Anthrax toxin edema factor: a bacterial adenylate cyclase that increases cyclic AMP concentrations of eukaryotic cells.

Leppla, Stephen H.

doi:10.1073/pnas.79.10.3162

Cited by 872 publications

(676 citation statements)

References 27 publications

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“…Edema factor acts as adenylyl cyclase and is dependent on calmodulin and calcium ions for its activity. Upon infection, edema toxin gains entry into the host cell cytoplasm through PA translocation channel and converts the cellular pool of adenosine triphosphate (ATP) into 3 0 , 5 0 cyclic adenosine monophosphate (cAMP), a secondary messenger crucial in diverse cellular processes [56]. Elevated and persistent level of cAMP causes loss of water from cells into the intercellular milieu (Fig.…”

Section: Edema Toxinmentioning

confidence: 99%

Bacterial Virulence Factors: Secreted for Survival

et al. 2016

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Virulence is described as an ability of an organism to infect the host and cause a disease. Virulence factors are the molecules that assist the bacterium colonize the host at the cellular level. These factors are either secretory, membrane associated or cytosolic in nature. The cytosolic factors facilitate the bacterium to undergo quick adaptive-metabolic, physiological and morphological shifts. The membrane associated virulence factors aid the bacterium in adhesion and evasion of the host cell. The secretory factors are important components of bacterial armoury which help the bacterium wade through the innate and adaptive immune response mounted within the host. In extracellular pathogens, the secretory virulence factors act synergistically to kill the host cells. In this review, we revisit the role of some of the secreted virulence factors of two human pathogens: Mycobacterium tuberculosis-an intracellular pathogen and Bacillus anthracis-an extracellular pathogen. The advances in research on the role of secretory factors of these pathogens during infection are discussed.

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Section: Edema Toxinmentioning

confidence: 99%

Bacterial Virulence Factors: Secreted for Survival

et al. 2016

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“…The cleavage events result in inactivation of the MAPK pathways thereby hampering a variety of cellular responses including cell division, apoptosis, and survival [7]. EF is a calmodulin-dependent adenylyl cyclase that elevates intracellular cAMP levels by converting ATP to cAMP, the classical second messenger, thereby causing diverse adverse side-effects [8]. These processes allow B. anthracis to evade the hosts` immune system and facilitate proliferation, resulting in the characteristic disease symptoms of anthrax that frequently lead to death.…”

Section: Introductionmentioning

confidence: 99%

Anthrax protective antigen is a calcium-dependent serine protease

et al. 2018

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Bacillus anthracis secretes a three component exotoxin-complex, which contributes to anthrax pathogenesis. Formation of this complex starts with the binding of protective antigen (PA) to its cellular receptor. In this study, we report that PA is a calcium-dependent serine protease and that the protein potentially uses this proteolytic activity for receptor binding. Additionally our findings shed new light on previous research describing the inhibition of anthrax toxins and exotoxin formation. Importantly, inhibition of the proteolytic activity of protective antigen could be a novel therapeutic strategy in fighting B. anthracis-related infections.

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“…Oedema toxin (EdTx) consists of PA and EF, a calmodulin-dependent adenylate cyclase. EdTx is thought to be responsible for phagocyte inhibition and the massive oedema that is seen during anthrax infection (Leppla, 1982(Leppla, , 1984. Genes required for capsule synthesis, capB, capC and capA, are carried by pXO2.…”

Section: Introductionmentioning

confidence: 99%

Early Bacillus anthracis-macrophage interactions: intracellular survival and escape

et al. 2000

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This study describes early intracellular events occurring during the establishment phase of Bacillus anthracis infections. Anthrax infections are initiated by dormant endospores gaining access to the mammalian host and becoming engulfed by regional macrophages (Mφ). During systemic anthrax, late stage events include vegetative growth in the blood to very high titres and the synthesis of the anthrax exotoxin complex, which causes disease symptoms and death. Experiments focus on the early events occurring during the first few hours of the B. anthracis infectious cycle, from endospore germination up to and including release of the vegetative cell from phagocytes. We found that newly vegetative bacilli escape from the phagocytic vesicles of cultured Mφ and replicate within the cytoplasm of these cells. Release from the Mφ occurs 4–6 h after endospore phagocytosis, timing that correlates with anthrax infection of test animals. Genetic analysis from this study indicates that the toxin plasmid pXO1 is required for release from the Mφ, whereas the capsule plasmid pXO2 is not. The transactivator atxA, located on pXO1, is also found to be essential for release, but the toxin genes themselves are not required. This suggests that Mφ release of anthrax bacilli is atxA regulated. The putative ‘escape’ genes may be located on the chromosome and/or on pXO1.

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Anthrax toxin edema factor: a bacterial adenylate cyclase that increases cyclic AMP concentrations of eukaryotic cells.

Cited by 872 publications

References 27 publications

Bacterial Virulence Factors: Secreted for Survival

Bacterial Virulence Factors: Secreted for Survival

Anthrax protective antigen is a calcium-dependent serine protease

Early Bacillus anthracis-macrophage interactions: intracellular survival and escape

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