IRBPPP particle size decreased from 220.54 to 67.89 µm, the specific surface area of IRBPPP particle increased from 993.47 to 2033.86 cm-1/g), and the microstructure of IRBPPP gradually showed an orderly network structure, which enhanced the IRBPPP dispersion stability and the Pickering emulsion stability. Pickering emulsion stability was highly correlated (P < 0.01) with the breakage efficiency of IRBPPP particles. Overall, the combined mechanical pretreatment improved the stability of the IRBPPP-stabilized Pickering emulsion. The study added value to rice bran products and offered a new way to create stable food-grade Pickering emulsions for functional foods using natural protein-polysaccharide-phenol complex particles.

Protein oxidation affected the encapsulation properties of rice bran protein fibril-high internal phase pickering emulsions: Enhanced stability and bioaccessibility of ß-carotene.

Rice bran protein fibril (RBPF)-high internal phase Pickering emulsions (HIPPEs) loaded with ß-carotene (CE) were constructed to enhance stability and bioavailability of CE. Rice bran (RB) protein with varying oxidation degrees was extracted from RB with varying storage period (0-10 days) to prepare RBPF by acid-heating (90 °C, 2-12 h) to stabilize HIPPEs. The influence of protein oxidation on the encapsulation properties of RBPF-HIPPEs was studied. The results showed that CE-HIPPEs could be stably stored for 56 days at 25 °C. When RB storage time was the same, the average particle size, lipid hydroperoxide content, and malondialdehyde content of CE-HIPPEs and the CE degradation rate initially fell, and then grew as the acid-heating time prolonged, while the ζ-potential value, viscosity, viscoelasticity, free fatty acid (FFA) release rate, and bioaccessibility first rose, and subsequently fell. When acid-heating time of RBPF was the same, the average particle size, lipid hydroperoxide content, and malondialdehyde content of CE-HIPPEs initially fell, and subsequently increased with RB storage time extended, while the ζ-potential value, viscosity, viscoelasticity, FFA release rate, and bioaccessibility initially increased, and then decreased. Overall, Moderate oxidation and moderate acid-heating enhanced the stability as well as rheological properties of CE-HIPPEs, thus improving the stability and bioaccessibility of CE. This study offered a new insight into the delivery of bioactive substances by protein fibril aggregates-based HIPPEs.

The synergistic effects of rice bran rancidity and dephenolization on digestive properties of rice bran protein.

Both rice bran (RB) rancidity and dephenolization could affect the structural characteristics and phenolics composition of rice bran protein (RBP), thereby affecting RBP digestibility. The synergistic effects of RB rancidity and dephenolization on RBP digestibility were investigated. Excessive RB rancidity (RB stored for 10 d) and non-dephenolization reduced RBP digestibility, while moderate RB rancidity (RB stored for 1 d) combined with dephenolization improved RBP digestibility to a maximum of 74.19%. Dephenolization reduced the antioxidant capacities of RBP digestive products. The digestibility of non-dephenolized RBP (NDRBP) was significantly (P < 0.05) related with its carbonyl content, surface hydrophobicity, and ζ-potential. The digestibility of dephenolized RBP (DRBP) was significantly related with its ß-sheet structure content, surface hydrophobicity, ζ-potential, and average particle size. Overall, moderate RB rancidity combined with dephenolization enhanced RBP digestibility by reducing the non-competitive inhibition of endogenous phenolics on protease and regulating the spatial structural characteristics of RBP.

Cigarette Smoke Extract Induces MUC5AC Expression Through the ROS/ IP3R/Ca2+ Pathway in Calu-3 Cells.

Background: Chronic obstructive pulmonary disease (COPD) is caused by exposure to noxious external particles, air pollution, and the inhalation of cigarette smoke. Airway mucus hypersecretion particularly mucin5AC (MUC5AC), is a crucial pathological feature of COPD and is associated with its initiation and progression. In this study, we aimed to investigate the effects of cigarette smoke extract (CSE) on MUC5AC expression, particularly the mechanisms by which reactive oxygen species (ROS) induce MUC5AC expression. Methods: The effects of CSE on the expression of MUC5AC and mucin5B (MUC5B) were investigated in vitro in Calu-3 cells. MUC5AC and MUC5B expression levels were measured using quantitative reverse transcription-polymerase chain reaction (qRT-PCR), immunofluorescence staining, and enzyme-linked immunosorbent assay (ELISA). Total cellular levels of ROS and Ca2+ were determined using DCFH-DA and Fluo-4 AM. Subsequently, the expression levels of IP3R, IRE1α, p-IRE1α and XBP1s were measured by Western blotting. Gene silencing was achieved by using small-interfering RNAs. Results: Our findings revealed that exposure to CSE increased MUC5AC levels and upregulated ROS, IP3R/Ca2+ and unfolded protein response (UPR)-associated factors. In addition, knockdown of IP3R using siRNA decreased CSE-induced Ca2+ production, UPR-associated factors, and MUC5AC expression. Furthermore, 10 mM N-acetyl-l-cysteine (NAC) treatment suppressed the effects of CSE, including ROS generation, IP3R/ Ca2+, UPR activation, and MUC5AC overexpression. Conclusion: Our results suggest that ROS regulates CSE-induced UPR and MUC5AC overexpression through IP3R/ Ca2+ signaling. Additionally, we identified NAC as a promising therapeutic agent for mitigating CSE-induced MUC5AC overexpression.

Association Between Biofilm Formation and Structure and Antibiotic Resistance in H. pylori.

Background: Persistent infections caused by Helicobacter pylori (H. pylori), which are resistant to antibiotic treatment, pose a growing global public health concern. Biofilm formation is known to be associated with persistent infections due to its role in enhancing antimicrobial resistance and the tolerance of many pathogenic bacteria. Objective: This study aims to evaluate the biofilm formation of clinical isolates of H. pylori and its impact on antibiotic eradication. Methods: The thickness, morphology, and structure of biofilms derived from nine H. pylori strains were examined using confocal laser scanning microscopy, scanning electron microscopy, and transmission electron microscopy. Subsequently, the susceptibility of both planktonic and biofilm bacteria was assessed through the determination of minimum inhibitory concentration and minimum biofilm eradication concentration for amoxicillin, clarithromycin, levofloxacin, and tetracycline. Results: The results revealed varying biofilm thicknesses and densities among the strains, characterised by the presence of numerous filaments intertwining and connecting bacterial cells. Additionally, several cases exhibited susceptibility based on MIC measurements but resistance according to MBEC measurements, with MBEC indicating a higher resistance rate. Pearson Correlation analysis demonstrated a positive correlation between biofilm thickness and MBEC results (0 < r < 1), notably significant for amoxicillin (r = 0.801, P = 0.009) and tetracycline (r = 0.696, P = 0.037). Conclusion: Different strains of H. pylori exhibit variations in their capacity to release outer membrane vesicles (OMVs) and form biofilms. Biofilm formation can influence the effectiveness of amoxicillin and tetracycline in eradicating susceptible bacterial strains.

CCR2+TREM-1+ monocytes promote natural killer T cell dysfunction contributing towards HBV disease progression.

Natural killer T (NKT) cells are amongst the most important innate immune cells against hepatitis B virus (HBV) infection. Moreover, previous studies have shown that HBV infection induced TREM-1+ expression in monocyte and secretion of inflammatory cytokines. Thus, this prompted us to elucidate the role of TREM-1+ monocytes in regulating the function of iNKT cells. Ninety patients and 20 healthy participants were enrolled in the study. The percentage and phenotype of iNKT cells and TREM-1+ monocytes were measured in the peripheral blood of healthy controls (HC), patients with chronic HBV infection (CHB), HBV-related liver cirrhosis (LC), and HBV-related acute-on-chronic liver failure (ACLF) via flow cytometry. Moreover, co-culture experiments with iNKT cells and TREM-1 overexpressing THP-1 cells were performed to determine the role of TREM-1 in the regulation of NKT cell function. We observed that the percentage of iNKT cells and CD4-iNKT cells gradually decreased, whereas the percentage of CCR2+TREM-1+ monocytes increased with the progression of the disease. In addition, activation of the TREM-1 signaling pathway induced the secretion of inflammatory cytokines leading to pyroptosis of iNKT cells and secretion of IL-17 contributing towards disease progression. Therefore, this study suggests that blocking the activation of TREM-1 in monocytes could promote the elimination of HBV by inhibiting pyroptosis of iNKT cells and restoring their function. However, further studies are required to validate these results that would help in developing new treatment strategies for patients with HBV infections.

[Feasibility of non-invasive prenatal testing for the detection of fetal chromosomal copy number variants].

OBJECTIVE: To explore the feasibility of non-invasive prenatal testing (NIPT) for detecting fetal chromosomal copy number variants (CNV). METHODS: A retrospective analysis was carried out on NIPT positive samples in Suzhou Municipal Hospital from January 1, 2019 to December 31, 2021. The effect of NIPT on fetal CNV detection was assessed by comparison with the results of karyotype analysis and/or chromosomal microarray analysis (CMA). RESULTS: Among the 525 NIPT positive samples, 146 were CNV cases, of which 84 were further verified by karyotyping and/or CMA, 29 (34.5%) were true positive. Among them, 12 cases were pathogenic variants, 2 cases were likely pathogenic variants and 15 cases were variants of uncertain significance. CONCLUSION: NIPT could detect CNV with high accuracy, and to combine CNV detection and chromosomal aneuploidy detection has great significance to improve the prenatal and postnatal care.

Bestatin attenuates breast cancer stemness by targeting puromycin-sensitive aminopeptidase.

Breast cancer is a prevalent malignant tumor among women with an increasing incidence rate annually. Breast cancer stem cells (BCSCs) are integral in impeding tumor advancement and addressing drug resistance. Bestatin serves as an adjuvant chemotherapy, triggering apoptosis in cancer cells. In this study, the effects of bestatin on sorted BCSCs from breast cancer cell lines have been studied. Our results indicated that bestatin inhibits the migration and proliferation of breast cancer cells by reducing the stemness of BCSCs both in vitro and in vivo. Puromycin-sensitive aminopeptidase is implicated in the process through the regulation of cell cycle, resulting in heightened cell apoptosis and diminished cell proliferation of BCSCs. Our study suggest that targeting cancer stem cell may offer a promising approach in breast cancer treatment, presenting noval therapeutic strategies for patients with breast cancer.

Identification of signaling pathways that specify a subset of migrating enteric neural crest cells at the wavefront in mouse embryos.

During enteric nervous system (ENS) development, pioneering wavefront enteric neural crest cells (ENCCs) initiate gut colonization. However, the molecular mechanisms guiding their specification and niche interaction are not fully understood. We used single-cell RNA sequencing and spatial transcriptomics to map the spatiotemporal dynamics and molecular landscape of wavefront ENCCs in mouse embryos. Our analysis shows a progressive decline in wavefront ENCC potency during migration and identifies transcription factors governing their specification and differentiation. We further delineate key signaling pathways (ephrin-Eph, Wnt-Frizzled, and Sema3a-Nrp1) utilized by wavefront ENCCs to interact with their surrounding cells. Disruptions in these pathways are observed in human Hirschsprung's disease gut tissue, linking them to ENS malformations. Additionally, we observed region-specific and cell-type-specific transcriptional changes in surrounding gut tissues upon wavefront ENCC arrival, suggesting their role in shaping the gut microenvironment. This work offers a roadmap of ENS development, with implications for understanding ENS disorders.

FAM83B regulates mitochondrial metabolism and anti-apoptotic activity in pulmonary adenocarcinoma.

Chemotherapy is an effective therapeutic modality; nevertheless, a significant proportion of patients diagnosed with lung adenocarcinoma (LUAD) demonstrate resistance to chemotherapy. Therefore, it is crucial to understand the potential regulatory mechanisms to develop novel treatment strategies. This study aims to understand how increased FAM83B expression impacts mitochondrial activity, cell apoptosis, and chemotherapy effectiveness in LUAD. Multiple assays, such as CCK8, wound healing, EdU, and transwell assays, were employed to confirm the augmented chemotherapy resistance, heightened cell proliferation, migration, and invasion caused by FAM83B overexpression in LUAD cells. Furthermore, MIMP, MTG, and ATP assays were utilized to quantify changes in mitochondrial metabolism. In vitro functional assays were performed to evaluate the influence of FAM83B overexpression on the malignant progression and resistance mechanisms to chemotherapy in LUAD. In the context of this study, it was determined that LUAD patients with increased FAM83B expression had shorter survival times, and tissue samples with FAM83B overexpression were more prone to metastasis compared to primary samples. As a result, FAM83B is identified as an adverse prognostic marker. The mechanistic analysis demonstrated that FAM83B impedes the translocation of calbindin 2 (CALB2) from the cytoplasm to the mitochondria, resulting in the inhibition of apoptosis and the promotion of mitochondrial activity. Consequently, this ultimately confers resistance to chemotherapy in LUAD. Furthermore, the administration of metformin, which blocks mitochondrial oxidative phosphorylation (OXPHOS), can restore sensitivity to drug resistance in LUAD. Taken together, these findings provide substantial evidence supporting the notion that FAM83B enhances chemotherapy resistance in LUAD through the upregulation of mitochondrial metabolism and the inhibition of apoptosis.

Mesenchymal Stem Cells Attenuates Hirschsprung diseases - Associated Enterocolitis by Reducing M1 Macrophages Infiltration via COX-2 Dependent Mechanism.

OBJECTIVE AND DESIGN: Hirschsprung disease-associated enterocolitis (HAEC) is a common life-threatening complication of Hirschsprung disease (HSCR). We aimed to investigate the effectiveness, long-term safety and the underlying mechanisms of Mesenchymal stem cells (MSCs) based therapy for HAEC. MATERIAL OR SUBJECTS: Specimens from HSCR and HAEC patients were used to assess the inflammatory condition. Ednrb knock-out mice was used as HAEC model. MSCs was intraperitoneally transplanted into HAEC mice. The therapy effects, long-term outcome, safety and toxicity and the mechanism of MSCs on the treatment of HAEC were explored in vivo and in vitro. RESULTS: Intestinal M1 macrophages infiltration and severe inflammation condition were observed in HAEC. After the injection of MSCs, HAEC mice showed significant amelioration of the inflammatory injury and inhibition of M1 macrophages infiltration. The expression levels of pro-inflammatory cytokines (TNF-α and IFN-γ) were decreased and anti-inflammatory cytokines (IL-10 and TGF-ß) were increased. In addition, we found that effective MSCs homing to the inflamed colon tissue occurred without long-term toxicity response. However, COX-2 inhibitor could diminish the therapeutic effects of MSCs. Using MSCs and macrophages co-culture system, we identified that MSCs could alleviate HAEC by inhibiting M1 macrophages activation through COX-2-dependent MAPK/ERK signaling pathway. CONCLUSIONS: MSCs ameliorate HAEC by reducing M1 macrophages polarization via COX-2 mediated MAPK/ERK signaling pathway, thus providing novel insights and potentially promising strategy for the treatment or prevention of HAEC.

Effect of epigallocatechin-3-gallate modification on the structure and emulsion stability of rice bran protein in the presence of soybean protein isolate.

For improving the emulsion stability of rice bran protein (RBP), RBP was modified by different concentrations of epigallocatechin-3-gallate (EGCG) in the presence of soybean protein isolate (SPI), and RBP-EGCG-SPI conjugate was prepared by alkaline pH-shifting. The results showed that the addition of EGCG led to an increase in the bound phenol content and the flexibility of the secondary structure, a decrease in the free sulfhydryl and disulfide bond content of the RBP-EGCG-SPI conjugate. EGCG covalently bound to RBP and SPI through non-disulfide bonds. When the concentration of EGCG was 10 % (w/v), the emulsifying activity index and emulsion stability index of conjugate reached the maximum value (36.61 m2/g and 255.61 min, respectively), and the conjugate had the best emulsion stability. However, an EGCG concentration above 10 % (w/v) negatively affected the emulsion stability, with increasing particle size due to protein aggregation. Summarily, the modification of EGCG improved the emulsion stability of conjugate by regulating the spatial structure of RBP-EGCG-SPI conjugate. The work provided an important guide to further improve the emulsion stability of RBP.

Effects of rice bran rancidity on the interfacial adsorption properties of rice bran protein fibril aggregates and stability of high internal phase Pickering emulsions.

The effects of rice bran rancidity-induced protein oxidation and heating time on the stability of rice bran protein fibril aggregates (RBPFA)-high internal phase Pickering emulsions (HIPPEs) were investigated. The optimal conditions for RBPFA-HIPPEs were 8 mg/mL RBPFA with an oil phase volume fraction of 75 %. Moderate oxidation (rice bran stored for 3 d) and moderate heating (8 h) enhanced the wettability, flexibility, diffusion rate, and adsorption rate of RBPFA, meanwhile, the rheological properties of RBPFA-HIPPEs increased. RBPFA-HIPPEs could be stably stored for 50 d at 25 °C. Moderate oxidized and moderate heated RBPFA-stabilized HIPPEs could remain stable after heat treatment and could be re-prepared after freeze-thaw (3 cycles). Additionally, the stability of RBPFA-HIPPEs was significantly related to the structural characteristics and interfacial properties of RBPFA. Overall, moderate oxidation and moderate heating enhanced the storage, thermal, and freeze-thaw stability of RBPFA-HIPPEs by improving the interfacial properties of RBPFA.

Intracellular presence of Helicobacter pylori antigen and genes within gastric and vaginal Candida.

BACKGROUND: Helicobacter pylori infections are generally acquired during childhood and affect half of the global population, but its transmission route remains unclear. It is reported that H. pylori can be internalized into Candida, but more evidence is needed for the internalization of H. pylori in human gastrointestinal Candida and vaginal Candida. METHODS: Candida was isolated from vaginal discharge and gastric mucosa biopsies. We PCR-amplified and sequenced H. pylori-specific genes from Candida genomic DNA. Using optical and immunofluorescence microscopy, we identified and observed bacteria-like bodies (BLBs) in Candida isolates and subcultures. Intracellular H. pylori antigen were detected by immunofluorescence using Fluorescein isothiocyanate (FITC)-labeled anti-H. pylori IgG antibodies. Urease activity in H. pylori internalized by Candida was detected by inoculating with urea-based Sabouraud dextrose agar, which changed the agar color from yellow to pink, indicating urease activity. RESULTS: A total of 59 vaginal Candida and two gastric Candida strains were isolated from vaginal discharge and gastric mucosa. Twenty-three isolates were positive for H. pylori 16S rDNA, 12 were positive for cagA and 21 were positive for ureA. The BLBs could be observed in Candida cells, which were positive for H. pylori 16S rDNA, and were viable determined by the LIVE/DEAD BacLight Bacterial Viability kit. Fluorescein isothiocyanate (FITC)-conjugated antibodies could be reacted specifically with H. pylori antigen inside Candida cells by immunofluorescence. Finally, H. pylori-positive Candida remained positive for H. pylori 16S rDNA even after ten subcultures. Urease activity of H. pylori internalized by Candida was positive. CONCLUSION: In the form of BLBs, H. pylori can internalize into gastric Candida and even vaginal Candida, which might have great significance in its transmission and pathogenicity.