A Microbial Strategy to Multiply in Macrophages: The Pregnant Pause

Swanson, Michele S.; Fernandez-Moreia, Esteban

doi:10.1034/j.1600-0854.2002.030302.x

Cited by 79 publications

(70 citation statements)

References 79 publications

(114 reference statements)

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“…Consequently, artificial elevation of phagosome pH (using NH 4 Cl, chloroquine, or bafilomycin A1) impairs killing of Aspergillus fumigatus [41], Staphylococcus aureus [42], and Bordetella pertussis [43]. Conversely, growth and survival of pathogens, which replicate in acidic compartments (such as Legionella pneumophila, Coxiella burnetii, Cryptococcus neoformans, Leishmania promastigotes, Brucella, and Salmonella), are impaired [44][45][46][47][48][49][50]. In these studies, all phagosome-neutralizing agents had similar effects on microbe survival [43][44][45][46][47][48].…”

Section: Discussionmentioning

confidence: 99%

“…Conversely, growth and survival of pathogens, which replicate in acidic compartments (such as Legionella pneumophila, Coxiella burnetii, Cryptococcus neoformans, Leishmania promastigotes, Brucella, and Salmonella), are impaired [44][45][46][47][48][49][50]. In these studies, all phagosome-neutralizing agents had similar effects on microbe survival [43][44][45][46][47][48]. By contrast, the results of our work indicate that NH 4 Cl prevented intracellular killing of urease null Hp, but bafilomycin A1 and chloroquine did not; as such, our data indicate that phagosome neutralization per se cannot prevent elimination of Hp.…”

Section: Discussionmentioning

confidence: 99%

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Role of urease in megasome formation and Helicobacter pylori survival in macrophages

Schwartz

Allen

2006

Journal of Leukocyte Biology

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Previous studies have demonstrated that Helicobacter pylori (Hp) delays its entry into macrophages and persists inside megasomes, which are poorly acidified and accumulate early endosome autoantigen 1. Herein, we explored the role of Hp urease in bacterial survival in murine peritoneal macrophages and J774 cells. Plasmid-free mutagenesis was used to replace ureA and ureB with cat in Hp Strains 11637 and 11916. ureAB null Hp lacked detectable urease activity and did not express UreA or UreB as judged by immunoblotting. Deletion of ureAB had no effect on Hp binding to macrophages or the rate or extent of phagocytosis. However, intracellular survival of mutant organisms was impaired significantly. Immunofluorescence microscopy demonstrated that (in contrast to parental organisms) mutant Hp resided in single phagosomes, which were acidic and accumulated the lysosome marker lysosome-associated membrane protein-1 but not early endosome autoantigen 1. A similar phenotype was observed for spontaneous urease mutants derived from Hp Strain 60190. Treatment of macrophages with bafilomycin A1, NH 4 Cl, or chloroquine prevented acidification of phagosomes containing mutant Hp. However, only ammonium chloride enhanced bacterial viability significantly. Rescue of ureAB null organisms was also achieved by surface adsorption of active urease. Altogether, our data indicate a role for urease and urease-derived ammonia in megasome formation and Hp survival.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Role of urease in megasome formation and Helicobacter pylori survival in macrophages

Schwartz

Allen

2006

Journal of Leukocyte Biology

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“…1). The biphasic developmental cycle of C. burnetii in the host cell and the bacterial factors used for the intracellular survival are well documented in Re-emergence of Q fever 331 several reviews [57,136,159]. The small and large forms express different genes that permit the bacterium to survive in the specific harsh compartment of each form.…”

Section: Entry and Survival Of C Burnetiimentioning

confidence: 99%

Is Q Fever an emerging or re-emerging zoonosis?

2005

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-Q fever is a zoonotic disease considered as emerging or re-emerging in many countries. It is caused by Coxiella burnetii, a bacterium developing spore-like forms that are highly resistant to the environment. The most common animal reservoirs are livestock and the main source of infection is by inhalation of contaminated aerosols. Although the culture process for Coxiella is laborious, advances on the knowledge of the life cycle of the bacterium have been made. New tools have been developed to (i) improve the diagnosis of Q fever in humans and animals, and especially animal shedders, (ii) perform epidemiological studies, and (iii) prevent the disease through the use of vaccines. This review summarizes the state of the knowledge on the bacteriology and clinical manifestations of Q fever as well as its diagnosis, epidemiology, treatment and prevention in order to understand what factors are responsible for its emergence or re-emergence. Coxiella burnetii / epidemiology / bacteriology / diagnostic / control

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“…Thereafter, some bacteria have adapted a pathogenic mechanism whereby they can highjack the resident macrophages in the Peyer's patches, allowing dissemination of bacteria via the circulatory system. For example, Listeria monocytogenes and Legionella pneumophila reside intracellularly in the macrophage, thereby avoiding an antimicrobial environment and promoting their dissemination throughout the host without being exposed to antibodies (Duclos & Desjardins, 2000;Pizarro-Cerda & Cossart, 2006;Swanson & Fernandez-Moreira, 2002). In contrast, Salmonella and Shigella can survive within macrophages as well as kill macrophages, depending on the physiological state of the macrophage (Navarre & Zychlinsky, 2000).…”

Section: Introductionmentioning

confidence: 99%

Type III secretion system 1 of Vibrio parahaemolyticus induces oncosis in both epithelial and monocytic cell lines

2009

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The Vibrio parahaemolyticus type III secretion system 1 (T3SS1) induces cytotoxicity in mammalian epithelial cells. We characterized the cell death phenotype in both epithelial (HeLa) and monocytic (U937) cell lines following infection with V. parahaemolyticus. Using a combination of the wild-type strain and gene knockouts, we confirmed that V. parahaemolyticus strain NY-4 was able to induce cell death in both cell lines via a T3SS1-dependent mechanism. Bacterial contact, but not internalization, was required for T3SS1-induced cytotoxicity. The mechanism of cell death involves formation of a pore structure on the surface of infected HeLa and U937 cells, as demonstrated by cellular swelling, uptake of cell membrane-impermeable dye and protection of cytotoxicity by osmoprotectant (PEG3350). Western blot analysis showed that poly ADP ribose polymerase (PARP) was not cleaved and remained in its full-length active form. This result was evident for seven different V. parahaemolyticus strains. V. parahaemolyticus-induced cytotoxicity was not inhibited by addition of the pan-caspase inhibitor carbobenzoxy-valyl-alanyl-aspartyl-[O-methyl]-fluoromethylketone (Z-VAD-FMK) or the caspase-1 inhibitor N-acetyl-tyrosyl-valylalanyl-aspartyl-aldehyde (Ac-YVAD-CHO); thus, caspases were not involved in T3SS1-induced cytotoxicity. DNA fragmentation was not evident following infection and autophagic vacuoles were not observed after monodansylcadaverine staining. We conclude that T3SS1 of V. parahaemolyticus strain NY-4 induces a host cell death primarily via oncosis rather than apoptosis, pyroptosis or autophagy. INTRODUCTIONVibrio parahaemolyticus is a Gram-negative food-borne pathogen that is commonly associated with consumption of raw or undercooked seafood (Joseph et al., 1982). Symptoms of infection include diarrhoea, nausea, vomiting, headache, fever and chills. In addition to typical gastrointestinal infections, approximately 5 % of V. parahaemolyticus infections advance to septicaemia (Hlady & Klontz, 1996) and these infections may be fatal, especially in immunocompromised patients or those with a preexisting medical condition such as liver disease or diabetes (Yeung & Boor, 2004).Thermostable direct haemolysin (TDH) is considered the primary virulence factor in V. parahaemolyticus. In addition to its ability to form pores in red blood cells, TDH causes increased short circuit current, increased Cl 2 secretion in human colonic epithelial cells, and enhanced Ca 2+ entry from the extracellular medium (Takahashi et al., 2001). An early study of a tdh deletion mutant demonstrated significantly reduced ability to cause fluid accumulation in ileal loops of a rabbit model (Nishibuchi et al., 1992). In contrast, Park et al. (2004) showed that a tdh deletion mutant has the ability to cause fluid accumulation in the ligated intestine of rabbits. Furthermore, both TDH-positive and -negative strains of V. parahaemolyticus can disrupt the epithelial tight junction, a precursor to dissemination of bacteria into the circulation (Lynch et a...

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A Microbial Strategy to Multiply in Macrophages: The Pregnant Pause

Cited by 79 publications

References 79 publications

Role of urease in megasome formation and Helicobacter pylori survival in macrophages

Role of urease in megasome formation and Helicobacter pylori survival in macrophages

Is Q Fever an emerging or re-emerging zoonosis?

Type III secretion system 1 of Vibrio parahaemolyticus induces oncosis in both epithelial and monocytic cell lines

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