scholarly journals LINFOMI ASSOCIATI ALL’INFEZIONE DA Helicobacter pylori, Borrelia burgdorferi e Campylobacter jejuni

2005 ◽  
Vol 20 (3) ◽  
Author(s):  
C. Doglioni
Planta Medica ◽  
2008 ◽  
Vol 74 (09) ◽  
Author(s):  
C Cwikla ◽  
K Schmidt ◽  
A Matthias ◽  
KM Bone ◽  
RP Lehmann ◽  
...  

GeroScience ◽  
2020 ◽  
Vol 42 (5) ◽  
pp. 1365-1376
Author(s):  
Marius Zeeb ◽  
Tobias Kerrinnes ◽  
Luka Cicin-Sain ◽  
Carlos A. Guzman ◽  
Wolfram Puppe ◽  
...  

Abstract Immunostimulation by chronic infection has been linked to an increased risk for different non-communicable diseases, which in turn are leading causes of death in high- and middle-income countries. Thus, we investigated if a positive serostatus for pathogens responsible for common chronic infections is individually or synergistically related to reduced overall survival in community dwelling elderly. We used data of 365 individuals from the German MEMO (Memory and Morbidity in Augsburg Elderly) cohort study with a median age of 73 years at baseline and a median follow-up of 14 years. We examined the effect of a positive serostatus at baseline for selected pathogens associated with chronic infections (Helicobacter pylori, Borrelia burgdorferi sensu lato, Toxoplasma gondii, cytomegalovirus, Epstein-Barr virus, herpes simplex virus 1/2, and human herpesvirus 6) on all-cause mortality with multivariable parametric survival models. We found a reduced survival time in individuals with a positive serostatus for Helicobacter pylori (accelerated failure time (AFT) − 15.92, 95% CI − 29.96; − 1.88), cytomegalovirus (AFT − 22.81, 95% CI − 36.41; − 9.22) and Borrelia burgdorferi sensu lato (AFT − 25.25, 95% CI − 43.40; − 7.10), after adjusting for potential confounders. The number of infectious agents an individual was seropositive for had a linear effect on all-cause mortality (AFT per additional infection − 12.42 95% CI − 18.55; − 6.30). Our results suggest an effect of seropositivity for Helicobacter pylori, cytomegalovirus, and Borrelia burgdorferi sensu lato on all-cause mortality in older community dwelling individuals. Further research with larger cohorts and additional biomarkers is required, to assess mediators and molecular pathways of this effect.


2019 ◽  
Vol 73 (1) ◽  
pp. 457-480 ◽  
Author(s):  
Jennifer A. Taylor ◽  
Sophie R. Sichel ◽  
Nina R. Salama

Helical cell shape appears throughout the bacterial phylogenetic tree. Recent exciting work characterizing cell shape mutants in a number of curved and helical Proteobacteria is beginning to suggest possible mechanisms and provide tools to assess functional significance. We focus here on Caulobacter crescentus, Vibrio cholerae, Helicobacter pylori, and Campylobacter jejuni, organisms from three classes of Proteobacteria that live in diverse environments, from freshwater and saltwater to distinct compartments within the gastrointestinal tract of humans and birds. Comparisons among these bacteria reveal common themes as well as unique solutions to the task of maintaining cell curvature. While motility appears to be influenced in all these bacteria when cell shape is perturbed, consequences on niche colonization are diverse, suggesting the need to consider additional selective pressures.


1992 ◽  
Vol 108 (3) ◽  
pp. 457-462 ◽  
Author(s):  
M. J. Webberley ◽  
J. M. Webberley ◽  
D. G. Newell ◽  
P. Lowe ◽  
V. Melikian

SUMMARYAn enzyme-linked immunosorbent assay has been used to diagnose serologically the prevalence ofHelicobacter pyloriinfection in Asian life-long vegans. There was no difference in the seropositivity between these individuals and a group of age-and sex-matched Asian meat-eaters, indicating the meat consumption is not a risk factor forH. pyloriinfection. However, both Asian groups had a higher prevalence of infection than age- and sex-matched Caucasian meat-eaters. Additionally, the Asian individuals had a wider range of specific IgG antibody concentrations than the Caucasians. This did not appear to be due to antigenic cross-reactivity betweenH. pyloriandCampylobacter jejuni. The significance of these observations to the establishment of cut-off levels for the serodiagnosis of certain ethnic groups is discussed.


2006 ◽  
Vol 51 (3) ◽  
pp. 868-876 ◽  
Author(s):  
Paul S. Hoffman ◽  
Gary Sisson ◽  
Matthew A. Croxen ◽  
Kevin Welch ◽  
W. Dean Harman ◽  
...  

ABSTRACT Nitazoxanide (NTZ) exhibits broad-spectrum activity against anaerobic bacteria and parasites and the ulcer-causing pathogen Helicobacter pylori. Here we show that NTZ is a noncompetitive inhibitor (Ki , 2 to 10 μM) of the pyruvate:ferredoxin/flavodoxin oxidoreductases (PFORs) of Trichomonas vaginalis, Entamoeba histolytica, Giardia intestinalis, Clostridium difficile, Clostridium perfringens, H. pylori, and Campylobacter jejuni and is weakly active against the pyruvate dehydrogenase of Escherichia coli. To further mechanistic studies, the PFOR operon of H. pylori was cloned and overexpressed in E. coli, and the multisubunit complex was purified by ion-exchange chromatography. Pyruvate-dependent PFOR activity with NTZ, as measured by a decrease in absorbance at 418 nm (spectral shift from 418 to 351 nm), unlike the reduction of viologen dyes, did not result in the accumulation of products (acetyl coenzyme A and CO2) and pyruvate was not consumed in the reaction. NTZ did not displace the thiamine pyrophosphate (TPP) cofactor of PFOR, and the 351-nm absorbing form of NTZ was inactive. Optical scans and 1H nuclear magnetic resonance analyses determined that the spectral shift (A 418 to A 351) of NTZ was due to protonation of the anion (NTZ−) of the 2-amino group of the thiazole ring which could be generated with the pure compound under acidic solutions (pKa = 6.18). We propose that NTZ− intercepts PFOR at an early step in the formation of the lactyl-TPP transition intermediate, resulting in the reversal of pyruvate binding prior to decarboxylation and in coordination with proton transfer to NTZ. Thus, NTZ might be the first example of an antimicrobial that targets the “activated cofactor” of an enzymatic reaction rather than its substrate or catalytic sites, a novel mechanism that may escape mutation-based drug resistance.


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