scholarly journals Failure to isolate Helicobacter pylori from stray cats indicates that H. pylori in cats may be an anthroponosis - an animal infection with a human pathogen

1997 ◽  
Vol 46 (5) ◽  
pp. 372-376 ◽  
Author(s):  
F. A. K. El-Zaatari ◽  
J. S. Woo ◽  
A. Badr ◽  
M. S. Osato ◽  
H. Serna ◽  
...  
2002 ◽  
Vol 70 (2) ◽  
pp. 606-611 ◽  
Author(s):  
Jetta J. E. Bijlsma ◽  
Barbara Waidner ◽  
Arnoud H. M. van Vliet ◽  
Nicky J. Hughes ◽  
Stephanie Häg ◽  
...  

ABSTRACT The only known niche of the human pathogen Helicobacter pylori is the gastric mucosa, where large fluctuations of pH occur, indicating that the bacterial response and resistance to acid are important for successful colonization. One of the few regulatory proteins in the H. pylori genome is a homologue of the ferric uptake regulator (Fur). In most bacteria, the main function of Fur is the regulation of iron homeostasis. However, in Salmonella enterica serovar Typhimurium, Fur also plays an important role in acid resistance. In this study, we determined the role of the H. pylori Fur homologue in acid resistance. Isogenic fur mutants were generated in three H. pylori strains (1061, 26695, and NCTC 11638). At pH 7 there was no difference between the growth rates of mutants and the parent strains. Under acidic conditions, growth of the fur mutants was severely impaired. No differences were observed between the survival of the fur mutant and parent strain 1061 after acid shock. Addition of extra iron or removal of iron from the growth medium did not improve the growth of the fur mutant at acidic pH. This indicates that the phenotype of the fur mutant at low pH was not due to increased iron sensitivity. Transcription of fur was repressed in response to low pH. From this we conclude that Fur is involved in the growth at acidic pH of H. pylori; as such, it is the first regulatory protein implicated in the acid resistance of this important human pathogen.


mBio ◽  
2011 ◽  
Vol 2 (5) ◽  
Author(s):  
Emily Goers Sweeney ◽  
Karen Guillemin

ABSTRACTFor almost 50 years,Escherichia colihas been the model for understanding how bacteria orient their movement in response to chemical cues, but recent studies of chemotaxis in other bacteria have revealed interesting variations from prevailing paradigms. Investigating the human pathogenHelicobacter pylori, Amieva and colleagues [mBio 2(4):e00098-11, 2011] discovered a new chemotaxis regulator, ChePep, which modulates swimming behavior through the canonical histidine-aspartate phosphorelay system. Functionally conserved among the epsilonproteobacteria, ChePep is essential forH. pylorito navigate deep into the stomach’s gastric glands and may be an attractive target for novel antibiotics.


2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Jiashen Zhou ◽  
Lin Zhang ◽  
Liping Zeng ◽  
Lu Yu ◽  
Yuanyuan Duan ◽  
...  

AbstractUnsaturated fatty acids (UFAs) are essential for functional membrane phospholipids in most bacteria. The bifunctional dehydrogenase/isomerase FabX is an essential UFA biosynthesis enzyme in the widespread human pathogen Helicobacter pylori, a bacterium etiologically related to 95% of gastric cancers. Here, we present the crystal structures of FabX alone and in complexes with an octanoyl-acyl carrier protein (ACP) substrate or with holo-ACP. FabX belongs to the nitronate monooxygenase (NMO) flavoprotein family but contains an atypical [4Fe-4S] cluster absent in all other family members characterized to date. FabX binds ACP via its positively charged α7 helix that interacts with the negatively charged α2 and α3 helices of ACP. We demonstrate that the [4Fe-4S] cluster potentiates FMN oxidation during dehydrogenase catalysis, generating superoxide from an oxygen molecule that is locked in an oxyanion hole between the FMN and the active site residue His182. Both the [4Fe-4S] and FMN cofactors are essential for UFA synthesis, and the superoxide is subsequently excreted by H. pylori as a major resource of peroxide which may contribute to its pathogenic function in the corrosion of gastric mucosa.


2012 ◽  
Vol 18 (S5) ◽  
pp. 27-28
Author(s):  
A. P. Alves de Matos ◽  
F. F. Vale ◽  
J. M. B. Vitor

Helicobacter pylori is a human pathogen involved in gastritis and gastric cancer whose mode of transmission remains unknown. Association of H. pylori with humans is thought to date from remote antiquity and the bacterium has apparently evolved together with the human host. A few studies have shown the presence of H. pylori in aquatic environments, which might provide a route of transmission of the bacteria to humans. A recent study has also disclosed the association of the bacteria with Acantamoeba castellanii. Amoeba are known to harbor and promote the persistence of several human pathogens in the environment, representing a significant source of contamination in community and hospital acquired infections.


Microbiology ◽  
2005 ◽  
Vol 151 (10) ◽  
pp. 3299-3311 ◽  
Author(s):  
María-Antonieta Jiménez-Pearson ◽  
Isabel Delany ◽  
Vincenzo Scarlato ◽  
Dagmar Beier

It is well established that motility is an essential virulence trait of the human gastric pathogen Helicobacter pylori. Accordingly, chemotaxis contributes to the ability of H. pylori to colonize animal infection models. Chemotactic signal transduction in H. pylori differs from the enterobacterial paradigm in several respects. In addition to a separate CheY response regulator protein (CheY1), H. pylori contains a CheY-like receiver domain (CheY2) which is C-terminally fused to the histidine kinase CheA. Furthermore, the genome of H. pylori encodes three CheV proteins consisting of an N-terminal CheW-like domain and a C-terminal receiver domain, while there are no orthologues of the chemotaxis genes cheB, cheR and cheZ. To obtain insight into the mechanisms controlling the chemotactic response of H. pylori, we investigated the phosphotransfer reactions between the purified two-component signalling modules in vitro. We demonstrate that both CheY1 and CheY2 are phosphorylated by CheA∼P and that the three CheV proteins mediate the dephosphorylation of CheA∼P, but with a clearly reduced efficiency as compared to CheY1 and CheY2. Furthermore, our data indicate retrophosphorylation of CheAY2 by CheY1∼P, suggesting a role of CheY2 as a phosphate sink to modulate the half-life of CheY1∼P.


2005 ◽  
Vol 19 (7) ◽  
pp. 421-424 ◽  
Author(s):  
Philip M Sherman ◽  
Frank YH Lin

Helicobacter pylori infection fulfills each of Koch's postulates as a human pathogen causing chronic active gastritis. Disease consequences that develop in a subset of infected subjects include peptic ulcerations, gastric adenocarcinoma and mucosa-associated lymphoid tissue lymphoma. More recently, multiple publications have advocated a role for H pylori infection in causing a variety of extraintestinal manifestations. Many of these reports suffer from being case reports or case series without adequate controls. As a result, purported manifestations may simply be coincidental in nature. On the other hand, increasing evidence supports H pylori infection as a cause of sideropenic (refractory iron deficiency) anemia. Moderate evidence supports H pylori gastric infection as a cause of some cases of immune thrombocytopenic purpura due to molecular mimicry. Guidelines should be adjusted in accordance with advancing knowledge in the field.


2005 ◽  
Vol 73 (2) ◽  
pp. 803-811 ◽  
Author(s):  
Karianne Terry ◽  
Susan M. Williams ◽  
Lynn Connolly ◽  
Karen M. Ottemann

ABSTRACT Helicobacter pylori is a human gastric pathogen associated with gastric and duodenal ulcers as well as specific gastric cancers. H. pylori infects approximately 50% of the world's population, and infections can persist throughout the lifetime of the host. Motility and chemotaxis have been shown to be important in the infection process of H. pylori. We sought to address the specific roles of chemotaxis in infection of a mouse model system. We found that mutants lacking cheW, cheA, or cheY are all nonchemotactic and infect FVB/N mice with an attenuated phenotype after 2 weeks of infection. If infections proceeded for 6 months, however, this attenuation disappeared. Histological and culture analysis revealed that nonchemotactic mutants were found only in the corpus of the stomach, while the wild type occupied both the corpus and the antrum. Further analysis showed that nonchemotactic H. pylori isolates had an increased 50% infectious dose and were greatly outcompeted when coinfected with the wild type. If nonchemotactic mutants were allowed to establish an infection, subsequent infection with the wild type partially displaced the nonchemotactic mutants, indicating a role for chemotaxis in maintenance of infection. The data presented here support four roles for chemotaxis in H. pylori mouse infections: (i) establishing infection, (ii) achieving high-level infection, (iii) maintaining an infection when there are competing H. pylori present, and (iv) colonizing all regions of the stomach.


1970 ◽  
Vol 1 (2) ◽  
pp. 129-135 ◽  
Author(s):  
M Zaidi ◽  
FA Jilani ◽  
Y Gupta ◽  
S Umair ◽  
M Gupta

Helicobacter pylori is a Gram negative, spiral-shaped, strictly micro-aerophilic and flagellate human pathogen that can inhabit many areas of stomach. H. pylori infection leads to the generation of oxygen free radicals. H. pylori infection might also aggravate the course of glaucoma by increasing the levels of nitric oxide, endothelin-1 and free radicals indirectly. This article briefly reviews the current perspectives on this issue. Keywords: Helicobacter pylori; glaucoma; free radicals DOI: 10.3126/nepjoph.v1i2.3688 Nep J Oph 2009;1(2):129-135


Author(s):  
A. R. Crooker ◽  
W. G. Kraft ◽  
T. L. Beard ◽  
M. C. Myers

Helicobacter pylori is a microaerophilic, gram-negative bacterium found in the upper gastrointestinal tract of humans. There is strong evidence that H. pylori is important in the etiology of gastritis; the bacterium may also be a major predisposing cause of peptic ulceration. On the gastric mucosa, the organism exists as a spiral form with one to seven sheathed flagella at one (usually) or both poles. Short spirals were seen in the first successful culture of the organism in 1983. In 1984, Marshall and Warren reported a coccoid form in older cultures. Since that time, other workers have observed rod and coccal forms in vitro; coccoid forms predominate in cultures 3-7 days old. We sought to examine the growth cycle of H. pylori in prolonged culture and the mode of coccoid body formation.


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