anthrax/hypoxia

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Anthrax lethal toxin inhibits translation of hypoxia-inducible factor 1α and causes decreased tolerance to hypoxic stress.

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Hypoxia is considered to be a contributor to the pathology associated with administration of anthrax lethal toxin (LT). However, we report here that serum lactate levels in LT-treated mice are reduced, a finding inconsistent with the anaerobic metabolism expected to occur during hypoxia. Reduced

Targeting Anthrax Toxin Receptor 2 Ameliorates Endometriosis Progression.

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Rationale: Endometriosis is a highly prevalent gynecological disease in women of reproductive age that markedly reduces life quality and fertility. Unfortunately, there is no cure for this disease, which highlights that more efforts are needed to investigate the underlying mechanism for

Persistent inhibition of oxygen-induced retinal neovascularization by anthrax lethal toxin.

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OBJECTIVE To evaluate the role of mitogen-activated protein kinase kinase (MKK) signaling in a mouse model of oxygen-induced retinopathy (OIR) that mimics retinopathy of prematurity (ROP). METHODS Postnatal day 7 mice were exposed to elevated oxygen for 5 days to induce retinopathy. Anthrax lethal

Bacillus anthracis cell wall produces injurious inflammation but paradoxically decreases the lethality of anthrax lethal toxin in a rat model.

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OBJECTIVE The in vivo inflammatory effects of the Bacillus anthracis cell wall are unknown. We therefore investigated these effects in rats and, for comparison, those of known inflammatory stimulants, Staphylococcus aureus cell wall or lipopolysaccharide (LPS). RESULTS Sprague-Dawley rats (n = 103)

The cytotoxic effect of anthrax lethal toxin on human lung cells in vitro and the protective action of bovine antibodies to PA and LF.

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The excretion of protein toxins by vegetative cells of Bacillus anthracis is critical to the development of the lethal consequences of anthrax, particularly inhalational anthrax. Whilst the lung macrophages and other phagocytic cells transfer the spores from the lung cavities into the lymphatic

Erythropoiesis suppression is associated with anthrax lethal toxin-mediated pathogenic progression.

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Anthrax is a disease caused by the bacterium Bacillus anthracis, which results in high mortality in animals and humans. Although some of the mechanisms are already known such as asphyxia, extensive knowledge of molecular pathogenesis of this disease is deficient and remains to be further

Histopathological effects of anthrax lethal factor on rat liver.

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Bacillus anthracis, the causative agent of anthrax, has become an increasingly important scientific topic due to its potential role in bioterrorism. The lethal toxin (LT) of B. anthracis consists of lethal factor (LF) and a protective antigen (PA). This study investigated whether only lethal factor

Bacillus anthracis lethal toxin induces TNF-alpha-independent hypoxia-mediated toxicity in mice.

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Bacillus anthracis lethal toxin (LT) is the major virulence factor of anthrax and reproduces most of the laboratory manifestations of the disease in animals. We studied LT toxicity in BALB/cJ and C57BL/6J mice. BALB/cJ mice became terminally ill earlier and with higher frequency than C57BL/6J mice.

The host response to anthrax lethal toxin: unexpected observations.

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Bacillus anthracis, the causative agent of anthrax, is believed to induce disease and death in humans in an endotoxic shock-like manner. A comprehensive study of the effects of anthrax toxin in mice demonstrates that toxin-induced death is mediated not by cytokine release, as previously thought, but

Lethality in a murine model of pulmonary anthrax is reduced by combining nuclear transport modifier with antimicrobial therapy.

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BACKGROUND In the last ten years, bioterrorism has become a serious threat and challenge to public health worldwide. Pulmonary anthrax caused by airborne Bacillus anthracis spores is a life-threatening disease often refractory to antimicrobial therapy. Inhaled spores germinate into vegetative forms

Anthrax Toxin Receptor 1 Is Essential for Arteriogenesis in a Mouse Model of Hindlimb Ischemia.

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Anthrax toxin receptor 1/tumor endothelial marker 8 (Antxr1 or TEM8) is up-regulated in tumor vasculature and serves as a receptor for anthrax toxin, but its physiologic function is unclear. The objective of this study was to evaluate the role of Antxr1 in arteriogenesis. The role of Antxr1 in

Fell-Muir Lecture: Regulatory mechanisms of skeletal and connective tissue development and homeostasis - lessons from studies of human disorders.

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Studies of proliferative hemangiomas have led to the discovery that interactions of endothelial cells with extracellular matrix and/or Vascular Endothelial Growth Factor (VEGF)-A stimulate the expression of VEGFR1, the VEGF decoy receptor, and suppress VEGF-dependent VEGFR2 signalling by a mechanism

Histologic Changes In Recreational Drug Misuse.

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Use of recreational drugs is associated with a number of histologic changes. These may be related to the method of administration or due to systemic effects of the drugs. This paper reviews the histopathological features seen following recreational drug use. With injection, there may be local

Crystal structure of prolyl 4-hydroxylase from Bacillus anthracis.

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Prolyl 4-hydroxylases (P4H) catalyze the post-translational hydroxylation of proline residues and play a role in collagen production, hypoxia response, and cell wall development. P4Hs belong to the group of Fe(II)/alphaKG oxygenases and require Fe(II), alpha-ketoglutarate (alphaKG), and O(2) for

Present-day conservative treatment retinopathy of prematurity.

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Retinopathy of prematurity occurs in prematurely born babies. Etiology of disease is multifactorial and frequency of retinopathy of prematurity diagnosis increases. Retinopathy is one of causes for major loss of vision and amaurosis in newborns around the world. Low efficacy of treatment leads to

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