Seroprevalence of fasciolosis and the difference of fasciolosis between rural area and city center in Isparta, Turkey.

OBJECTIVE: To investigate the seroprevalence of fasciolosis and the possible causes of differences between rural and city center. METHODS: We undertook a multi-stage sampling analysis of data from Isparta, Turkey, between March and June 2004. Four hundred and fifteen individuals participants from Isparta center and 171 from Asagi Gokdere village were included in the study. Fasciola hepatica (F. hepatica) specific antibodies were analyzed using excretory-secretory (ES)-enzyme-linked immunosorbent assay (ELISA) method. RESULTS: Fasciola hepatica antibodies were detected as positive in 10 (2.4%) of 415 people whose sera were collected from the city center and 16 (9.3%) of 171 people from Asagi Gokdere village. The positivity rates between village and city center were found statistically significant. A statistical difference was noted for fasciolosis positivity between individuals who have ingested water cress and who have not. Fasciolosis was not detected in the individuals who used to wash vegetables with water containing vinegar. CONCLUSION: Most of the patients in this region reported consumption of uncooked or unwashed water cress. Watering channel is one of the major risk factors of fasciolosis. Therefore, it is essential to determine the watering systems in this region. Moreover, ES-ELISA would be useful in investigating the laboratory diagnosis of fasciolosis.

Infection with Chlamydia pneumoniae but not Helicobacter pylori is related to elevated apolipoprotein B levels.

OBJECTIVE: Results of many studies show that apolipoprotein B (apo B) is a better marker of risk of vascular disease than other lipid markers including LDL and HDL-cholesterol and triglycerides. We investigated the association between two infectious agents: C. pneumoniae and H. pylori, known to have an atherogenic effect, and apo B, to evaluate the effects of chronic infections on apo B levels. METHODS AND RESULTS: The study group consisted of 257 patients in whom diagnostic coronary angiography was performed. C. pneumoniae IgG and IgM and H. pylori IgG and IgA antibodies were measured by enzyme-linked immunosorbent assay and apo B levels were measured by the nephelometry method. Established risk factors of atherosclerosis were recorded. Of 257 patients recruited, 104 had normal vessels, 88 had 3 or more vessels obstructed and 65 had ectatic vessels without atherosclerosis. Mean apo B concentration was significantly higher in C. pneumoniae IgG and IgM positive healthy subjects compared with C. pneumoniae negatives (0.954 vs. 0.722 and 0.973 vs. 0.851, p < 0.001 and p = 0.007, respectively). Apo B levels were significantly higher in severe atherosclerotic patients (0.985 +/- 0.234 g/l) compared with control subjects (0.892 +/- 0.244 g/l) (p = 0.008), but the difference was not significant in ectatic subjects (0.946 +/- 0.272 g/l) when compared with controls (p = 0.18). Apo B levels were higher but not statistically significant in H. pylori antibody positive cases when compared with negatives. CONCLUSIONS: Apo B levels increased with C. pneumoniae infection. This finding supports the hypothesis that lipid profiles change to atherogenic lipid profile in chronic infections.

Detection of Helicobacter pylori and Chlamydia pneumoniae DNA in human coronary arteries and evaluation of the results with serologic evidence of inflammation.

OBJECTIVE: Atherosclerosis is pathologically similar to a chronic inflammatory response. Recent reports have suggested that Chlamydia pneumoniae (C. pneumoniae) and Helicobacter pylori (H. pylori) play a role in the pathogenesis of atherosclerosis but this relation has not been confirmed on an inflammatory background. METHODS: Twenty-nine consecutive patients admitted to Suleyman Demirel University Medical School Cardiovascular Surgery Department, Isparta, Turkey between May 2002 to June 2003 were included in the study and the presence of C. pneumoniae and H. pylori DNA in atherosclerotic plaques of 14 coronary endarterectomy specimens and 15 left internal mammarian artery (LIMA) specimens as control subjects were determined by polymerase chain reaction. Serologic evidence of infection and inflammatory markers were also determined in both groups. RESULTS: Two C. pneumoniae DNA cases from the plaque group (14.3%) and 4 H. pylori DNA cases; 3 from plaque (21.4%) and one from the LIMA groups (6.7%) were detected. The C-reactive protein (mg/L) were higher in DNA positive samples of C. pneumoniae (66.58) and H. pylori (21.93) compared to DNA negatives of C. pneumoniae (8.49) and H. pylori (10.98), similarly interleukin-6 (U/L) levels were higher in DNA positive samples of C. pneumoniae (42.25) and H. pylori (56.37) compared with DNA negatives of C. pneumoniae (17.52) and H. pylori (13.28), but the differences were not statistically significant. Apolipoprotein B levels were significantly higher in C. pneumoniae immunoglobulin M positive cases (0.844 g/L) compared with negatives (0.661 g/L) (p=0.004). CONCLUSION: Chronic infections modify the serum lipid profile in a way that increases the risk of atherosclerosis. The increased titers of inflammation markers in DNA positive patients support inflammation in atherosclerosis, however, the results should be reproduced in a larger cohort.

Preventive effect of probiotics and α-tocopherol on ethanol-induced gastric mucosal injury in rats.

The protective effect of a probiotic mixture of 13 different bacteria and α-tocopherol on 98% ethanol-induced gastric mucosal injury was evaluated. Levels of gastric mucosal pro- and anti-inflammatory cytokines, malondialdehyde, and secretory immunglobulin A were measured. Rats were allocated into four groups: control, ethanol, probiotic, and α-tocopherol. The control and ethanol groups received skim milk for 14 days. Probiotic and α-tocopherol groups were administered probiotic mixture suspended in skim milk and 100 mg/kg α-tocopherol, respectively, by daily gavage for 14 days. On Day 15, gastric lesions were induced by administration of ethanol 98% (1 mL) to all rats except those in the control group. Probiotic, but not α-tocopherol, seemed to inhibit ethanol-induced gastric mucosal tumor necrosis factor-α, interferon-γ, and interleukin-2 production (P > .05). Ethanol caused the elevation of mucosal interleukin-4 level (compared to the control, P < .05). Probiotic pretreatment significantly suppressed the ethanol-induced increase of gastric mucosal interleukin-4 levels. Pretreatment with either probiotic or α-tocopherol inhibited the ethanol-induced increase of mucosal malondialdehyde concentration (P < .01 and P < .05, respectively). Probiotic pretreatment enhanced the gastric mucosal secretory immunoglobulin A concentration (P < .001). In conclusion, probiotic mixture and α-tocopherol reduced ethanol-induced gastric mucosal lipid peroxidation, suggesting that they may be beneficial for gastric lesions induced by lower ethanol concentration.

Effect of probiotics on aspirin-induced gastric mucosal lesions.

BACKGROUND/AIMS: We aimed to investigate the role of a probiotic mixture, including 13 different bacteria, in the prevention of aspirin-induced gastric mucosal injury. METHODS: Forty rats were allocated into 4 groups: normal control, aspirin, probiotic control, and probiotic plus aspirin. Normal control and aspirin groups received 0.2 ml of skim milk by daily gavage for 14 days. Probiotic control and probiotic plus aspirin groups were administered 0.2 ml/day of probiotic mixture (1.3 x 10(10) cfu/ml) suspended in skim milk by daily gavage for 14 days. On day 15, gastric lesions were induced by administration of aspirin (200 mg/kg) in the aspirin and probiotic plus aspirin groups. Normal control and probiotic control groups were given saline. RESULTS: Pretreatment with probiotic mixture reduced aspirin-induced gastric damage scores (4.50 ± 0.43 and 2.60 ± 0.40, p<0.01) and exerted tendency of downregulation of proinflammatory cytokines elicited by aspirin (p>0.05). We also found that the probiotic mixture increased sIgA production approximately 7.5-fold in the stomach, and significantly reduced the malondialdehyde (MDA) increase in the gastric mucosa elicited by aspirin (p<0.001). Additionally, pretreatment with the probiotic mixture alleviated aspirin-induced reduction of mast cell count in the gastric mucosa. CONCLUSIONS: Probiotic mixture pretreatment attenuates the aspirin-induced gastric lesions by reducing the lipid peroxidation, enhancing mucosal sIgA production, and stabilizing mucosal mast cell degranulation into the gastric mucosa.