1.Mechanism of Helicobacter pylori metabolites antagonizing host innate immunity
Zhi CHEN ; Huanxiong LIN ; Huitian YANG
Chinese Journal of Immunology 2024;40(3):478-483
Objective:To investigate potential mechanism of Helicobacter pylori metabolites antagonizing host innate immunity.Methods:RNA sequencing and pathway enrichment analysis were used to analyze only LPS-stimulated gastric mucosal cells GES-1,GES-1 cells co-treated with LPS and Helicobacter pylori culture supernatant,and untreated GES-1 cells.The culture supernatant of He-licobacter pylori was filtered by a 3KD ultrafiltration tube,and the filtered filtrate(metabolite part)and the retained solution(protein part)were treated with LPS-stimulated GES-1 cells to detect activity of NF-κB pathway,phosphorylation level of NF-κB,secretion levels of NF-κB pathway effectors TNF-α,IL-6 and IL-8.Identification of key metabolites by untargeted metabolic mass spectrometry.Results:Compared with GES-1 cells stimulated only by LPS,after co-treated with LPS and Helicobacter pylori culture supernatant,expression levels of various genes were regulated and tended to the level of GES-1 in untreated gastric mucosal cells,mainly in the NF-κB pathway.After co-treatment with LPS and culture supernatant of Helicobacter pylori,activity of NF-κB pathway was inhibited(P<0.05).Helicobacter pylori metabolites could inhibit the activity of NF-κB pathway,inhibit phosphorylation of NF-κB,and inhibit the secretion of NF-κB pathway effectors TNF-α,IL-6 and IL-8(P<0.05).1,5 and 25 μmol/L of Helicobacter pylori metabolite 2-D-Glu-copyranose(2DG)treatment inhibited activity of NF-κB pathway and phosphorylation of NF-κB in GES-1 cells,and secretion of NF-κB pathway effectors TNF-α,IL-6 and IL-8 were inhibited(P<0.05).After 2DG treatment,activity of NF-κB in GES-1 cells with TLR3,TLR4,TLR5,TLR6,TLR7,TLR8,TLR9 and TLR10 knockout were significantly decreased(P<0.05);while there was no significant changes in activity of NF-κB in TLR1 and TLR2 knockout GES-1 cells.Both TLR1 and TLR2 interactions were attenuated in GES-1 cells after 2DG treatment.Molecular docking showed that 2DG could bind to TLR2 amino acid disabled R321,K347 and F349,the binding energy was-12 kcal/mol.TLR2 wild-type and mutant plasmids(R321K,K347R,F349A)were constructed,and TLR2-knockout GES-1 cells were respectively transfected.It was found that 2DG treatment did not reduce NF-κB activity in GES-1 cells transfected with TLR2 mutant.Conclusion:Helicobacter pylori metabolite 2DG can interact with TLR2,reduce the formation of het-erodimers between TLR2 and TLR1,and inhibit the activity of innate immune NF-κB pathway.
2.Research progress on pedicle screw placement safety in orthopedic treatment of type 1 neurofibromatosis scoliosis
Wenbo WANG ; Sanquan TANG ; Guojun LI ; Huanxiong CHEN
Chongqing Medicine 2024;53(23):3633-3638,3644
Neurofibromatosis(NF)as an autosomal dominant disease usually involves multiple sys-tems throughout the body and is classified as type 1 or type 2 NF.Neurofibromatosis scoliosis(NFS)is main-ly type 1,and severe neurofibromatosis scoliosis type 1(NF1-S)is manifested by abnormalities in spinal anat-omy and morphology,such as rotation of the parietal vertebrae and abnormal morphology of the pedicles,which leads to the difficulty and maximal risk of pedicle screw placement in scoliosis orthopedic surgery.In or-der to improve the safety of surgery,this paper discusses the morphology and anatomical structure of the pedi-cles in the patients with NF1-S,and analyzes the accuracy and safety of different pedicle-assisted screw place-ment techniques to provide reference for clinical surgery and promote the improvement of treatment level.
3.Unstable pelvic fractures treated with cancellous bone screw fixation:inflammatory factor levels
Mengfan XU ; Huanxiong ZHUANG ; Huqiang MAI ; Shixiong CHEN
Chinese Journal of Tissue Engineering Research 2016;20(22):3272-3278
BACKGROUND:After different metal fixation materials areimplanted into the human body, peripheral tissue inflammatory response to varying degrees wil appear in the early stage. Poor biocompatibility of the corresponding materials wil lead to prolonged duration of inflammatory reaction.
OBJECTIVE:To investigate the inflammatory factor level changes and biocompatibility of cancelous bone screw fixation in treatment of unstable pelvic fractures.
METHODS:A total of 61 patients with unstable pelvic fractures were randomly divided into the observation group (29cases) and the control group (32 cases). The 29 patients in the observation group underwent cancelous bone screw fixation. The 32 patients in the control group underwent conventional therapy. During 12 months of folow-up, Majeed function score and inflammatory factor level changes and adverse events were observed and compared between the two groups.
RESULTS AND CONCLUSION:(1) Majeed function scores were significantly higher in both groups after treatment as compared with that preoperatively (alP< 0.05). The Majeed function scores were significantly higher in the observation group than in the control group 12 months after treatment (P< 0.05). (2) Inflammatory factor levels: Interleukin 6, C-reactive protein, and tumor necrosis factor alpha levels were significantly lower in both groups after treatment as compared with that preoperatively (alP< 0.05). No significant difference in above indexes was found between the two groups before and after treatment (P> 0.05). (3) Adverse events: one case affected incision infection after operation in the observation group. In the control group, four patients experienced incision infection. One suffered from nonunion, and one had bone necrosis. Above patients were treated in time, and were cured, so there wereno deaths. There were significant differences in the incidence of adverse events between the 2 groups (P< 0.05). (4) The research results show that cancelous bone screw fixation for unstable pelvic fractures can obtain satisfactory clinical results, andhave good biocompatibility.

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