Chittoor M. Habibullah

Antimicrobial activities of Eugenol and Cinnamaldehyde against the human gastric pathogen Helicobacter pylori

BackgroundEradication of Helicobacter pylori is an important objective in overcoming gastric diseases. Many regimens are currently available but none of them could achieve 100% success in eradication. Eugenol and cinnamaldehyde that are commonly used in various food preparations are known to possess antimicrobial activity against a wide spectrum of bacteria.AimThe present study was performed to assess the in vitro effects of eugenol and cinnamaldehyde against indigenous and standard H. pylori strains, their minimum inhibitory concentrations (MICs) and time course lethal effects at various pH.MethodsA total of 31 strains (29 indigenous and one standard strain of H. pylori ATCC 26695, one strain of E. coli NCIM 2089) were screened. Agar dilution method was used for the determination of drug sensitivity patterns of isolates to the commonly used antibiotics and broth dilution method for the test compounds.ResultsEugenol and cinnamaldehyde inhibited the growth of all the 30 H. pylori strains tested, at a concentration of 2 μg/ml, in the 9th and 12th hours of incubation respectively. At acidic pH, increased activity was observed for both the compounds. Furthermore, the organism did not develop any resistance towards these compounds even after 10 passages grown at sub-inhibitory concentrations.ConclusionThese results indicate that the two bioactive compounds we tested may prevent H. pylori growth in vitro, without acquiring any resistance.

Study of duodenal ulcer disease in 100 families using total serum pepsinogen as a genetic marker.

Although various markers have been used in attempts to elucidate the mode of inheritance of duodenal ulcer, they have not significantly contributed to a clear understanding of the problem. In the present study total serum pepsinogen was used as a genetic marker and its concentrations were estimated in 100 ulcer patients and their family members up to three generations. Eighty three per cent of the ulcer patients had hyperpepsinogenaemia on a familial basis, and it followed an autosomal dominant mode of inheritance. Thus a large majority of ulcer patients have associated hyperpepsinogenaemia which forms a genetic basis of their disease. The remaining 17% ulcer patients did not have associated hyperpepsinogenaemia nor was the ulcer inherited by the family. Based on these observations we wish to suggest that duodenal ulcer associated with hyperpepsinogenaemia may be considered a genetic disease. This type may be termed primary duodenal ulcer. In the remaining patients without hyperpepsinogenaemia or affected relatives the ulcer may be called secondary duodenal ulcer. Thus total serum pepsinogen may be considered a reliable genetic marker in helping to delineate the genetic disorder from the non-genetic, thereby improving the predictive ability in duodenal ulcer.

Analysis of mutations within the 5' untranslated region, interferon sensitivity region, and PePHD region as a function of response to interferon therapy in hepatitis C virus-infected patients in India.

ABSTRACT Mutations in several subgenomic regions have been implicated in influencing response to interferon therapy; however, a comprehensive picture of Indian patients was lacking. Based on the viral load and clinical factors, 10 out of 15 patients were found to be complete responders, whereas 5 patients were nonresponders. The pretreatment viral RNA load of the patients was found to be between 5.20 and 6.13 log10 IU/ml, which eventually fell to 2.77 log10 IU/ml after 24 weeks of treatment, whereas in the case of nonresponders, the average was 5.38 log10 IU/ml. In order to study the influence of the hepatitis C virus genotype on the response to interferon therapy, the 5′ untranslated region sequences of the samples were analyzed, which showed that genotype 3 patients responded better than genotype 1 patients. Additionally, the mutations in the interferon sensitivity-determining region (ISDR) of the NS5A protein and the double-stranded RNA-activated protein kinase-eukaryotic initiation factor 2 alpha phosphorylation homology domain (PePHD) of the E2 envelope protein, before and after treatment, were compared with nonresponder prototype J. Although, no clear correlation was found in the case of the mutated ISDR, some significant changes in residues were observed in the PePHD region, which could be helpful in understanding the molecular basis of resistance to therapy. Interestingly, analysis of the quasispecies variations showed a change in genotype in one sample during treatment, which might have contributed to the resistance. The results suggest that the mutations in different regions of the viral genome might have a concerted effect on the response to interferon therapy.

Implications of Molecular Genotyping of Helicobacter pylori Isolates from Different Human Populations by Genomic Fingerprinting of Enterobacterial Repetitive Intergenic Consensus Regions for Strain Identification and Geographic Evolution

ABSTRACT Biogeographic partitioning of the genome is typical of the gastric pathogen Helicobacter pylori. Such population-specific evolution could serve as a model for understanding host-pathogen interaction and the impact of genetic drift and recombination on insular populations. With a total of 320 isolates from six geographic regions (Japan, India, England, Spain, Ireland, Africa, and Peru) analyzed by enterobacterial repetitive intergenic consensus (ERIC)-based genotyping, we examined genetic affinities among various H. pylori populations in the world. Several strain-specific and region-specific differences were observed by ERIC-based typing. Polymorphic ERIC patterns indicated that the ERIC sequences are in fact dispersed in the H. pylori chromosome at different locations separated by various distances. Phylogenetic analysis of 61 representative isolates revealed three distinct genetic clusters populated by isolates with shared ERIC types independent of the cag right-junction motif type and vacA allele status. Among the notable genetic relationships were the genotypic similarities between Irish and Japanese and between Peruvian and Japanese isolates. Insular genotypic characteristics of Irish isolates amid genetic similarity to East Asian, as well as North European, strains have been once again proved in this study. Peruvian genotypes were more similar to those of Japanese isolates than to those of Iberian or European isolates. Given the current debate on the origin and age of present-day H. pylori, this is a significant finding that supports the possibility of ancient colonization of Amerindians with East Asian strains. Genotypic data presented here will be additionally helpful in realizing the importance of H. pylori geographical genomics in the development of gastroduodenal pathology.

Serum alpha1-antitrypsin and haptoglobin phenotypes in vitiligo

The role of genetic factors in the etiology of vitiligo has been discussed by some workers [5, 8], and the familial incidence of vitiligo transmitted by an autosomally dominant gene of variable penetrance has already been established [8]. About 40% of patients report a positive family history of the disease [5]. Dermatoglyphic patterns, such as increased frequency of whorls and arches and decreased total finger ridge count have been associated with vitiligo [5]. In view of the reported genetic markers associated with vitiligo we studied the serum alphal-antitrypsin and haptoglobin (Hp) phenotypes in vitiligo patients to further establish the role of genetic factors in the etiology of this disease. From the Central Research Institute for Unani Medicine in Hyderabad, 90 vitiligo patients of both sexes, aged between 15 and 40 years (mean age 28.3 • 9.2 years), were selected. The study was conducted in the Department of Gastroenterology at Osmania General Hospital, Hyderabad, India. Blood samples were collected from patients and controls; serum was separated on the same day. Serum alphal.antitrypsin was measured on the basis of serum trypsin inhibitor capacity (STIC) using denatured hemoglobin substrate as described by Jaccobson [6]. Hp typing was analysed in accordance with the method of Clark [3]. In controls, STIC and Hp typing was not seen in the same individuals; different individuals were taken for each test. In patients, both tests were made in the same individuals. The statistical significance of the difference in distribution of STIC in patients and controls was determined using Students t-test. The frequency of Hp types in the patients and controls was compared and the variati-

Xenogenic transplantation of microencapsulated hepatocytes: ureagenesis of retrieved encapsulated hepatocytes

Abstract The microencapsulation technique is being used successfully in various types of cells for providing a substratum for long-term survival and immunoprotection to immobilized transplanted cells. Rat hepatocytes were microencapsulated in alginic acid poly-l-lysine membrane and transplanted intraperitoneally in rabbits. The animals were followed up to study the functional capacity of transplanted hepatocytes by assessing ureagenesis and the efficacy of the capsule membrane to provide a physical barrier between the hosts immune system and the encapsulated hepatocytes, assessed by no evidence of hepatocyte rejection by the host for up to 2 months. The transplanted animals were sacrificed by cervical dislocation after 15, 30, 45 and 60 days. The transplanted capsules were retrieved and the hepatocytes were studied for their capacity for ureagenesis. The capsules were found intact even after 60 days of transplantation. The retrieval was 75% with 80% of viable cells displaying normal functional capacity to produce urea. Therefore, it may be concluded that the microencapsulation technique is effective in maintaining functional capacity and providing a physical barrier between the hosts immune system and immobilized cells.

Elevated Urinary Pepsinogen: A Subclinical Marker of Ulcer Diathesis

DOI: http://dx.doi.org/10.5915/22-3-14307 Urinary pepsinogen levels were determined in 314 patients with peptic ulcer and in 100 healthy controls to see if possible role in pathogenesis of peptic ulcer and to recognize elevated levels of urinary pepsinogen as a subclinical marker of ulcer diathesis. All patients studied were endoscopically proved to have peptic ulcer. Significantly elevated urinary pepsinogen levels were observed in patients with duodenal ulcer, pyloric ulcer and stomal ulcer, but increased level of urinary pepsinogen in gastric ulcer was not statistically significant when compared with controls. Sixteen percent of patients with duodenal ulcer had pepsinogen levels similar to the control group.

The Role of Constitutional and Environmental Factors in Susceptibility to Duodenal Ulcer

DOI: http://dx.doi.org/10.5915/21-4-13512 We studied 1250 duodenal ulcer patients during an eight year period to see the role of constitutional and environmental factors in the etiology of duodenal ulcer disease. All the patients studied were endoscopically proven to have duodenal ulcer. In our area, duodenal ulcer was found 15 times more frequently than gastic ulcer. It was more common in males and the highest incidence was recorded between 20 and 40 years of age. The disease was unaffected by the seasons and no significant ethnic variation was observed; however, the disease was associated with belonging to low income groups and unskilled professions. It was more common among rice eaters, those who were irregular in taking meals, and it was common in nonvegetarians. Consumption of alcohol, tea or coffee was not associated with the disease, but the disease was more prevalent among smokers than nonsmokers. Pan chewing habit did not have any bearing on the disease pattern.

Genetic Markers in Duodenal Ulcer Disease

DOI: http://dx.doi.org/10.5915/20-2-13284 A study has been carried out on 100 endoscopically proven duodenal ulcer patients and in 100 healthy controls to examine the role of genetic factors in the development of duodenal ulcer disease. Serum pepsinogen levels, serum alpha-J-antitrypsin, haptoglobin phenotyping and ABO blood groups served as genetic markers. Hyperpepsinogenemia, deficiency of alpha-1-antitrypsin, haptoglobin 2-2 typing and O blood group were found to be associated with duodenal ulcer disease.