Helicobacter pylori infection in pregnant women and it’s correlation with the alterations of some trace elements levels in the serum at Maternity Teaching Hospital in Erbil City

2018 ◽  
pp. 41-50
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Pregnant Women ◽  
Zinc Level ◽  
Serum Copper ◽  
Vital Role ◽  
Human Gastric Mucosa ◽  
Significant Difference ◽  
H Pylori ◽  
Human Infections

Helicobacter pylori (H. pylori) is a spiral-shaped pathogenic bacterium found on the human gastric mucosa, Warren and Marshall isolated H pylori for the first time in 1982. It is one of the most common worldwide human infections [1]. H. pylori play a vital role in the development of chronic gastritis, gastric ulcer, duodenal ulcer, gastric adenocarcinoma, and gastric mucosa-associated lymphoid tissue lymphoma [2]. The current study included (120) pregnant women, (50) positive anti -H. Pylori Ig and (70) negative anti- H. Pylori Ig with pregnancy for first, second and third semester at mean age/ years 28.36 for the positive anti-H. Pylori and 26.17 for the negative anti-H. Pylori appeared that an alteration of zinc level in serum of positive anti- H. Pylori Ig groups was (48.904 ± 18.3486) (μg/dl) comparing with the negative groups (90.757 ± 9.2727) with the highly significant difference (P < 0.01). While serum copper levels of positive anti-H. Pylori Ig group was (μg/dl), (100.412 ± 23.8234), documented as normal highly significant (P < 0.01) compared to the negative anti- H. Pylori Ig group (114.971 ± 20.4995).In this study, the GIT disorder with anti-H. Pylori Ig positive groups were (32, 64%) and anti-H. Pylori Ig negative groups were (32, 45.7%), with significant difference (P < 0.05).

Helicobacter pylori infection in pregnant women and it’s correlation with the alterations of some trace elements levels in the serum at Maternity Teaching Hospital in Erbil City

2018 ◽  
pp. 41-50
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Pregnant Women ◽  
Zinc Level ◽  
Serum Copper ◽  
Vital Role ◽  
Human Gastric Mucosa ◽  
Significant Difference ◽  
H Pylori ◽  
Human Infections

Helicobacter pylori (H. pylori) is a spiral-shaped pathogenic bacterium found on the human gastric mucosa, Warren and Marshall isolated H pylori for the first time in 1982. It is one of the most common worldwide human infections [1]. H. pylori play a vital role in the development of chronic gastritis, gastric ulcer, duodenal ulcer, gastric adenocarcinoma, and gastric mucosa-associated lymphoid tissue lymphoma [2]. The current study included (120) pregnant women, (50) positive anti -H. Pylori Ig and (70) negative anti- H. Pylori Ig with pregnancy for first, second and third semester at mean age/ years 28.36 for the positive anti-H. Pylori and 26.17 for the negative anti-H. Pylori appeared that an alteration of zinc level in serum of positive anti- H. Pylori Ig groups was (48.904 ± 18.3486) (μg/dl) comparing with the negative groups (90.757 ± 9.2727) with the highly significant difference (P < 0.01). While serum copper levels of positive anti-H. Pylori Ig group was (μg/dl), (100.412 ± 23.8234), documented as normal highly significant (P < 0.01) compared to the negative anti- H. Pylori Ig group (114.971 ± 20.4995).In this study, the GIT disorder with anti-H. Pylori Ig positive groups were (32, 64%) and anti-H. Pylori Ig negative groups were (32, 45.7%), with significant difference (P < 0.05).

Helicobacter pylori (H. pylori) infection increases IL-8 and IL-6 production from human gastric mucosa

1995 ◽  
Vol 108 (4) ◽  
pp. A769
Author(s):  
T. Ando ◽  
K. Kusugami ◽  
M. Sakakibara ◽  
T. Shimizu ◽  
M. Shinoda ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Human Gastric Mucosa ◽  
H Pylori

scholarly journals Serum trace metals in Pre-Eclamptic Nigerians

2016 ◽  
Vol 7 (3) ◽  
pp. 78-83 ◽  
Author(s):  
Ikechukwu Chidiebere Ikaraoha ◽  
Nkeiruka Chigaekwu Mbadiwe ◽  
John Ibhagbemien Anetor ◽  
Isreal Agware Ojareva
Keyword(s):  
Trace Metals ◽  
Pregnant Women ◽  
Serum Levels ◽  
Zinc Level ◽  
Serum Copper ◽  
Copper Level ◽  
Medical Sciences ◽  
Lower Serum ◽  
Significant Difference

Background: The role of trace metals in Pathogenesis of Pre-eclampsia has received insufficient attention in Nigeria.Materials and Methods: We examined the effect of serum levels of some trace metals; selenium (Se), zinc (Zn), copper (Cu), cobalt (Co), and manganese (Mn) in the development of pre-eclampsia in Nigeria. Blood samples were collected from 59 pre-eclamptic, 150 normal pregnant and 122 non pregnant women. Serum Se, Zn, Cu, Co and Mn were determined by AAS.Results: Result shows significantly lower serum Se, Zn, Cu, Cu: Zn ratio, Co and Mn in pre-eclamptics compared to normal pregnant women (p<0.001). Comparison of normal pregnant women and controls showed non significant difference in the zinc level (P>0.05), significantly lower levels of serum Se, Co, Mn (p<0.00011, p=0.0022, p<0.0001 respectively) and significantly raised copper level (p<0.001) in normal pregnant women compared to controls.  Serum Se, Zn, Co and Mn were significantly lower (p<0.001) while serum copper and Cu: Zn ratio were significantly higher (p<0.001) in pregnant women compared to controls. ANOVA shows significant progressive decreases in serum Se, Zn Co and Mn, from controls to normal pregnant women and pre-eclamptics (p<0.0001).Conclusion: Decreases in serum level of Se, Zn, Cu, Cu: Zn ratio, Co and Mn may play important role in the pathogenesis of pre-eclampsia.Asian Journal of Medical Sciences Vol. 7(3) 2016 78-83

scholarly journals Helicobacter pylori–binding nonacid glycosphingolipids in the human stomach

2018 ◽  
Vol 293 (44) ◽  
pp. 17248-17266 ◽  
Author(s):  
Chunsheng Jin ◽  
Angela Barone ◽  
Thomas Borén ◽  
Susann Teneberg
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Structural Complexity ◽  
Human Stomach ◽  
Carbohydrate Binding ◽  
Human Gastric Mucosa ◽  
H Pylori ◽  
Contrast Information

Helicobacter pylori has a number of well-characterized carbohydrate-binding adhesins (BabA, SabA, and LabA) that promote adhesion to the gastric mucosa. In contrast, information on the glycoconjugates present in the human stomach remains unavailable. Here, we used MS and binding of carbohydrate-recognizing ligands to characterize the glycosphingolipids of three human stomachs from individuals with different blood group phenotypes (O(Rh−)P, A(Rh+)P, and A(Rh+)p), focusing on compounds recognized by H. pylori. We observed a high degree of structural complexity, and the composition of glycosphingolipids differed among individuals with different blood groups. The type 2 chain was the dominating core chain of the complex glycosphingolipids in the human stomach, in contrast to the complex glycosphingolipids in the human small intestine, which have mainly a type 1 core. H. pylori did not bind to the O(Rh−)P stomach glycosphingolipids, whose major complex glycosphingolipids were neolactotetraosylceramide, the Lex, Lea, and H type 2 pentaosylceramides, and the Ley hexaosylceramide. Several H. pylori-binding compounds were present among the A(Rh+)P and A(Rh+)p stomach glycosphingolipids. Ligands for BabA-mediated binding of H. pylori were the Leb hexaosylceramide, the H type 1 pentaosylceramide, and the A type 1/ALeb heptaosylceramide. Additional H. pylori-binding glycosphingolipids recognized by BabA-deficient strains were lactosylceramide, lactotetraosylceramide, the x2 pentaosylceramide, and neolactohexaosylceramide. Our characterization of human gastric receptors required for H. pylori adhesion provides a basis for the development of specific compounds that inhibit the binding of this bacterium to the human gastric mucosa.

scholarly journals Follow-up analysis and histopathological study of gastric mucosa in patients with Helicobacter pylori infection

2021 ◽  
Vol 49 (12) ◽  
pp. 030006052110553
Author(s):  
Guang Zhao ◽  
Zhishang Zhang ◽  
Baohui Li ◽  
Silin Huang ◽  
Wensi Li ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Intraepithelial Neoplasia ◽  
Mucosal Damage ◽  
Helicobacter Pylori Infection ◽  
Gastric Mucosal Damage ◽  
Histopathological Study ◽  
Significant Difference ◽  
H Pylori

Objective To investigate the histomorphological characteristics of the gastric mucosa and the prognosis in patients with Helicobacter pylori infection. Methods Progressive damage to the gastric mucosa was examined by immunohistochemistry in 2294 patients with H. pylori infection and follow-up information was analyzed. Results H. pylori initially colonized the mucus layer covered by the gastric mucosa epithelium, then selectively adhered to and destroyed the surface mucus cells causing intra-gastric and extra-gastric lesions. Gastric mucosal damage induced by H. pylori was divided into five stages according to the depth of H. pylori invasion and degree of lesion deterioration: mucilaginous, surface mucocellular, lamina propria lesion, mucosal atrophy, and intraepithelial neoplasia stages. Morphological follow-up analysis revealed no significant difference in 6-month curative effects between stage I and stage II, but significant differences were found between stages II and III, stages III and IV, and between stages IV and stage V, respectively. Conclusions This novel staging strategy may be a valuable tool for diagnosing and predicting the results of gastric mucosal damage induced by H. pylori infection.

scholarly journals Gene structure of the Helicobacter pylori cytotoxin and evidence of its key role in gastric disease.

1994 ◽  
Vol 179 (5) ◽  
pp. 1653-1658 ◽  
Author(s):  
J L Telford ◽  
P Ghiara ◽  
M Dell'Orco ◽  
M Comanducci ◽  
D Burroni ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Peptic Ulcer ◽  
Gastric Mucosa ◽  
Chronic Infection ◽  
Gastric Disease ◽  
Human Gastric Mucosa ◽  
Gastric Lesions ◽  
Gram Negative ◽  
H Pylori ◽  
Cytotoxin Gene

The gram negative, microaerophilic bacterium Helicobacter pylori colonizes the human gastric mucosa and establishes a chronic infection that is tightly associated with atrophic gastritis, peptic ulcer, and gastric carcinoma. Cloning of the H. pylori cytotoxin gene shows that the protein is synthesized as a 140-kD precursor that is processed to a 94-kD fully active toxin. Oral administration to mice of the purified 94-kD protein caused ulceration and gastric lesions that bear some similarities to the pathology observed in humans. The cloning of the cytotoxin gene and the development of a mouse model of human gastric disease will provide the basis for the understanding of H. pylori pathogenesis and the development of therapeutics and vaccines.

scholarly journals Downregulation of Interleukin- (IL-) 17 through Enhanced Indoleamine 2,3-Dioxygenase (IDO) Induction by Curcumin: A Potential Mechanism of Tolerance towards Helicobacter pylori

2018 ◽  
Vol 2018 ◽  
pp. 1-7 ◽  
Author(s):  
Tiziana Larussa ◽  
Serena Gervasi ◽  
Rita Liparoti ◽  
Evelina Suraci ◽  
Raffaella Marasco ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Antimicrobial Properties ◽  
Human Gastric Mucosa ◽  
T Cell Apoptosis ◽  
Indoleamine 2,3 Dioxygenase ◽  
Treated Sample ◽  
Tryptophan Catabolism ◽  
Gastric Biopsies ◽  
H Pylori

The anti-inflammatory and antimicrobial properties of curcumin suggest its use as an anti-Helicobacter pylori (H. pylori) agent, but mechanisms underlying its helpful activity are still not clear. Indoleamine 2,3-dioxygenase (IDO) promotes the effector T cell apoptosis by catalyzing the rate-limiting first step in tryptophan catabolism, and its high expression in H. pylori-infected human gastric mucosa attenuates Th1 and Th17 immune response. The aim of this study was to investigate the role of curcumin in modulating the expression of IL-17 and IDO in H. pylori-infected human gastric mucosa. In an organ culture chamber, gastric biopsies from 35 patients were treated with and without 200 μM curcumin. In H. pylori-infected patients (n=21), IL-17 was significantly lower, both in gastric biopsies (p=0.0003) and culture supernatant (p=0.0001) while IDO significantly increased (p<0.00001) in curcumin-treated sample compared with untreated samples. In a subgroup of H. pylori-infected patients (n=15), samples treated with curcumin in addition to IDO inhibitor 1-methyl-L-tryptophan (1-MT) showed a higher expression of IL-17 compared with untreated samples and curcumin-treated alone (p<0.00001). Curcumin downregulates IL-17 production through the induction of IDO in H. pylori-infected human gastric mucosa, suggesting its role in dampening H. pylori-induced immune-mediated inflammatory changes.

scholarly journals Interleukin-12 Drives the Th1 Signaling Pathway in Helicobacter pylori-Infected Human Gastric Mucosa

2007 ◽  
Vol 75 (4) ◽  
pp. 1738-1744 ◽  
Author(s):  
Antonia Pellicanò ◽  
Ladislava Sebkova ◽  
Giovanni Monteleone ◽  
Giovanni Guarnieri ◽  
Maria Imeneo ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Transcription Factors ◽  
Gastric Mucosa ◽  
Enzyme Linked Immunosorbent Assay ◽  
Human Gastric Mucosa ◽  
Organ Cultures ◽  
Gastric Biopsies ◽  
Ifn Γ ◽  
H Pylori ◽  
Cell Commitment

ABSTRACT In this study we examined mechanisms that regulate T-helper lymphocyte 1 (Th1) commitment in Helicobacter pylori-infected human gastric mucosa. The levels of gamma interferon (IFN-γ), interleukin-4 (IL-4), and IL-12 in total extracts of gastric biopsies taken from H. pylori-infected and uninfected patients were determined by an enzyme-linked immunosorbent assay. The levels of signal transducer and activator of transcription 4 (STAT4), STAT6, and T-box expressed in T cells (T-bet) in total proteins extracted from gastric biopsies were determined by Western blotting. Finally, the effect of a neutralizing IL-12 antibody on expression of Th1 transcription factors and the levels of IFN-γ in organ cultures of H. pylori-infected biopsies was examined. Increased levels of IFN-γ and IL-12 were found in gastric biopsy samples of H. pylori-infected patients compared to the levels in uninfected patients. In addition, H. pylori-infected biopsies exhibited high levels of expression of phosphorylated STAT4 and T-bet. Higher levels of IFN-γ and expression of Th1 transcription factors were associated with greater infiltration of mononuclear cells in the gastric mucosa. By contrast, production of IL-4 and expression of phosphorylated STAT6 were not associated with the intensity of mononuclear cell infiltration. In ex vivo organ cultures of H. pylori-infected biopsies, neutralization of endogenous IL-12 down-regulated the expression of phosphorylated STAT4 and T-bet and reduced IFN-γ production. Our data indicated that IL-12 contributes to the Th1 cell commitment in H. pylori-infected human gastric mucosa.

scholarly journals Tissue transglutaminase activity in human gastric mucosa according to Helicobacter pylori infection

2018 ◽  
Vol 243 (15-16) ◽  
pp. 1161-1164
Author(s):  
Maria Pina Dore ◽  
Giovanni Mario Pes ◽  
Alessandra Errigo ◽  
Alessandra Manca ◽  
Giuseppe Realdi
Keyword(s):  
Helicobacter Pylori ◽  
Animal Models ◽  
Gastric Mucosa ◽  
Natural History ◽  
Tissue Transglutaminase ◽  
Helicobacter Pylori Infection ◽  
Human Gastric Mucosa ◽  
Antral Mucosa ◽  
History Of ◽  
H Pylori

Tissue transglutaminase (t-TG) is a multifunctional protein involved in the healing of gastric erosions and ulcers in animal models. The aim of this study was to measure gastric t-TG activity in patients with dyspepsia according to Helicobacter pylori infection and cytotoxin-associated gene A (cagA) and vacuolating cytotoxin (vacA) subtype status. Patients undergoing upper endoscopy not taking any medications were enrolled. Tissue-TG activity was determined in homogenates of antral specimens using a radiometric assay and was expressed in pmol/mg. The cagA and vacA genotypes were determined by PCR amplification using gene-specific oligoprimers. Data from 46 patients were available (17 of them were positive for H. pylori). Antral t-TG activity was significantly increased in H. pylori positive patients compared to H. pylori negative patients (6437 ± 3691 vs. 3773 ± 1530 pmol/mg; P = 0.001) according to Mann–Whitney U test. Patients with H. pylori negative gastritis had higher t-TG activity than patients with normal gastric mucosa. The specimens infected with cagA positive strains (72%) displayed greater t-TG activity than cagA negative samples (7358 ± 4318 vs. 4895 ± 1062 pmol/mg; P = 0.237). Similarly, t-TG activity was higher in H. pylori vacA s1/m1 strains vs. vacA s1/m2 (7429 vs. 5045 pmol/mg; P = 0.744), and vacA s1/m1 vs. s2/m2 (7429 vs. 4489 pmol/mg; P = 0.651) but the results were not significant. No differences were found between histology, endoscopy features and t-TG activity. These results show that t-TG activity is significantly greater in gastritis associated with H. pylori infection, suggesting that this enzyme is induced by inflammation and may have an important role in the natural history of human gastritis. Impact statement Tissue transglutaminase (t-TG) is unique among TG enzymes because of its additional role in several physiological and pathological activities, including inflammation, fibrosis, and wound healing. The presence of t-TG has previously been described in the intestine of human and animal models, yet studies on t-TG activity in human gastric mucosa are missing. Helicobacter pylori infection is the major cause of gastritis and peptic ulcers. For the first time, our results show that t-TG activity was significantly higher in antral specimens of patients with chronic active gastritis associated with H. pylori infection compared to H. pylori negative chronic gastritis and normal antral mucosa. These findings suggest that t-TG has a role in the natural history of human gastritis, which requires further investigation but may be an avenue for new therapeutic options.

scholarly journals Variations in Helicobacter pylori Lipopolysaccharide To Evade the Innate Immune Component Surfactant Protein D

2005 ◽  
Vol 73 (11) ◽  
pp. 7677-7686 ◽  
Author(s):  
Wafa Khamri ◽  
Anthony P. Moran ◽  
Mulugeta L. Worku ◽  
Q. Najma Karim ◽  
Marjorie M. Walker ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Phase Variation ◽  
Surfactant Protein ◽  
Clinical Isolates ◽  
Surfactant Protein D ◽  
Human Gastric Mucosa ◽  
H Pylori

ABSTRACT Helicobacter pylori is a common and persistent human pathogen of the gastric mucosa. Surfactant protein D (SP-D), a component of innate immunity, is expressed in the human gastric mucosa and is capable of aggregating H. pylori. Wide variation in the SP-D binding affinity to H. pylori has been observed in clinical isolates and laboratory-adapted strains. The aim of this study was to reveal potential mechanisms responsible for evading SP-D binding and establishing persistent infection. An escape variant, J178V, was generated in vitro, and the lipopolysaccharide (LPS) structure of the variant was compared to that of the parental strain, J178. The genetic basis for structural variation was explored by sequencing LPS biosynthesis genes. SP-D binding to clinical isolates was demonstrated by fluorescence-activated cell sorter analyses. Here, we show that H. pylori evades SP-D binding through phase variation in lipopolysaccharide. This phenomenon is linked to changes in the fucosylation of the O chain, which was concomitant with slipped-strand mispairing in a poly(C) tract of the fucosyltransferase A (fucT1) gene. SP-D binding organisms are predominant in mucus in vivo (P = 0.02), suggesting that SP-D facilitates physical elimination. Phase variation to evade SP-D contributes to the persistence of this common gastric pathogen.

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