scholarly journals The dps Gene of Symbiotic “Candidatus Legionella jeonii” in Amoeba proteus Responds to Hydrogen Peroxide and Phagocytosis

2006 ◽  
Vol 188 (21) ◽  
pp. 7572-7580 ◽  
Author(s):  
Miey Park ◽  
Seong Tae Yun ◽  
Sue-Yun Hwang ◽  
Choong-Ill Chun ◽  
Tae In Ahn
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Host Cell ◽  
Genomic Library ◽  
Amoeba Proteus ◽  
Host Cells ◽  
Intracellular Pathogens ◽  
Protective Mechanisms ◽  
Dps Protein ◽  
Cloned Gene

ABSTRACT To survive in host cells, intracellular pathogens or symbiotic bacteria require protective mechanisms to overcome the oxidative stress generated by phagocytic activities of the host. By genomic library tagging, we cloned a dps (stands for DNA-binding protein from starved cells) gene of the symbiotic “Candidatus Legionella jeonii” organism (called the X bacterium) (dps X) that grows in Amoeba proteus. The gene encodes a 17-kDa protein (pI 5.19) with 91% homology to Dps and DNA-binding ferritin-like proteins of other organisms. The cloned gene complemented the dps mutant of Escherichia coli and conferred resistance to hydrogen peroxide. DpsX proteins purified from E. coli transformed with the dps X gene were in oligomeric form, formed a complex with pBlueskript SKII DNA, and protected the DNA from DNase I digestion and H2O2-mediated damage. The expression of the dps X gene in “Candidatus Legionella jeonii” was enhanced when the host amoeba was treated with 2 mM H2O2 and by phagocytic activities of the host cell. These results suggested that the Dps protein has a function protective of the bacterial DNA and that its gene expression responds to oxidative stress generated by phagocytic activities of the host cell. With regard to the fact that invasion of Legionella sp. into respiratory phagocytic cells causes pneumonia in mammals, further characterization of dps X expression in the Legionella sp. that multiplies in a protozoan host in the natural environment may provide valuable information toward understanding the protective mechanisms of intracellular pathogens.

scholarly journals Prison Break: Pathogens' Strategies To Egress from Host Cells

2012 ◽  
Vol 76 (4) ◽  
pp. 707-720 ◽  
Author(s):  
Nikolas Friedrich ◽  
Monica Hagedorn ◽  
Dominique Soldati-Favre ◽  
Thierry Soldati
Keyword(s):  
Host Cell ◽  
Pathogenic Bacteria ◽  
Wide Spectrum ◽  
Host Cells ◽  
Host Immune System ◽  
Intracellular Pathogens ◽  
Pathogenic Yeast ◽  
Apicomplexan Parasites ◽  
Strategic Process ◽  
Intimate Association

SUMMARYA wide spectrum of pathogenic bacteria and protozoa has adapted to an intracellular life-style, which presents several advantages, including accessibility to host cell metabolites and protection from the host immune system. Intracellular pathogens have developed strategies to enter and exit their host cells while optimizing survival and replication, progression through the life cycle, and transmission. Over the last decades, research has focused primarily on entry, while the exit process has suffered from neglect. However, pathogen exit is of fundamental importance because of its intimate association with dissemination, transmission, and inflammation. Hence, to fully understand virulence mechanisms of intracellular pathogens at cellular and systemic levels, it is essential to consider exit mechanisms to be a key step in infection. Exit from the host cell was initially viewed as a passive process, driven mainly by physical stress as a consequence of the explosive replication of the pathogen. It is now recognized as a complex, strategic process termed “egress,” which is just as well orchestrated and temporally defined as entry into the host and relies on a dynamic interplay between host and pathogen factors. This review compares egress strategies of bacteria, pathogenic yeast, and kinetoplastid and apicomplexan parasites. Emphasis is given to recent advances in the biology of egress in mycobacteria and apicomplexans.

scholarly journals THE CYTONUCLEOPROTEINS OF AMEBAE

1963 ◽  
Vol 19 (3) ◽  
pp. 453-466 ◽  
Author(s):  
Thomas J. Byers ◽  
Dorothy B. Platt ◽  
Lester Goldstein
Keyword(s):  
Host Cell ◽  
Cell Nucleus ◽  
Amoeba Proteus ◽  
Host Cells ◽  
Binucleate Cell ◽  
Donor Nucleus ◽  
Random Manner ◽  
Host Cell Nucleus ◽  
Long Term Behavior

Autoradiographs of whole Amoeba proteus host cells fixed after the implantation of single nuclei from A. proteus donors labeled with any one of 8 different radioactive amino acids showed that the label had become highly concentrated in the host cell nucleus as well as in the donor nucleus and that the cytoplasmic activity was relatively low. When these amebae were sectioned, the radioactivity was found to be homogeneously distributed throughout the nuclei. The effect of unlabeled amino acid "chaser," the solubility of the labeled material, and the long-term behavior of the labeled material gave evidence that the radioactivity was in protein. At equilibrium, the host cell nucleus contained approximately 30 per cent of the radioactivity distributed between the two nuclei. This unequal nuclear distribution is attributed to the presence of two classes of nuclear proteins: a non-migratory one that does not leave the nucleus during interphase, and a migratory one, called cytonucleoprotein, that shuttles between nucleus and cytoplasm in a non-random manner. It is estimated that between 12 per cent and 44 per cent of the cytonucleoproteins are present in the cytoplasm of a binucleate cell at any one moment. Nuclei of Chaos chaos host cells also concentrated label acquired from implanted radioactive A. proteus nuclei.

Targeting of host cell receptor tyrosine kinases by intracellular pathogens

2019 ◽  
Vol 12 (599) ◽  
pp. eaau9894 ◽  
Author(s):  
Gholamreza Haqshenas ◽  
Christian Doerig
Keyword(s):  
Host Cell ◽  
Tyrosine Kinases ◽  
Receptor Tyrosine Kinases ◽  
Cell Receptor ◽  
Host Cells ◽  
Target Cells ◽  
Intracellular Pathogens ◽  
Host Cell Receptor ◽  
Host Signaling ◽  
Mediate Cell

Intracellular pathogens use complex and tightly regulated processes to enter host cells. Upon initial interactions with signaling proteins at the surface of target cells, intracellular microbes activate and co-opt specific host signaling pathways that mediate cell surface–cytosol communications to facilitate pathogen internalization. Here, we discuss the roles of host receptor tyrosine kinases (RTKs) in the establishment of productive infections by major intracellular pathogens. We evaluate the gaps in the current understanding of this process and propose a comprehensive approach for assessing the role of host cell signaling in the biology of intracellular microorganisms and viruses. We also discuss RTK-targeting strategies for the treatment of various infections.

scholarly journals The OxyR Regulon in Nontypeable Haemophilus influenzae

2006 ◽  
Vol 189 (3) ◽  
pp. 1004-1012 ◽  
Author(s):  
Alistair Harrison ◽  
William C. Ray ◽  
Beth D. Baker ◽  
David W. Armbruster ◽  
Lauren O. Bakaletz ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Haemophilus Influenzae ◽  
Host Cells ◽  
Chronic Obstructive ◽  
Upper Respiratory Tract ◽  
Nontypeable Haemophilus Influenzae ◽  
Intracellular Iron ◽  
Regulatory Pathways ◽  
Iron Utilization

ABSTRACT Nontypeable Haemophilus influenzae (NTHi) is a gram-negative bacterium and a common commensal organism of the upper respiratory tract in humans. NTHi causes a number of diseases, including otitis media, sinusitis, conjunctivitis, exacerbations of chronic obstructive pulmonary disease, and bronchitis. During the course of colonization and infection, NTHi must withstand oxidative stress generated by insult due to multiple reactive oxygen species produced endogenously by other copathogens and by host cells. Using an NTHi-specific microarray containing oligonucleotides representing the 1821 open reading frames of the recently sequenced NTHi isolate 86-028NP, we have identified 40 genes in strain 86-028NP that are upregulated after induction of oxidative stress due to hydrogen peroxide. Further comparisons between the parent and an isogenic oxyR mutant identified a subset of 11 genes that were transcriptionally regulated by OxyR, a global regulator of oxidative stress. Interestingly, hydrogen peroxide induced the OxyR-independent upregulation of expression of the genes encoding components of multiple iron utilization systems. This finding suggested that careful balancing of levels of intracellular iron was important for minimizing the effects of oxidative stress during NTHi colonization and infection and that there are additional regulatory pathways involved in iron utilization.

scholarly journals Manipulation of Rab GTPase Function by Intracellular Bacterial Pathogens

2007 ◽  
Vol 71 (4) ◽  
pp. 636-652 ◽  
Author(s):  
John H. Brumell ◽  
Marci A. Scidmore
Keyword(s):  
Host Cell ◽  
Bacterial Pathogens ◽  
Endocytic Pathway ◽  
Host Cells ◽  
Eukaryotic Cells ◽  
Rab Gtpase ◽  
Host Immune System ◽  
Intracellular Pathogens ◽  
Cell Trafficking ◽  
Rab Gtpases

SUMMARY Intracellular bacterial pathogens have evolved highly specialized mechanisms to enter and survive within their eukaryotic hosts. In order to do this, bacterial pathogens need to avoid host cell degradation and obtain nutrients and biosynthetic precursors, as well as evade detection by the host immune system. To create an intracellular niche that is favorable for replication, some intracellular pathogens inhibit the maturation of the phagosome or exit the endocytic pathway by modifying the identity of their phagosome through the exploitation of host cell trafficking pathways. In eukaryotic cells, organelle identity is determined, in part, by the composition of active Rab GTPases on the membranes of each organelle. This review describes our current understanding of how selected bacterial pathogens regulate host trafficking pathways by the selective inclusion or retention of Rab GTPases on membranes of the vacuoles that they occupy in host cells during infection.

scholarly journals Distinct H2O2-Scavenging System in Yersinia pseudotuberculosis: KatG and AhpC Act Together to Scavenge Endogenous Hydrogen Peroxide

2021 ◽  
Vol 12 ◽  
Author(s):  
Fen Wan ◽  
Xue Feng ◽  
Jianhua Yin ◽  
Haichun Gao
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Yersinia Pseudotuberculosis ◽  
Cellular Responses ◽  
Host Cells ◽  
Ros Scavenging ◽  
Nadh Peroxidase ◽  
Catalase Peroxidase ◽  
Low Levels ◽  
Simultaneous Loss

To colonize in the digestive tract of animals and humans, Yersinia pseudotuberculosis has to deal with reactive oxygen species (ROS) produced by host cells and microbiota. However, an understanding of the ROS-scavenging systems and their regulation in this bacterium remains largely elusive. In this study, we identified OxyR as the master transcriptional regulator mediating cellular responses to hydrogen peroxide (H2O2) in Y. pseudotuberculosis through genomics and transcriptomics analyses. OxyR activates transcription of diverse genes, especially the core members of its regulon, including those encoding catalases, peroxidases, and thiol reductases. The data also suggest that sulfur species and manganese may play a particular role in the oxidative stress response of Y. pseudotuberculosis. Among the three H2O2-scavenging systems in Y. pseudotuberculosis, catalase/peroxidase KatE functions as the primary scavenger for high levels of H2O2; NADH peroxidase alkyl hydroperoxide reductase (AhpR) and catalase KatG together are responsible for removing low levels of H2O2. The simultaneous loss of both AhpC (the peroxidatic component of AhpR) and KatG results in activation of OxyR. Moreover, we found that AhpC, unlike its well-characterized Escherichia coli counterpart, has little effect on protecting cells against toxicity of organic peroxides. These findings provide not only novel insights into the structural and functional diversity of bacterial H2O2-scavenging systems but also a basic understanding of how Y. pseudotuberculosis copes with oxidative stress.

scholarly journals DNA damage and oxidative stress in human cells infected by Trypanosoma cruzi

2021 ◽  
Vol 17 (4) ◽  
pp. e1009502
Author(s):  
Pilar T. V. Florentino ◽  
Davi Mendes ◽  
Francisca Nathalia L. Vitorino ◽  
Davi J. Martins ◽  
Julia P. C. Cunha ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Dna Repair ◽  
Trypanosoma Cruzi ◽  
Host Cell ◽  
Dna Lesions ◽  
Host Cells ◽  
Antioxidant Defenses ◽  
Related Factor ◽  
Infected Cells

Trypanosoma cruzi is the etiologic agent of Chagas’ disease. Infected cells with T. cruzi activate several responses that promote unbalance of reactive oxygen species (ROS) that may cause DNA damage that activate cellular responses including DNA repair processes. In this work, HeLa cells and AC16 human cardiomyocyte cell line were infected with T. cruzi to investigate host cell responses at genome level during parasites intracellular life cycle. In fact, alkaline sensitive sites and oxidized DNA bases were detected in the host cell genetic material particularly in early stages of infection. These DNA lesions were accompanied by phosphorylation of the histone H2Ax, inducing γH2Ax, a marker of genotoxic stress. Moreover, Poly [ADP-ribose] polymerase) and 8-oxoguanine glycosylase (OGG1) are recruited to host cell nuclei, indicating activation of the DNA repair process. In infected cells, chromatin-associated proteins are carbonylated, as a possible consequence of oxidative stress and the nuclear factor erythroid 2–related factor 2 (NRF2) is induced early after infection, suggesting that the host cell antioxidant defenses are activated. However, at late stages of infection, NRF2 is downregulated. Interestingly, host cells pretreated with glutathione precursor, N-acetyl cysteine, NRF2 activator (Sulforaphane), and also Benznidonazol (BNZ) reduce parasite burst significantly, and DNA damage. These data indicate that the balance of oxidative stress and DNA damage induction in host cells may play a role during the process of infection itself, and interference in these processes may hamper T. cruzi infection, revealing potential target pathways for the therapy support.

The Dps-like protein Fri of Listeria monocytogenes promotes stress tolerance and intracellular multiplication in macrophage-like cells

Microbiology ◽  
2005 ◽  
Vol 151 (3) ◽  
pp. 925-933 ◽  
Author(s):  
Katja N. Olsen ◽  
Marianne H. Larsen ◽  
Cormac G. M. Gahan ◽  
Birgitte Kallipolitis ◽  
Xenia A. Wolf ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Listeria Monocytogenes ◽  
Bacterial Species ◽  
Wild Type ◽  
Gene Encoding ◽  
Iron Storage ◽  
Food Borne ◽  
Dps Protein

Members of the ferritin-like Dps protein family are found in a number of bacterial species, where they demonstrate the potential to bind iron, and have been implicated in tolerance to oxidative stress. In this study of the food-borne pathogen Listeria monocytogenes, the fri gene encoding a Dps homologue was deleted, and, compared to wild-type cells, it was found that the resulting mutant was less resistant to hydrogen peroxide, and demonstrated reduced survival following long-term (7–11 days) incubation in laboratory media. In view of this, it is shown that fri gene expression is controlled by the hydrogen peroxide regulator PerR, as well as the general stress sigma factor σ B. When fri mutant cells were transferred to iron-limiting conditions, growth was retarded relative to wild-type cells, indicating that Fri may be required for iron storage. This notion is supported by the observation that the L. monocytogenes genome appears not to encode other ferritin-like proteins. Given the role of Fri in resistance to oxidative stress, and growth under iron-limiting conditions, the ability of the fri mutant to infect mice was examined. When injected by the intraperitoneal route, the fri mutant demonstrated a reduced capacity to proliferate in the organs of infected mice relative to the wild-type, whereas when the bacteria were supplied intravenously this effect was mitigated. In addition, the mutant was impaired in its ability to survive and grow in J774.A1 mouse macrophage cells. Thus, the data suggest that Fri contributes to the ability of L. monocytogenes to survive in environments where oxidative stress and low iron availability may impede bacterial proliferation.

Effect of Turmeric and Ginger on Lipid Profile in Male Rats Exposed to Oxidative Stress

2019 ◽  
Vol 10 (01) ◽  
Author(s):  
Eman A. Al-Rekabi ◽  
Dheyaa K. Alomer ◽  
Rana Talib Al-Muswie ◽  
Khalid G. Al-Fartosi
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Drinking Water ◽  
Lipid Profile ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Male Rats ◽  
Control Group ◽  
Very Low Density Lipoprotein ◽  
Low Density

The present study aimed to investigate the effect of turmeric and ginger on lipid profile of male rats exposed to oxidative stress induced by hydrogen peroxide H2O2 at a concentration of 1% given with consumed drinking water to male rats. Methods: 200 mg/kg from turmeric and ginger were used, and the animals were treatment for 30 days. Results: the results showed a significant increase in cholesterol, triglycerides, low density lipoprotein (LDL), very low density lipoprotein (VLDL), whereas it explained a significant decrease in high density lipoprotein (HDL) of male rats exposed to oxidative stress when compared with control group. the results showed a significant decrease in cholesterol, triglycerides, (LDL), (VLDL), whereas it explained a significant increase in (HDL) of rats treated with turmeric and ginger at dose 200 mg/kg when compared with male rats exposed to oxidative stress.

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