Human live anthrax vaccine in the former USSR

Shlyakhov, E. N.; Rubinstein, Ethan

doi:10.1016/0264-410x(94)90223-2

Cited by 102 publications

(52 citation statements)

References 7 publications

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“…Further evidence that infection induces superior cellular immune response to anthrax in comparison with vaccination comes from the results of trials of live spore vaccines (42), in which it was shown by skin test positivity that cellular immune responses rapidly declined after vaccination. In contrast, the same research previously demonstrated that .90% of cutaneously infected individuals remained skin test positive a year postinfection (43).…”

Section: Discussionmentioning

confidence: 78%

Natural Exposure to Cutaneous Anthrax Gives Long-Lasting T Cell Immunity Encompassing Infection-Specific Epitopes

Ingram

Metan²,

Maillère³

et al. 2010

The Journal of Immunology

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Section: Discussionmentioning

confidence: 78%

Natural Exposure to Cutaneous Anthrax Gives Long-Lasting T Cell Immunity Encompassing Infection-Specific Epitopes

Ingram

Metan²,

Maillère³

et al. 2010

The Journal of Immunology

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“…The live STI-1 (Sanitary Technical Institute) vaccine provides effective protection against these strains (46). However, once B. anthracis is engineered with genes from closely related B. cereus to express high levels of SMase C and PC-PLC, the vaccine becomes ineffective (44).…”

Section: Discussionmentioning

confidence: 99%

Inhibition of CFTR Cl ⁻ channel function caused by enzymatic hydrolysis of sphingomyelin

Ramu

Lü

2007

Proc. Natl. Acad. Sci. U.S.A.

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Numerous mutations in the cystic fibrosis (CF) transmembrane conductance regulator (CFTR, a Cl − channel) disrupt salt and fluid transport and lead to the formation of thick mucus in patients' airways. Obstruction by mucus predisposes CF patients to chronic infections and inflammation, which become gradually harder to control and eventually fatal. Aggressive antibiotic therapy and supportive measures have dramatically lengthened CF patients' lives. Here, we report that sphingomyelinases (SMase) from human respiratory pathogens strongly inhibit CFTR function. The hydrolysis of sphingomyelin by SMase makes it more difficult to activate CFTR by phosphorylation of its regulatory domain. By inhibiting CFTR currents, SMase-producing respiratory tract bacteria may not only aggravate pulmonary infection in some CF patients but may also elicit a condition, analogous to CFTR deficiency, in non-CF patients suffering from bacterial lung infection.

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“…Strains of B. anthracis lacking capsule have markedly reduced virulence in animal models (40), and such strains have been used successfully for more than 50 years to prevent anthrax in domesticated animals (51). Similar vaccines have also been used to control anthrax in humans in countries of the former Soviet Union and the People's Republic of China (48). Capsule synthesis is regulated by factors encoded on both of the virulence plasmids pX01 (11,12,20,53) and pX02 (3,53,57) and is induced by the presence of serum and carbon dioxide (26,35).…”

mentioning

confidence: 99%

Poly-γ-Glutamate Capsule-Degrading Enzyme Treatment Enhances Phagocytosis and Killing of EncapsulatedBacillus anthracis

Scorpio

Chabot

Day

et al. 2007

Antimicrob Agents Chemother

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The poly-␥-D-glutamic acid capsule confers antiphagocytic properties on Bacillus anthracis and is essential for virulence. In this study, we showed that CapD, a ␥-polyglutamic acid depolymerase encoded on the B. anthracis capsule plasmid, degraded purified capsule and removed the capsule from the surface of anthrax bacilli. Treatment with CapD induced macrophage phagocytosis of encapsulated B. anthracis and enabled human neutrophils to kill encapsulated organisms. A second glutamylase, PghP, a ␥-polyglutamic acid hydrolase encoded by Bacillus subtilis bacteriophage ⌽NIT1, had minimal activity in degrading B. anthracis capsule, no effect on macrophage phagocytosis, and only minimal enhancement of neutrophil killing. Thus, the levels of both phagocytosis and killing corresponded to the degree of enzyme-mediated capsule degradation. The use of enzymes to degrade the capsule and enable phagocytic killing of B. anthracis offers a new approach to the therapy of anthrax.

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Human live anthrax vaccine in the former USSR

Cited by 102 publications

References 7 publications

Natural Exposure to Cutaneous Anthrax Gives Long-Lasting T Cell Immunity Encompassing Infection-Specific Epitopes

Natural Exposure to Cutaneous Anthrax Gives Long-Lasting T Cell Immunity Encompassing Infection-Specific Epitopes

Inhibition of CFTR Cl ⁻ channel function caused by enzymatic hydrolysis of sphingomyelin

Poly-γ-Glutamate Capsule-Degrading Enzyme Treatment Enhances Phagocytosis and Killing of EncapsulatedBacillus anthracis

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Human live anthrax vaccine in the former USSR

Cited by 102 publications

References 7 publications

Natural Exposure to Cutaneous Anthrax Gives Long-Lasting T Cell Immunity Encompassing Infection-Specific Epitopes

Natural Exposure to Cutaneous Anthrax Gives Long-Lasting T Cell Immunity Encompassing Infection-Specific Epitopes

Inhibition of CFTR Cl − channel function caused by enzymatic hydrolysis of sphingomyelin

Poly-γ-Glutamate Capsule-Degrading Enzyme Treatment Enhances Phagocytosis and Killing of EncapsulatedBacillus anthracis

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Product

Resources

About

Inhibition of CFTR Cl ⁻ channel function caused by enzymatic hydrolysis of sphingomyelin