Effects of anthrax toxin components on human neutrophils

O’Brien, J.; Friedlander, A. M.; Dreier, Thomas M.; Ezzell, John W.; Leppla, Stephen H.

doi:10.1128/iai.47.1.306-310.1985

Cited by 204 publications

(71 citation statements)

References 10 publications

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“…Many bacterial pathogens have developed specific strategies to survive challenge with professional phagocytes, including the induction of macrophage apoptosis, inhibition of phagocytosis, escape from the phagocytic vacuole, or diversion of intracellular routing (Knodler et al, 2001). Ca 2+ has been implicated as a second messenger during macrophage response to infectious agents, and bacterial pathogens have developed strategies to divert Ca 2+ -dependent responses, including phagocytosis or superoxide production in macrophages (O'Brien et al, 1985;Takei et al, 1998).…”

Section: Ca 2+ Signalling During Bacterial Infection Of Professional mentioning

confidence: 99%

Calcium signalling during cell interactions with bacterial pathogens

Nhieu

Clair

Grompone

et al. 2004

Biology of the Cell

108

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The ability of a pathogenic microorganism to cause a disease is conditioned by its ability to colonise a given niche and implicates the expression of specific determinants, i.e. virulence factors, that allow the pathogen to adhere to or to invade epithelial cells. Diseases may be induced by bacteria that replicate extracellularly and alter the epithelial mucosa by producing toxins. Ca2+ signalling has been implicated in various steps of bacterial infection. Bacterial toxins can induce an increase in free cytosolic Ca2+ in host cells, itself required for the toxin-mediated effects. Such toxins, by diffusing in the extracellular media, can act at a distance from the site of infection and have a global effect on the integrity of the epithelium by promoting the expression of pro-inflammatory cytokines. Independent on toxins, bacteria can induce Ca2+ responses that play a role in cytoskeletal rearrangements required for cell binding or internalisation of the microorganism. In some instances, invasion of the epithelium may be followed by bacterial access to deeper tissue, dissemination to other organs, and sometimes persistence in host cells in a parasitic-like mode. Such strategies underline the pathogen abilities to control innate defence cells such as professional phagocytes, and may implicate the diversion of Ca(2+)-dependent cellular processes that normally result in killing of the ingested bacteria. Finally, bacterial pathogens can also induce the cell release of ATP, a Ca2+ agonist, that may expand bacterial cell signalling by a paracrine or autocrine route, leading to enhanced colonisation or enhanced host cell responses to the invading microorganism.

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Section: Ca 2+ Signalling During Bacterial Infection Of Professional mentioning

confidence: 99%

Calcium signalling during cell interactions with bacterial pathogens

Nhieu

Clair

Grompone

et al. 2004

Biology of the Cell

108

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“…PA binds the cell surface receptors ANTXR1 (TEM8) and ANTXR2 (CMG2) (Bradley et al ., 2001;Scobie et al ., 2003) and delivers the enzymatic moieties to the mammalian cytosol. The enzymatic component of edema toxin is edema factor, an adenylate cyclase that reduces the phagocytic capacity of neutrophils by raising intracellular cAMP levels (Leppla, 1982;O'Brien et al ., 1985). Lethal factor (LF), a zinc-dependent protease, is the enzymatic moiety of LT.…”

Section: Introductionmentioning

confidence: 99%

Differentiation of human monocytic cell lines confers susceptibility to Bacillus anthracis lethal toxin

Kassam

Der

Mogridge

2004

Cellular Microbiology

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SummaryAnthrax lethal toxin (LT) is comprised of protective antigen and lethal factor. Lethal factor enters mammalian cells in a protective antigen-dependent process and cleaves mitogen-activated protein kinase kinases. Although LT has no observable effect on many cell types, it causes necrosis in macrophages derived from certain mouse strains and apoptosis in activated mouse macrophages. In this study, we observed that LT treatment of three different human monocytic cell lines U-937, HL-60 and THP-1 did not induce cell death. Cells did become susceptible to the toxin, however, after differentiation into a macrophage-like state. Treatment with LT resulted in decreased phosphorylation of p38, ERK1/2 and JNK in both undifferentiated and differentiated HL-60 cells, suggesting that the change in susceptibility does not result from differences in toxin delivery or substrate cleavage. Death of differentiated HL-60 cells was accompanied by chromosome condensation and DNA fragmentation, but was not inhibited by the pan-caspase inhibitor Z-VAD-FMK. In addition, we observed that the macrophage differentiation process could be inhibited by LT. Our results indicate that LTmediated death of mouse and human macrophages may occur through distinct processes and that the differentiation state of human cells can determine susceptibility or resistance to LT.

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“…Anthrax infections end either in recovery or death of the host. When B. anthracis spores are ingested, the spores germinate into fast-multiplying vegetative forms that produce three soluble factors that assemble to form toxic complexes: edema factor (EF), an adenylate cyclase that impairs immune cell function (Leppla, 1982;Brien et al, 1985;Collier & Young, 2003;Comer et al, 2005); lethal factor (LF), a zinc metalloprotease that cleaves mitogen-activated protein (MAP)-kinase-kinases thereby suppressing production of several types of cytokines and immune cell functions (Duesbery, 1998;Vitale et al, 1998;Pellizzari et al, 1999;Erwin et al, 2001;Agrawal et al, 2003;Ribot et al, 2006); and protective antigen (PA), which complexes with the other two factors and allows them to enter host cells through oligomeric PA pores (Mogridge, Cunningham & Collier, 2002). The PA and LF bind to form the anthrax lethal toxin, the key virulence factor of B. anthracis that kills macrophages and dendritic cells through a caspase-1-dependent cell death program known as pyroptosis (Fink, Bergsbaken & Cookson, 2008).…”

Section: (3) Immunologymentioning

confidence: 99%

Spores and soil from six sides: interdisciplinarity and the environmental biology of anthrax (Bacillus anthracis)

et al. 2018

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Environmentally transmitted diseases are comparatively poorly understood and managed, and their ecology is particularly understudied. Here we identify challenges of studying environmental transmission and persistence with a six-sided interdisciplinary review of the biology of anthrax (Bacillus anthracis). Anthrax is a zoonotic disease capable of maintaining infectious spore banks in soil for decades (or even potentially centuries), and the mechanisms of its environmental persistence have been the topic of significant research and controversy. Where anthrax is endemic, it plays an important ecological role, shaping the dynamics of entire herbivore communities. The complex eco-epidemiology of anthrax, and the mysterious biology of Bacillus anthracis during its environmental stage, have necessitated an interdisciplinary approach to pathogen research. Here, we illustrate different disciplinary perspectives through key advances made by researchers working in Etosha National Park, a long-term ecological research site in Namibia that has exemplified the complexities of the enzootic process of anthrax over decades of surveillance. In Etosha, the role of scavengers and alternative routes (waterborne transmission and flies) has proved unimportant relative to the long-term * Authors for correspondence: (Colin J. Carlson-Tel.: +1 (510) 990 2258; E-mail: ccarlson@sesync.org; Wayne M. Getz-Tel.: +1 510 642 8745; E-mail: wgetz@berkeley.edu; Nils C. Stenseth-Tel.: +47-22854584/+47-22854400; E-mail: n.c.stenseth@ibv.uio.no).Biological Reviews (2018) 000-000 © 2018 Cambridge Philosophical Society 2 Colin J. Carlson and others persistence of anthrax spores in soil and their infection of herbivore hosts. Carcass deposition facilitates green-ups of vegetation to attract herbivores, potentially facilitated by the role of anthrax spores in the rhizosphere. The underlying seasonal pattern of vegetation, and herbivores' immune and behavioural responses to anthrax risk, interact to produce regular 'anthrax seasons' that appear to be a stable feature of the Etosha ecosystem. Through the lens of microbiologists, geneticists, immunologists, ecologists, epidemiologists, and clinicians, we discuss how anthrax dynamics are shaped at the smallest scale by population genetics and interactions within the bacterial communities up to the broadest scales of ecosystem structure. We illustrate the benefits and challenges of this interdisciplinary approach to disease ecology, and suggest ways anthrax might offer insights into the biology of other important pathogens. Bacillus anthracis, and the more recently emerged Bacillus cereus biovar anthracis, share key features with other environmentally transmitted pathogens, including several zoonoses and panzootics of special interest for global health and conservation efforts. Understanding the dynamics of anthrax, and developing interdisciplinary research programs that explore environmental persistence, is a critical step forward for understanding these emerging threats.

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Effects of anthrax toxin components on human neutrophils

Cited by 204 publications

References 10 publications

Calcium signalling during cell interactions with bacterial pathogens

Calcium signalling during cell interactions with bacterial pathogens

Differentiation of human monocytic cell lines confers susceptibility to Bacillus anthracis lethal toxin

Spores and soil from six sides: interdisciplinarity and the environmental biology of anthrax (Bacillus anthracis)

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