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BACKGROUND AND OBJECTIVES: There is evidence that patients with irritable bowel syndrome (IBS) have a low degree of inflammation in the intestinal mucosa. The aim of the study was to evaluate the profile of pro- and anti-inflammatory cytokines in plasma in Mexican pediatric patients with IBS. PATIENTS AND METHODS: Fifteen patients with IBS according to Rome III criteria for childhood and 15 healthy children, matched by age and sex, were included in the study. Plasma levels of tumoral necrosis factor alpha (TNF-α), interleukins 10 and 12 (IL-10, IL-12) and transforming growth factor beta (TGF-ß) were quantified and compared between groups. RESULTS: Plasma levels of IL-10 were lower in patients with IBS (86.07+21.3 pg/mL vs. 118.71+58.62 pg/mL: P=.045) and IL-12 levels were higher in patients with IBS compared to the control group of healthy children (1,204.2±585.9 pg/mL vs. 655.04±557.80 pg/mL; P=.011). The IL-10/IL-12 index was lower in patients with IBS (0.097±0.07 vs. 0.295±0.336; P=.025). Plasma concentration of TGF-ß was higher in patients with IBS (545.67±337.69 pg/mL vs. 208.48±142.21 pg/mL; P=.001). There was no difference in plasma levels of TNF-α between groups. CONCLUSIONS: This study suggests that children with IBS have a state of altered immune regulation. This is consistent with the theory of low-grade inflammatory state in these patients. Further studies are needed to elucidate the role played by these cytokines, specifically TGF-ß in the pathogenesis of IBS.

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Genotypic differences in Helicobacter pylori play an important role in infection. We characterized the diversity of the cagA, cagE, babA2, and vacA genes in H. pylori strains isolated from pediatric patients and the relationship between these genes and clinical disease. Additionally, we employed the Neighbor-net algorithm to predict the behavior of the genotypes of the strains isolated from patients. Of 93 patients analyzed, 32 were positive for infection. A total of 160 H. pylori strains (five isolates per positive patient) were analyzed. A total of 91% and 83% of strains possessed the cagA and cagE genes, respectively. For the vacA gene, 84% of strains possessed the s1 allele, 15% the s2 allele, 81% the m1 allele and 13.8% the m2 allele. The babA2 gene was present in 79% of strains. Infection with H. pylori strains with the vacA (s1m1) genotype was associated with risk of esophagitis and gastritis (p=0.0001). The combination of cagA and vacA (s1m1) was significantly associated with abdominal pain (p=0.002); however, EPIYA type was not significantly associated with abdominal pain. A total of 16 different genotypes were identified; the most common genotype was vacAs1m1cagA+cagE+babA2+ (47.5%). A total of 84% of pediatric patients were infected by at least two and up to five different genotypes. The network recovered two genotype groups (A: strains with vacAs1 and B: strains with vacAs2). The presence of multiple paths in the network suggests that reticulate events, such as recombination or reinfection, have contributed to the observed genotypic diversity.

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Infection with Helicobacter pylori has been shown to be at the origin of various gastric pathologies. However, it has not yet been established whether the etiology of such diseases, particularly of gastric cancer, is related to the production of free radicals or to mutagenesis. The aim of this study was to determine whether a six-month infection with Helicobacter pylori increased the amount of lipid peroxidation, nitric oxide, and DNA damage in Mongolian gerbils (Meriones unguiculatus). H. pylori was characterized genotypically and administered orally to the animals. Four tests were applied to identify the presence of bacteria at one, two, four, and six months after the inoculation, namely, isolation and identification in culture, the urease test, the ELISA assay, and immunohistochemical staining of gastric biopsies. The infection was considered to be successful when three of the above-mentioned tests were positive. The infection occurred in 30% of the animals in the first month after the H. pylori inoculation and in 60-70% of the animals in the later stages. Levels of malondialdehyde, nitric oxide, and DNA damage (using the "comet" assay) were determined in the gastric tissue of the animals at one, two, four, and six months. We found statistically significant increases in malondialdehyde and nitric oxide levels from the second month on. The comet assay in animals infected with H. pylori showed a significant increase in the mean tail length throughout the observation period. We conclude that our results support the assumption that oxidative damage and DNA breakage produced by the infection with H. pylori are some of the initial alterations occurring in the development of gastric diseases.

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Aflatoxin B(1) (AFB(1)) is a potent mutagenic and carcinogenic agent found in numerous agricultural and dairy products consumed by humans. Therefore, we evaluated the capacity of mannan to cope with its genotoxic potential. We prepared a diet constituted of corn (90%) plus the recommended amount of other nutrients, as well as with the tested compounds (mannan and/or AFB(1)). Mice were fed this diet during 4 weeks as follows: one group with AFB(1)-contaminated corn (0.25 mg/kg of corn), three groups with mannan (50, 250, and 500 mg/kg of corn) plus AFB(1) (0.25 mg/kg), another group with only mannan (500 mg/kg), and the last group with an uncontaminated diet and no mannan added. We determined the weight, the micronucleated normochromatic erythrocyte rate (MNNE), the polychromatic/normochromatic index, and the sister chromatid exchange rate (SCE). We also examined the recovery response of mice during 4 additional weeks, when they were fed only the normal diet without AFB(1) or mannan. The results in the first period revealed the following: a) mice fed with mannan alone presented values in the range determined for the control group; b) mice fed AFB(1) had a significant weight decrease, as well as a significant increase in the rate of MNNE and SCE; and c) animals fed the combined regimen (AFB(1) plus mannan) presented a 25% weight increase with respect to the animals treated with AFB(1) alone, as well as a significant reduction in the level of MNNE and SCE with the two high doses tested. In the second (recovery) period, the control and the mannan fed groups maintained values similar to those exhibited in the previous phase, and the AFB(1) group as well as the groups fed the regimen combined with mannan showed an improvement in all evaluated parameters; the best response was that found in mice fed AFB(1) plus 500 mg/kg of mannan. Our study established an antigenotoxic effect of mannan that could be due to its adsorbent capacity.

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