Colostrum IgA1 antibodies recognize antigens from Helicobacter pylori and prevent cytoskeletal changesin human epithelial cells.

Helicobacter pylori is a Gram-negative bacterium found on the luminal surface of the gastric mucosa in at least 50% of the world's human population. The protective effect of breastfeeding against H. pylori infection has been extensively reported; however, the mechanisms behind this protection remain poorly understood. Human IgA from colostrum has reactivity against H. pylori antigens. Despite that IgA1 and IgA2 display structural and functional differences, their reactivity against H. pylori had not been previously determined. We attested titers and reactivity of human colostrum-IgA subclasses by ELISA, immunoblot, and flow cytometry. Colostrum samples from healthy mothers had higher titers of IgA; and IgA1 mostly recognized H. pylori antigens. Moreover, we found a correlation between IgA1 reactivity and their neutralizing effect determined by inhibition of cytoskeletal changes in AGS cells infected with H. pylori. In conclusion, colostrum-IgA reduces H. pylori infection of epithelial gastric cells, suggesting an important role in preventing the bacteria establishment during the first months of life. As a whole, these results suggest that IgA1 from human colostrum provides protection that may help in the development of the mucosal immune system of newborn children.

Mechanism of berberine in treating Helicobacter pylori induced chronic atrophic gastritis through IRF8-IFN-γ signaling axis suppressing.

AIMS: In this study, we will investigate the therapeutic effects of berberine (BBR) in Helicobacter pylori (H. pylori) induced chronic atrophic gastritis (CAG). Furthermore, potential mechanisms of BBR in regulating IRF8-IFN-γ signaling axis will also be investigated. MATERIALS AND METHODS: H. pylori were utilized to establish CAG model of rats. Therapeutic effects of BBR on serum supernatant indices, and histopathology of stomach were analyzed in vivo. Moreover, GES-1 cells were infected by H. pylori, and intervened with BBR in vitro. Cell viability, morphology, proliferation, and quantitative analysis were detected by high-content screening (HCS) imaging assay. To further investigate the potential mechanisms of BBR, relative mRNA, immunohistochemistry and protein expression in IRF8-IFN-γ signaling axis were measured. KEY FINDINGS: Results showed serum supernatant indices including IL-17, CXCL1, and CXCL9 were downregulated by BBR intervention, while, G-17 increased significantly. Histological injuries of gastric mucosa induced by H. pylori also were alleviated. Moreover, cell viability and morphology changes of GES-1 cells were improved by BBR intervention. In addition, proinflammatory genes and IRF8-IFN-γ signaling axis related genes, including Ifit3, Upp1, USP18, Nlrc5, were suppressed by BBR administration in vitro and in vivo. The proteins expression related to IRF8-IFN-γ signaling axis, including Ifit3, IRF1 and Ifit1 were downregulated by BBR intervention.

Effect of Celastrus orbiculatus in inhibiting Helicobacter pylori induced inflammatory response by regulating epithelial mesenchymal transition and targeting miR-21/PDCD4 signaling pathway in gastric epithelial cells.

BACKGROUND: The extract of Celastrus orbiculatus (COE) have been studied for anti-Helicobacter pylori (H. pylori) activity and anti-cancer effects in vitro and in vivo. However, the molecular mechanism by which COE inhibits H. pylori-induced inflammatory response has not been fully elucidated so far. METHODS: The effects of COE on viability, morphological changes, inflammatory cytokine secretion, protein and mRNA expression were analyzed by MTT assay, enzyme-linked immunosorbent assay (ELISA), immunofluorescence, western blot and real-time PCR (RT-PCR), respectively. The methylation level of programmed cell death 4 (PDCD4) promoter was investigated by methylation-specific PCR. (MSP) . RESULTS: COE effectively inhibited the H.pylori-induced inflammatory response by regulating epithelial-mesenchymal transition (EMT). The methylation level of PDCD4 promoter was suppressed by COE, which increased the expression ofPDCD4. Moreover, COE could inhibit microRNA-21 (miR-21) expression, as shown by an enhancement of its target gene PDCD4. Furthermore, both miR-21 over-expression and PDCD4 silencing attenuated the anti-inflammatory effect. of COE. CONCLUSIONS: COE inhibits H. pylori induced inflammatory response through regulating EMT, correlating with inhibition of miR-21/PDCD4 signal pathways in gastric epithelial cells.

A modified pectic polysaccharide from turmeric (Curcuma longa) with antiulcer effects via anti-secretary, mucoprotective and IL-10 mediated anti-inflammatory mechanisms.

Antiulcer potency and inhibitory effects on Helicobacter pylori of structurally defined low molecular weight modified pectin from turmeric (MTrPP) has been previously demonstrated by us. Given that ulcer is a disorder characterized by inflammatory responses leading to initiation, aggravation and perpetuation of disease conditions, the present study aims to understand the possible anti-inflammatory mechanisms through which MTrPP delivered antiulcer effects. Rats triggered with early phase gastric inflammation (LPS) followed by ulcer induction (swim-stress) were pretreated with MTrPP (150 mg/kg b.w.) for 14 days. Inflammation and ulcer-specific markers were screened to assess the protective effects. MTrPP offered up to 91% protection by limiting the production of pro-inflammatory factors (TNF-α, IL-8, NF-κB) and by the tight differential regulation of cyclooxygenase (COX-1, 2), mitogen-activated-protein-kinase (p-p38, p-ERK-1/2) and matrix metalloproteinase (pro-MMP-9). MTrPP showed modulatory effects through inhibition of galectin-3, oxidative stress, H+,K+-ATPase and elicitation of gastro-protective mediators such as, mucin, prostaglandin E2, NOx, zinc, IgA etc. Results revealed that MTrPP mediated the overall protection by creating an environment conducive to protection by switching from the inflammatory to anti-inflammatory phase via IL-10 over expression.

Serum Concentrations of 15 Elements Among Helicobacter Pylori-Infected Residents from Lujiang County with High Gastric Cancer Risk in Eastern China.

Helicobacter pylori (H. pylori) infection can interfere with the absorption of most elements, and the variations of some element levels are related to the incidence of gastric cancer. However, there have been conflicting results concerning the influence of H. pylori infection on serum element levels. The present study aimed to compare the serum element concentrations of H. pylori-infected local residents with uninfected residents from Lujiang County with high gastric cancer risk in Eastern China. We used data and serum samples from the H. pylori screening-survey program which was a cross-sectional study. We took 155 samples randomly from the screening survey, identified 74 H. pylori-positive residents and 81 H. pylori-negative residents by a serological test. The serum concentrations of 15 elements (calcium, magnesium, iron, zinc, selenium, copper, molybdenum, chromium, cobalt, nickel, lead, cadmium, mercury, arsenic, and aluminum) were determined using inductively coupled plasma mass spectrometry. Serum cobalt was found at higher levels in the H. pylori-infected residents than the H. pylori-uninfected residents (0.246 vs 0.205 µg/L, P = 0.022), but no statistically significant differences in the serum levels of other elements were found. This is the first study to report the serum concentrations of 15 elements and their relationships with the infection status of H. pylori among local residents from Lujiang County with high gastric cancer risk. Although the International Agency for Research on Cancer has classified cobalt and other soluble cobalt salts as possibly carcinogenic to human beings, our results may provide a clue to the relationships between cobalt, H. pylori, and gastric cancer.

Berberine demonstrates anti-inflammatory properties in Helicobacter pylori-infected mice with chronic gastritis by attenuating the Th17 response triggered by the B cell-activating factor.

Berberine (BBR) is an isoquinoline alkaloid derived from various medicinal herbs. Previous studies have suggested that BBR exerts antimicrobial, antitumor, and antidiabetic effects and can be used to treat Helicobacter pylori-induced chronic gastritis. However, the exact mechanism by which BBR inhibits H. pylori infection is not fully understood. We investigated the anti-inflammatory properties and potential mechanism of BBR in H. pylori-infected mice with chronic gastritis. We found that BBR can suppress the expression of pro-inflammatory genes IL-6, TGF-ß, and IL-1ß and upregulate anti-inflammatory gene IL-10 expression in the mucosa and RAW 264.7 macrophages. Exposure to BBR also reduced the expression and accumulation of IL-17 in the mucosa and CD4+ T cells activated by anti-CD3 and anti-CD28, and it decreased the frequency of IL-17-producing CD4+ T cells. B cell-activating factor (BAFF) production was inhibited by BBR and by cultured dendritic and CD4+ T cells. Furthermore, we demonstrated that BAFF can trigger the Th17 response by promoting the production of pro-Th17 cytokines IL-6, TGF-ß, and IL-1ß, which are strongly associated with the anti-inflammatory role of BBR in chronic gastritis caused by H. pylori. In conclusion, we determined that BBR has anti-inflammatory effects on H. pylori-induced chronic gastritis by attenuating the BAFF-triggered Th17 response.

The Suppressive Effects of Geniposide and Genipin on Helicobacter pylori Infections In Vitro and In Vivo.

Geniposide and genipin have been found in Gardenia jasminoides Ellis, a traditional Chinese medicine that exhibits multiple biological functions. However, no report showing the effects of geniposide and genipin on gastric protection in Helicobacter pylori infections in vitro and in vivo has been done. In this study, we clarified how geniposide and genipin suppress H. pylori-mediated inflammation in gastric AGS cells and C57BL/6 mice. Our results demonstrated that genipin shows a strong ability to inhibit H. pylori growth and is able to reduce vacA and cagA gene expression of H. pylori in infected AGS cells. Genipin also attenuates the abilities of adhesion and invasion of H. pylori to AGS cells. An attenuation of interleukin (IL)-8 and IFN-γ production caused by genipin was observed to inhibit cell inflammatory responses. In the in vivo experiments, geniposide and genipin both showed suppressive effects on the vacA gene expression in mice after H. pylori infection. The serum levels of IFN-γ, IL-1ß, immunoglobulin A, and Immunoglobulin M were decreased by geniposide and genipin in infected mice. The inflammatory maker COX2 was downregulated in H. pylori-infected mice after exposure to geniposide and genipin. Together, geniposide and genipin effectively exert a healthy promotion to reduce H. pylori infections in vivo by interfering with the growth and virulence of H. pylori as well as attenuating the gastric inflammation caused by an H. pylori infection. PRACTICAL APPLICATION: Geniposide and genipin have a healthy promotion to eradicate H. pylori infections by interfering with the growth and virulence of H. pylori and to attenuate the gastric inflammation caused by an H. pylori infection.

INHIBITORY ACTIVITY OF MANGIFERIN ON HELICOBACTER PYLORI-INDUCED INFLAMMATION IN HUMAN GASTRIC CARCINOMA AGS CELLS.

BACKGROUND: Gastric cancer is a serious health issue caused by H. pylori and claims more lives in developing and undeveloped countries. Hence, the need for a natural drug with several pharmacological activities with no adverse effect are highly recommended. The target of this study was to verify the anti-H. pyloric efficacy of mangiferin (MF) on H. pylori-infected AGS cells. MATERIALS AND METHODS: AGS cells were co-cultured with H. pylori and incubated with increased concentration of MF (10, 20, 50 and 100 µg/mL) or amoxicillin (AMX) and DMSO (control) group to assess its anti-H. pyloric effect by checking inhibitory zone, bacterial drug sensitivity test (MIC and MBC), adhesion and invasive property and various inflammatory markers. RESULTS: Co-culturing of H. pylori-infected AGS cells with MF (100 µg) considerably increased (p<0.05) the inhibitory zone as well as substantially lowered (p<0.05) in the levels of MBC and MIC with decreased adhesion and invasive property in a dose-dependent manner and thus endorsing its anti H. pyloric activity and are almost equivalent to antibiotic AMX. Meanwhile, inflammatory markers such as NF-κΒ subunit p65, interleukins-1ß, IL-8, and TNF-α were also markedly suppressed (p<0.01) on treatment with MF. In addition, the protein expression of inflammatory enzymes like COX-2 and iNOS were notably downregulated (p<0.05) in AGS cells incubated with MF. CONCLUSION: We, concluded that MF treatment with H. pylori-infected AGS cells significantly suppressed the adhesion and invasion process as well as deactivated NF-p65 thereby blocking inflammatory response and thus lower the incidence of gastric carcinoma.

Effect of Rumex Aquaticus Herba Extract Against Helicobacter pylori-Induced Inflammation in Gastric Epithelial Cells.

The purposes of this study were to examine the characteristics of Helicobacter pylori and the effect of Rumex Aquaticus Herba extract on the expression of cytokines in H. pylori-infected gastric epithelial cells. Cultured human adenocarcinoma gastric cells (AGS) were infected by H. pylori in RPMI 1640 media. Cell growth was measured by trypan blue assay. Western blot analysis was performed to investigate effect of extract containing Quercetin-3-O-ß-d-glucuronopyranoside (ECQ) on the expression of inflammatory factors and the inhibition on cell growth. Furthermore, we compared the inhibitory effects with various combinations of clarithromycin, amoxicillin, omeprazole, and ECQ. The urease test with Christensen's Urea Agar was performed to identify the urease activity of H. pylori and the effect ECQ has on urease activity. When the cells were exposed to H. pylori, the trypan blue assay revealed a decrease in the rate of cell growth. Western blot analysis showed that H. pylori-infected cells had increased levels of degraded IκB-α and inflammatory factors. Pretreatment with ECQ inhibited interleukin expression induced by H. pylori in a dose-dependent manner. A combination of ECQ and antibiotics inhibited cytokine expression more effectively than other treatments. H. pylori displayed significant urease activity. ECQ did not significantly inhibit urease activity. These data suggest that H. pylori infection has cytotoxic effects against AGS cells, and ECQ may inhibit the production of proinflammatory cytokines in H. pylori-infected AGS cells.

EVIDENCE BASE OF LACTOBACILLUS REUTERI EFFICACY IN THE TREATMENT OF DISEASES ASSOCIATED WITH HELICOBACTER PYLORI.

Helicobocterpylori (HP) - the human infection that persists for a long time in the stomach and can cause chronic gastritis, gastric and duodenal ulcer, MALT-lymphoma, gastric adenocarcinoma. There is a well-adapted niche-specific microbial community in the stomach represented by Lactobocillus, Streptococcus ahd other bacteria. Use of probiotics is considered to be an alternative or supplement to eradication therapy Among the Lactobacillus the most promising is Loctobocillus reutert who are able to have the anti-HP activity L. reureri produces powerful antimicrobial compounds such as reuterin, reuteritsin 6, reutetsiklin and metabolites that inhibit the growth of I-/P (volatile fatty acids, lactic acid, hydrogen peroxide, etc.). These compounds could reduce the adhesion of HP to gastric epithelial cells, inhibit growth HP, which leads to a significant reduction in the degree of contamination of HP and the severity of gastric mucosal inflammation. The data on the effectiveness of L. re uteri as monotherapy in patients with HP without absolute indications for eradication, and as an additional component, which increase the effectiveness of eradication are presented.

Recombinant human lactoferrin enhances the efficacy of triple therapy in mice infected with Helicobacter pylori.

Helicobacter pylori (H. pylori) is a life-threatening pathogen which causes chronic gastritis, gastric ulcers and even stomach cancer. Treatment normally involves bacterial eradication; however, this type of treatment only has a rate of effectiveness of <80%. Thus, it is a matter of some urgency to develop new therapeutic strategies. Lactoferrin, a member of the transferrin family of iron-binding proteins, has been proven to be effective in removing a vast range of pathogens, including H. pylori. In the present study, we examined the effectiveness of recombinant human lactoferrin (rhLf) isolated from transgenic goats as a treatment for H. pylori in vitro and in vivo. For the in vivo experiments, BALB/c mice received an intragastric administration of 0.1 ml of a suspension of H. pylori. The mice were then divided into 4 groups: group A, treated with saline; group B, treated with 1.5 g of rhLF; group C, treated with the standard triple therapy regimen; and group D, treated with the standard triple therapy regimen plus.5 g of rhLF. Following sacrifice, the stomach tissues of the mice were histologically examined for the presence of bacteria. For the in vitro experiments, the bacteria were cultured in BHI broth and RT-qPCR and western blot analysis were carried out to determine the mRNA and protein levels of virulence factors (CagA and VacA) in the cultures. Our results revealed that rhLf not only inhibited the growth of H. pylori, but also suppressed the expression of two major virulence factors. Moreover, rhLf markedly increased bacterial eradication and effectively reduced the inflammatory response when combined with the standard triple therapy regimen. These results provide evidence supporting the use of rhLF as an adjuvant to traditional therapeutic strategies in the treatment of H. pylori.

Helicobacter pylori: a pathogenic threat to the gastric mucosal barrier.

Peptic ulcer disease is a multi-factorial disorder of the gastrointestinal tract with a global prevalence affecting about 4.6 million people annually and having a mortality of one death per 10,000 cases. Helicobacter pylori (H. pylori) plays a profound role in the pathogenesis of chronic gastritis, peptic ulcer, including gastric mucosa-associated lymphoid tissue and carcinoma. Any compromise to the gastric mucosal barrier will greatly affect the integrity of the stomach. H. pylori is an organism which mediates a compromise of the gastric mucosal barrier by stimulating increased gastric acid secretion, causing alteration of certain immune factors, penetration of the mucosal layer and provoking persistent inflammation even without invading the mucus membrane. All the different lines of therapy have not shown maximal efficacy in the eradication/cure of the infection in patients. Consequently, alternative therapies including phytomedicines and probiotics have been introduced both in the quest for better eradication therapies and in addressing the problem of H. pylori relapse. In the light of the increasing antibiotic resistance associated with current therapies, the use of herbal preparations or its concomitant use with current therapy has the potential to contribute additive and synergistic effect in the eradication of the H. pylori infection. This review highlights the anti-H. pylori herbal preparations tested and in current use.

[Serumimmunological study of moxibustion on helicobacter pylori gastritis in rats].

OBJECTIVE: To explore the immune mechanism of moxibustion on protecting gastric mucosa injury. METHODS: Forty healthy SD rats were randomly divided into four groups: a blank group, a model group, a moxibustion acupoint group and a moxibustion non-acupoint group, 10 rats in each one. Eight days before model establishment, moxibustion at "Zusanli" (ST 36), "Zhongwan" (CV 12), "Guanyuan" (CV 4), "Pishu" (BL 20) and "Weishu" (BL 21) was applied in the moxibustion acupoint group while these acupoints' controlled points were selected in the moxibustion non-acupoint group, and no treatment was given in the model group, once a day in three groups for continuous 16 days. The helicobacter pylori (Hp) model was established by intragastric administration of Hp. HE staining microscopic examination was used to observe inflammation severity in gastric mucosa, and enzyme-linked immunosorbent assay (ELISA) was adapted to measure content of heat shock protein (HSP) 72, TNF-alpha and IL-1beta, and real-time quantitative PCR was used to measure the expression of TLR2 mRNA, TLR4 mRNA, CD14 mRNA and MyD88 mRNA in peripheral blood mononuclear cells, and western blot method was used to measure content of NFkappaB and IkappaBalpha in peripheral blood mononuclear cells. RESULTS: Compared with the blank group, the expression of HP could be seen in the smear of gastric mucosa by Gram's staining in the model group; the inflammation severity score was obviously increased as well as content of serum HSP 72 and TNF-alpha and IL-1beta in gastric tissue; and expression of TLR2, 4 mRNA, CD14 mRNA, MyD88 mRNA, NFkappaB was increased (P < 0.01), but the expression of IkappaBalpha was reduced (P < 0.05). After the moxibustion, the inflammation severity score was reduced in the moxibustion acupoint group, and the content of serum HSP 72 was increased, and the expression of TNF-alpha and IL-1beta in gastric tissue and expression of TLR2 mRNA, TLR4 mRNA, CD14 mRNA, MyD88 mRNA and NFkappaB were reduced (P < 0.01), but the expression of IkappaBalpha was increased (P < 0.05). The differences between the moxibustion non-acupoint group and the model group were not significant (P > 0.05). CONCLUSION: The pretreatment of moxibustion at acupoints could induce the over expression of serum HSP 72. By combining TLR 2 and 4 receptors to trigger receptor signal transduction pathways, the releases of downstream signal substances are regulated; as a result, the releases of related immune substances are regulated to relieve the gastric mucosa injury of rats with HP gastritis.

Helicobacter canis bacteremia in a renal transplant patient.

Here we present a case report of a 41-year-old woman suffering from high fever and bacteremia due to Helicobacter canis, 11 months after kidney transplantation. Identification of H. canis was achieved by 16s rDNA sequence analysis of a positive blood culture. The patient was restored fully to health after antibiotics therapy (cefuroxime and ciprofloxacin). Until now, only 4 human clinical cases have been described with H. canis bacteremia. This study describes for the first time, to our knowledge, an infection with H. canis in a kidney transplant patient.

Hyperimmune bovine colostrum for treatment of GI infections: a review and update on Clostridium difficile.

Hyperimmune bovine colostrum (HBC), produced by vaccination of a cow during gestation, is rich in targeted immunoglobulins, and can be used to treat a variety of diseases. The published history of HBC use for treating gastrointestinal infections in humans has developed over the past several decades and demonstrates the promise of this type of therapeutic for GI infectious disease. HBC, or purified derivative products, have been used successfully for treatment or prevention of cryptosporidiosis, shigellosis, rotavirus, enterotoxigenic E. coli, and C. difficile infection (CDI). Given the positive results of previous studies using HBC for treatment of CDI, we have produced HBC with antibodies against the two most important virulence factors of C. difficile, TcdA and TcdB, using a novel recombinant vaccine. Our preliminary results demonstrate efficacy of the HBC product for treatment of CDI in the gnotobiotic piglet model, and warrant more thorough investigation. HBC may provide an effective treatment alternative to antibiotics, which can spare the normal gut microflora, and reduce rates of recurrence and antibiotic resistance.

[Study of Th1/Th2 balance in peripheral blood of chronic gastritis patients with Pi-Wei damp-heat syndrome].

OBJECTIVE: To study the correlation between the Th1/Th2 balance in the peripheral blood and Pi-Wei damp-heat syndrome (PDS) in chronic gastritis (CG). METHODS: Fifty-one patients with CG of PDS were recruited, including 22 cases with predominant damp (PDS-D), 9 case with predominant heat (PDS-H), and 20 case with simultaneous onset of damp and Heat (PDS-DH). Besides, 10 healthy volunteers were recruited as the healthy control group. H. pylori (HP) infection was detected by fast urea enzyme, and the expressions of Th1 type cytokines interferon-gamma (IFN-gamma), interleukin-12 (IL-12), and Th2 type cytokines interleukin-4 (IL-4), interleukin-10 (IL-10) in serum were detected by luminex technology. RESULTS: The HP infection rate was 41.18% (21/51) in the PDS patients, obviously higher than that in the healthy control group (10.00%,1/10), showing statistical difference (P<0.05). The HP infection rate was 45.45% (10/22) in PDS-D, 22.22% (2/9) in PDS-H, and 45.00% (9/20) in PDS-DH. The HP infection rate in PDS-D and PDS-DH was significantly higher than that of the healthy control group, showing statistical difference (P<0.05). There was no statistically significant difference in the expressions of peripheral blood IFN-gamma, IL-12, IL-4, and IL-10 between the PDS patient group and the healthy control group (P>0.05). But the expressions of IFN-gamma and IL-12 showed an increasing trend in the PDS patient group, while the expression of IL-4 showed a decreasing trend. The expressions of IFN-gamma, IL-12, IL-4, and the ratios of IFN-gamma/IL-4 and IL-12/IL-4 were also higher in PDS-DH group than in the PDS-D group and the PDS-H group, but with no statistical significance (P>0.05). CONCLUSION: The occurrence of Pi-Wei damp-heat CG was possibly correlated with the imbalance of Th1/Th2. Damp and heat pathogen might be important pathogenic factors leading to Th1 type cytokine immunoreaction.

Effects of alpha tocopherol and ascorbic acid on Helicobacter pylori colonization and the severity of gastric inflammation.

BACKGROUND AND AIM: We aimed to evaluate the changes in histopathologic features, concentrations of vitamins C and E in gastric mucosa, and total antioxidant capacity of the body after ingestion of ascorbic acid and alpha tocopherol in patients with Helicobacter pylori. MATERIAL AND METHOD: Patients with H. pylori-positive nonulcer dyspepsia were included in this study. Tissue samples were taken from the lesser and greater curvature in both prepyloric antrum and corpus for histopathologic examination and measurement of vitamins C and E concentrations. Blood samples were obtained for measurement of the total antioxidant capacity of the body. The patients were given vitamin C 500 mg BID and vitamin E 200 IU BID for 4 weeks orally. At the end of the 4th week, the initial procedures were repeated. Histopathologic examination of the tissue samples were carried out by two pathologists. RESULTS: The mean vitamins C and E concentrations in gastric mucosa at the 4th week were higher than those at the beginning (p = .000 and p = .006, respectively). Mean total antioxidant capacity of the body at the beginning and that at the 4th week were similar (p = .689). H. pylori intensity in the antrum at the beginning was higher than that at the 4th week for both pathologists (p = .007 and p = .039). Neutrophilic activity in the antrum at the beginning was higher than that at the 4th week for both pathologists (p = .000 and p = .025). Neutrophilic activity in the corpus at the beginning was higher than that at the 4th week for pathologist 1 (p = .033), and they were similar for pathologist 2 (p = .763). CONCLUSION: The findings that H. pylori intensity and neutrophilic activity decrease through increasing gastric ascorbic acid and alpha tocopherol concentrations suggest that supplementation with vitamins C and E increases the eradication rates via impairing the microenvironment created by the bacteria and facilitating the diffusion of antibiotics into gastric mucosa.

Reduction of inflammatory hyperplasia in the intestine in colon cancer-prone mice by water-extract of Cistanche deserticola.

Cistanche deserticola has commonly been used in traditional Chinese medicine to treat many health problems including irritable bowel syndrome or constipation. This study was designed to test the efficacy of a water-extract of C. deserticola in the prevention of colorectal cancer in a mouse model. Polysaccharide-rich water-extract of C. deserticola was prepared by boiling its stem powder in distilled water. Tgfb1Rag2 null mice were used as an experimental model. Here we showed that feeding of water-extract of C. deserticola significantly reduced the number of mucosal hyperplasia and intestinal helicobacter infection in mice. This beneficial effect correlated with significant stimulation of the immune system, evidenced by the enlargement of the spleens with increased number of splenic macrophage and natural killer cells, and with more potent cytotoxicity of splenocytes. In vitro water-extract of C. deserticola enhanced the cytotoxicity of naïve splenocytes against a human colon cancer cell line, and in macrophage cultures up-regulated nitric oxide synthase II expression and stimulated phagocytosis. In conclusion, our data indicate that oral administration of C. deserticola extract reduces inflammatory hyperplastic polyps and helicobacter infection in mice by its immune-stimulatory activity, suggesting that C. deserticola extract may have potential in preventing intestinal inflammation disorders including colorectal cancer.

[Use of the immunopotentiator N-acetyl-glucosamine-N-acetylmuramyl dipeptide during triple anti-Helicobacter pylori therapy].

AIM: To evaluate the efficiency of first-line Helicobacter pylori eradication therapy with glucosaminylmuramyldipeptide (Licopid JSC "Peptek", Russia). SUBJECTS AND METHODS: Eradication therapy was performed in 128 patients (84 men and 34 women; mean age 44.1 +/- 13.5 years) with duodenal bulb ulcer associated with H. pylori. The latter was detected in the gastroduodenal mucosa by a morphological study and rapid urease test before and 6-8 weeks after treatment and discontinuation of all drugs. Gastric metaplasia areas in the duodenum were revealed by periodic acid-Schiff and Alcian blue staining. The patients were divided into 4 groups according to the treatment protocol: 1) omeprazole (O) 0.04 g/day, clarithromycin (C) 1 g/day, amoxicillin (A) 2 g/day for 7 days (OCA7; n = 33); 2) the above drugs for 14 days (OCA14; n = 34); 3) O 0.04 g/day, C 1 g/day, A 2.0 g/day for 7 days, and glucosaminylmuramyldipeptide (Licopid) (L) 0.001 g/day for a day (OCA7L1; n = 34) and 4) the above drugs and L 0.01 g/day for 10 (OCA7L10; n = 27). RESULTS: According to the data of intention-to-treat analysis and per protocol, the H. pylori eradication rate was 81.8 and 87.1% for OCA7; 82.4 and 93.3% for OCA14; 88.2 and 93.8% for OCA7L1; 88.9 and 96% for OCA7L10 after PT and RRT, respectively. The rate of side effects was as follows: 6.1% for OCA7; 17.6% for OCA14 (5.9% stopped treatment); 5.9% for OCA7L1; 7.4% for OCA7L10. The cost of the treatment protocols was $ 32 for OCA7; $ 64 for OCA14; $ 40 for OCA7L1; $ 67 for OCA7L10. The intake of glucosaminylmuramyldipeptide (licopid) 0.001 g/day during 7-day triple anti-Helicobacter pylori therapy increased eradication by 6.4% (ITT) and 6.7% (PP), without raising the rate of side effects. CONCLUSION: H. pylori-positive patients with duodenal bulb ulcer should be given glucosaminylmuramyldipeptide (Licopid) 0.001 g/day during 7-day first-line eradication therapy as alternative to the 14-day treatment regimen.