Double-stranded RNA induces IL-8 and MCP-1 gene expression via TLR3 in HaCaT-keratinocytes.

In the present study, we investigated the gene expression of IL-8 and MCP-1 in HaCaT keratinocytes in response to poly(I:C), a synthetic dsRNA analogon. Both gene inductions were found to be mediated by TLR3 and downstream signalling pathways. While poly(I:C) induced IL-8 gene expression was solely inhibited by the NF-κB inhibitor III, MCP-1 gene induction was also blocked by PKA, p38 MAPK and JAK-STAT inhibitors. Moreover, Brefeldin A, an inhibitor of the anterograde transport, suppressed MCP-1 but not IL-8 gene expression, indicating that poly(I:C)-induced cytokines are involved in the chemokine gene expression. Both chemokines were expressed in response to the pro-inflammatory cytokines TNFα and IL-1ß; however, MCP-1 gene induction was also found in response to IFNγ. These data are indicative for distinct signalling pathways in the poly(I:C)-induced gene expression of IL-8 and MCP-1 in HaCaT keratinocytes.

Prevalence of Helicobacter pylori in the adolescent oral cavity: dependence on orthodontic therapy, oral flora and hygiene.

BACKGROUND: Helicobacter pylori (HP) infection usually occurs in childhood. While there are various studies on the prevalence of HP in dental plaque, ours is the first to analyze its prevalence during orthodontic therapy and its interaction with competitive bacteria in adolescents. SUBJECTS AND METHODS: The prevalence of HP was examined before and during the first 12 weeks of orthodontic therapy with fixed appliances in 11 patients with a mean age of 12.7 years. A total of 93 plaque samples were analyzed using PCR. The data acquired at every consultation were the following: PCR analysis of dental plaque and (13)C urea breath tests for HP, quantitative analyses of saliva for Lactobacilli and Streptococcus mutans, the interproximal plaque index (API), and sulcus bleeding index (SBI). RESULTS: The prevalence of HP in plaque was 82% before orthodontic therapy, dropping to 54% during therapy (t test, p≤0.05). In contrast to HP's prevalence, the Lactobacilli count rose (p≤0.05). The number of Streptococcus mutans bacteria in saliva decreased during orthodontic therapy (p≤0.05). CONCLUSION: The prevalence of HP in dental plaque amounted to 82%. Orthodontic treatment did not reduce its prevalence. The prevalence of Lactobacilli was inversely proportional to that of HP.

Helicobacter pylori-specific immune response in maternal serum, cord blood, and human milk among mothers with and without current Helicobacter pylori infection.

We assessed the patterns of Helicobacter pylori (H. pylori) specific maternal antibodies in maternal serum, cord blood, and milk, which might play a role in prevention of H. pylori infection because transferred to the infant. Between November 2000 and November 2001, mothers were recruited after delivery of their offspring. H. pylori infection status was determined by 13C-urea breath test (UBT). Specific H. pylori antibody profiles were analysed using commercial H. pylori-specific enzyme-linked immunosorbent assay and Western blots. Among 898 mothers, 23% had a current H. pylori infection. Median H. pylori IgG antibody titers in serum and cord blood of UBT-positive mothers were 23.8 U/mL and 24.0 U/mL, respectively. Whereas prevalences of H. pylori-specific antibodies in serum of UBT-negative mothers were clearly lower than those among UBT-positive mothers, patterns of H. pylori-specific IgA antibodies in milk were similar among UBT-positive and UBT-negative mothers. Neonates born from H. pylori-infected women are provided with large amounts of transplacentally transferred specific IgG H. pylori antibodies. Breast-fed neonates are additionally provided with specific IgA antibodies in human milk. Notably, the latter may also be activated if exposure of the mother to H. pylori might have been long time ago and been cleared in the meantime.

Role of Helicobacter pylori infection in iron deficiency during pregnancy.

OBJECTIVE: We investigated the possible role of Helicobacter pylori infection in iron deficiency during pregnancy in a large group of mothers in Germany after the birth of their baby under special consideration of iron supplementation. STUDY DESIGN: All women who were delivered of their baby between November 2000 and November 2001 at the Department of Gynecology and Obstetrics at the University of Ulm, Germany, were recruited for the study. Hemoglobin levels at various points of time during pregnancy were obtained from the mothers' health charts. Current H pylori infection was determined by 13 C-urea breath test. We used multiple linear regression analyses to assess the impact of infection status on hemoglobin level at the beginning of pregnancy and on hemoglobin change during pregnancy. RESULTS: Twenty-three percent of the 898 mothers had a H pylori infection, and 20% of the mothers had a hemoglobin level below 12 g/dL at the beginning of pregnancy. Compared with uninfected mothers, mothers with H pylori infection had a lower mean hemoglobin level at the beginning of pregnancy (-0.25 g/dL; 95% CI, -0.49, -0.003) and a more unfavorable change in hemoglobin level during pregnancy (-0.14 g/dL; 95% CI, -0.38, 0.10). CONCLUSION: This study supports a possible moderate, but still relevant, independent role of H pylori infection in iron deficiency during pregnancy.

Role of Lewis A and Lewis B blood group antigens in Helicobacter pylori infection.

BACKGROUND AND AIMS: We investigated the prevalence of Helicobacter pylori infection in a large group of women to determine whether there was an association of current infection status with Lewis blood group antigen A and B phenotype. METHODS: Between November 2000 and November 2001, mothers were recruited after delivery of their offspring at the Department of Gynecology and Obstetrics at the University of Ulm, Ulm, Germany. The H. pylori infection status of the women was determined by 13C urea breath test. Their Lewis A and Lewis B phenotype was determined using standard laboratory techniques. RESULTS: In total, 22.2% of the 712 women included in the study (mean age 30.7 years) had a current H. pylori infection. The prevalence of infection varied from 15.5% in women of German nationality to 75.0% in women of Turkish nationality (p < .001). Most women (68.1%) had a Le(a-b+) phenotype. The prevalence of H. pylori infection in women with Le(a-b+) phenotypes was lower than in other women (p = .02). In multivariate analysis, the odds ratio (OR) for a current H. pylori infection given Le(a-b+) was 0.56 [95% confidence interval (CI) 0.33-0.95] compared to women with Le(a-b-). CONCLUSION: Le(a-b+) blood group phenotype in combination with secretor status may hinder colonization of H. pylori in the population studied.

Comparison of different criteria for interpretation of immunoglobulin G immunoblotting results for diagnosis of Helicobacter pylori infection.

Gastric infection with Helicobacter pylori is one of the most common chronic infections in humans, causing substantial morbidity and mortality. The diagnosis of H. pylori infection usually involves upper endoscopy with biopsy since the only noninvasive method of comparable accuracy, the [(13)C]urea breath test, requires technical equipment that is not available in most gastroenterological units. Serological methods for detection of H. pylori infection have reached sufficient accuracy to be used as screening tests before endoscopy or for seroepidemiological surveys. In the present study we evaluated different interpretation criteria for use with immunoglobulin G immunoblotting for the diagnosis of H. pylori infection. We applied five different sets of interpretation criteria, four of which had been published previously, to the Western blot results of 294 patients with different gastrointestinal symptoms. Since it is known that less than 2% of patients who are infected with H. pylori fail to seroconvert, an optimally sensitive Western blotting system should be able to detect approximately 98% of active infections. When the different criteria were applied to our patient population, it became apparent that the abilities of the systems to detect active H. pylori infection were quite varied. The results for the sensitivity and specificity, according to the different applied criteria, ranged from 62.8 to 95.9% and from 85.7 to 100.0%, respectively. Positive predictive values and negative predictive values, according to the published criteria, ranged from 97.2 to 100.0% and from 37.7 to 82.4%, respectively. Recommendations for the optimal use of the different interpretation criteria are discussed.

Recurrent abdominal pain in children: evidence from a population-based study that social and familial factors play a major role but not Helicobacter pylori infection.

OBJECTIVE: To analyze the relationship between social and familial factors, Helicobacter pylori infection and recurrent abdominal pain (RAP) in children in a population-based cross-sectional study among 1221 preschool children aged 5-8 years. METHODS: H. pylori infection status was determined by 13C-urea breath test (13C-UBT) and information on medical history of the child and on RAP as well as on family demographics was obtained by a standardized questionnaire. RESULTS: Overall, 129 children (11.3%) were infected with H. pylori and 29 children were identified as having RAP within the past 3 months (2.5%). Analysis by multiple logistic regression demonstrated a clear relationship of RAP with living in a single parent household [odds ratio (OR) 2.9, 95% confidence interval (95% CI) 1.2-6.7], with parental history of peptic ulcer (OR 3.7, 95% CI 1.3-10.4) and with parental history of nonulcer gastrointestinal disorders (OR 5.3, 95% CI 2.1-13.2). By contrast, there was a nonsignificant relation between H. pylori infection and occurrence of RAP (OR 1.6, 95% CI 0.5-5.5). CONCLUSION: Social and familial factors play a major role but not H. pylori infection in RAP.

Helicobacter pylori-specific immune responses of children: implications for future vaccination strategy.

We analyzed the specific anti-Helicobacter pylori immunoglobulin G (IgG) antibody profile for a sample of 824 asymptomatic schoolchildren in southern Germany (mean age, 10.7 +/- 0.65 years) with an H. pylori-specific IgG enzyme-linked immunosorbent assay and Western blot analysis. The prevalence of infection was 19.8% (95% confidence interval, 17.1 to 22.7%). The immunoresponses were characterized predominantly by antibodies against low-molecular-mass antigens of 14 and 29 kDa, with a significant difference between children of German and Turkish nationalities (P = 0.0012 and P < 0.0001, respectively).

Risk of gastric cancer among smokers infected with Helicobacter pylori.

Infection with the gastric bacterium Helicobacter pylori (in particular infection with CagA-positive strains) and smoking have been identified as risk factors for the development of gastric cancer. Both risk factors are typically acquired early in life and prevail over decades if not for life. We assessed the individual and joint impact of both risk factors on gastric cancer risk in a population-based case-control study from Germany including 71 patients with histologically verified gastric cancer and 363 patients with colorectal cancer who served as controls. Information on smoking and potential confounding factors was collected by standardized interviews. H. pylori infection was measured serologically by immunoglobulin G antibody titers against H. pylori. In addition, antibodies against the CagA antigen were determined by Western blot. Twenty-seven percent of cases compared with 15% of controls were smokers, and 43% of cases compared with 23% of controls were infected with CagA-positive H. pylori strains. After control for potential confounders, the relative risk of gastric cancer was 2.6 (95% CI 1.2-5.7) for nonsmoking subjects with CagA-positive H. pylori infections and 7.2 (95% CI 2.2-23.6) for smoking subjects with CagA-positive H. pylori infections compared with subjects without these risk factors. The corresponding relative risks for noncardia gastric cancer were 6.1 ( 95% CI 2.3-16.5) and 16.6 (95% CI 4.3-64.2). We conclude that smoking subjects with CagA-positive H. pylori infections have a strongly increased risk of gastric cancer and may be an important group for targeting efforts of prevention and early detection.