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Helicobacter pylori infection is the major risk factor associated with the development of gastric cancer. Currently, administration of standard antibiotic therapy combined with probiotics and postbiotics has gained significant attention in the management of H. pylori infection. In this work, the immunomodulatory effects of Lactobacillus crispatus-derived extracellular vesicles (EVs) and cell-free supernatant (CFS) were investigated on H. pylori-induced inflammatory response in human gastric adenocarcinoma (AGS) cells. L. crispatus-derived EVs were isolated by ultracentrifugation and physically characterized by dynamic light scattering (DLS), transmission electron microscopy (TEM), and scanning electron microscopy (SEM). Furthermore, the protein content of L. crispatus-derived EVs was also evaluated by SDS-PAGE. Cell viability of AGS cells exposed to varying concentrations of EVs and CFS was assessed by MTT assay. The mRNA expression of IL-1β, IL-6, IL-8, TNF-α, IL-10, and TGF-ß genes was determined by RT-qPCR. ELISA was used for the measurement of IL-8 production in AGS cells. In addition, EVs (50 μg/mL) and CFS modulated the H. pylori-induced inflammation by downregulating the mRNA expression of IL-1β, IL-6, IL-8, and TNF-α, and upregulating the expression of IL-10, and TGF-ß genes in AGS cells. Furthermore, H. pylori-induced IL-8 production was dramatically decreased after treatment with L. crispatus-derived EVs and CFS. In conclusion, our observation suggests for the first time that EVs released by L. crispatus strain RIGLD-1 and its CFS could be recommended as potential therapeutic agents against H. pylori-triggered inflammation., (© 2024. Institute of Microbiology, Academy of Sciences of the Czech Republic, v.v.i.)

Over time, mounting evidence has demonstrated extra-gastric manifestations of Helicobacter pylori infection. As such, a number of studies demonstrated the potential contribution of H. pylori infection to the incidence and progression of Alzheimer's disease (AD). Considering unanswered questions regarding the effect of H. pylori infection on brain activity, we sought to investigate the impact of H. pylori infection on the expression of AD-associated risk factors. We used two H. pylori clinical strains obtained from two patients with peptic ulcer and evaluated their influence on the expression level of AD-associated genes ( APP , ApoE2 , ApoE4 , ABCA7 , BIN1 , Clu , CD33 ) and genes for inflammatory markers (TLR-4, IL-8, TNF-α) by RT-qPCR in human glioblastoma (U87MG) and astrocyte (1321N1) cell lines. The expression of inflammatory cytokines was further assessed by ELISA assay. The exposure of U97MG and 1321N1 cells to H. pylori strains resulted in a significant enhancement in the expression level of the risk allele ApoE4 , while reducing the expression of the protective allele ApoE2 . H. pylori infection remarkably increased the expression level of main AD-associated risk genes, and also pro-inflammatory cytokines. Furthermore, we noticed a substantial elevation in the mRNA expression level of transmembrane receptor TLR-4 following H. pylori infection. Our findings presented the potential for H. pylori to stimulate the expression of AD-associated risk genes and trigger neuroinflammation in the brain tissue. This, in principle, leads to the recommendation that AD patients should perhaps test for H. pylori infection and receive treatments upon positive detection., Competing Interests: The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (© 2023 The Authors.)

Background: Helicobacter pylori infection is considered as the major risk factor for gastric adenocarcinoma. Today, the increasing emergence of antibiotic-resistant strains has drastically decreased the eradication rate of H. pylori infection. This study was aimed to investigate the inhibitory and modulatory effects of live and pasteurized Lactobacillus crispatus strain RIGLD-1 on H. pylori adhesion, invasion, and inflammatory response in AGS cell line., Methods and Results: The probiotic potential and properties of L. crispatus were evaluated using several functional and safety tests. Cell viability of AGS cells exposed to varying concentrations of live and pasteurized L. crispatus was assessed by MTT assay. The adhesion and invasion abilities of H. pylori exposed to either live or pasteurized L. crispatus were examined by gentamycin protection assay. The mRNA expression of IL-1β, IL-6, IL-8, TNF-α, IL-10, and TGF-ß genes was determined by RT-qPCR from coinfected AGS cells. ELISA was used for the detection of IL-8 secretion from treated cells. Both live and pasteurized L. crispatus significantly decreased H. pylori adhesion/invasion to AGS cells. In addition, both live and pasteurized L. crispatus modulated H. pylori-induced inflammation by downregulating the mRNA expression of IL-1β, IL-6, IL-8, and TNF-α and upregulating the expression of IL-10, and TGF-ß cytokines in AGS cells. Furthermore, H. pylori-induced IL-8 production was dramatically decreased after treatment with live and pasteurized L. crispatus., Conclusions: In conclusion, our findings demonstrated that live and pasteurized L. crispatus strain RIGLD-1 are safe, and could be suggested as a potential probiotic candidate against H. pylori colonization and inflammation., (© 2023. The Author(s), under exclusive licence to Springer Nature B.V.)

The gut microbiome plays a critical role in maintaining overall health and immune function. However, dysbiosis, an imbalance in microbiome composition, can have profound effects on various aspects of human health, including susceptibility to viral infections. Despite numerous studies investigating the influence of viral infections on gut microbiome, the impact of gut dysbiosis on viral infection and pathogenesis remains relatively understudied. The clinical variability observed in SARS-CoV-2 and seasonal influenza infections, and the presence of natural HIV suppressors, suggests that host-intrinsic factors, including the gut microbiome, may contribute to viral pathogenesis. The gut microbiome has been shown to influence the host immune system by regulating intestinal homeostasis through interactions with immune cells. This review aims to enhance our understanding of how viral infections perturb the gut microbiome and mucosal immune cells, affecting host susceptibility and response to viral infections. Specifically, we focus on exploring the interactions between gamma delta (γδ) T cells and gut microbes in the context of inflammatory viral pathogenesis and examine studies highlighting the role of the gut microbiome in viral disease outcomes. Furthermore, we discuss emerging evidence and potential future directions for microbiome modulation therapy in the context of viral pathogenesis.

The human gut microbiota are critical for preserving the health status because they are required for digestion and nutrient acquisition, the development of the immune system, and energy metabolism. The gut microbial composition is greatly influenced by the colonization of the recalcitrant pathogen Helicobacter pylori ( H. pylori ) and the conventional antibiotic regimens that follow. H. pylori is considered to be the main microorganism in gastric carcinogenesis, and it appears to be required for the early stages of the process. However, a non- H. pylori microbiota profile is also suggested, primarily in the later stages of tumorigenesis. On the other hand, specific groups of gut microbes may produce beneficial byproducts such as short-chain fatty acids (acetate, butyrate, and propionate) that can modulate inflammation and tumorigenesis pathways. In this review, we aim to present how H. pylori influences the population of the gut microbiota to modify the host immunity and trigger the development of gastric carcinogenesis. We will also highlight the effect of the gut microbiota on immunotherapeutic approaches such as immune checkpoint blockade in cancer treatment to present a perspective for further development of innovative therapeutic paradigms to prevent the progression of H. pylori -induced stomach cancer., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Fakharian, Asgari, Nabavi-Rad, Sadeghi, Soleimani, Yadegar and Zali.)

Objectives: In this study, the preemptive effect of a small dose of ketamine on postoperative wound pain and morphine consumption in patients undergoing elective cesarean section was evaluated., Methods: In a randomized, double-blind clinical trial, 60 women with American Society of Anesthesiologists class I and II identification undergoing elective cesarean section were enrolled. In the case group, the patients received 0.5 mg/kg ketamine, and in the control group, they received isotonic saline, 5 minutes before the induction of anesthesia. Anesthesia was induced with 4 mg/kg thiopental followed by 1.5 mg/kg succinylcholine. A further neuromuscular block was achieved by using 0.2 mg/kg of atracurium. Anesthesia was maintained with nitrous oxide 50% and halothane in oxygen. The lungs were mechanically ventilated. After fetus delivery, fentanyl (2 microg/kg) and morphine (0.15 mg/kg) were given intravenously. In the postanesthesia care unit and in the ward, all patients received morphine. Pain was assessed by the Visual Analog Scales at 2, 6, 12, and 24 hours postoperatively; the amount of morphine used and side effects were recorded., Results: There was no significant difference between the patients considering their operative details, homodynamic variables, side effects, and Apgar scores of their babies at first and fifth minutes. Significantly, lower amounts of morphine were used in the case group (4.8 mg+/-2.5 mg vs. 8.1 mg+/-4.2 mg) during the first 2 hours after surgery (P=0.01), but the difference was not significant during 2 to 24 hours (3.2+/-2.2 vs. 3.1+/-2.3). There were no statistical differences between the groups in pain 2, 6, 12, and 24 hours postoperatively., Discussion: Intraoperative low-dose ketamine had no effect on morphine consumption during 2 to 24 hours after surgery. No significant differences were seen in the pain scores of the 2 groups during the study period. The preoperative administration of 0.5 mg/kg ketamine in patients undergoing cesarean section did not elicit a preemptive analgesic effect.

To evaluate the impact of preemptive local analgesia at the incision site for postoperative pain in patients undergoing disc operation. In this prospective, randomized, double-blinded, placebo-controlled study 166 patients were assigned to either lidocaine (n = 83) or placebo (n = 83) groups. The incision site was infiltrated with either 20 mL of 2% lidocaine and 0.9% saline in lidocaine group or 0.9% saline before the incision. Morphine (5 mg) was used for postoperative pain treatment. Postoperative pain was measured with Visual Analog Scale (VAS) in 6, 12, 24 and 48 h. Data were analyzed with SPSS software, using Chi-square and t-tests. The groups were matched for age, sex, type of operation, mean length of hospital stay and mean length of operation. Statistical analysis revealed no significant difference in visual analog scores of pain severity at 6, 12, 24 and 48 h after surgery between lidocaine and placebo groups (6 h: 38.22 +/- 26.87 vs. 34.52 +/- 24.43, p = 0.35; 12 h: 33.26 +/- 28.83 vs. 28.01 +/- 24.71, p = 0.20; 24 h: 26.71 +/- 23.31 vs. 22.85 +/- 22.48, p = 0.27; 48 h 16.35 +/- 10.16 vs. 15.23 +/- 8.90 p = 0.45). The amount of narcotics used post operatively had no meaningful difference in the groups (lidocaine 10.07 +/- 8.24 mg vs. placebo 10.54 +/- 9.31 mg p = 0.73). Preemptive analgesia with lidocaine 2% used subcutaneously before skin incision has no effect in reducing postoperative pain, narcotics demand and duration of hospital stay.