A Phospholipase in Staphylococcal Toxin which hydrolyses Sphingomyelin

Doery, Hazel M.; Magnusson, Björn; Cheyne, I. M.; Gulasekharam, J.

doi:10.1038/1981091a0

Cited by 92 publications

(44 citation statements)

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“…Beta-hemolysin was found in 1963 to have phosphorylase c activity (48). This activity requires the presence of Mg 2ϩ and is limited with specificity for sphingomyelin and lyso-phosphatidylcholine.…”

Section: Beta-hemolysin (Sphingomyelinase C)mentioning

confidence: 99%

Exotoxins of Staphylococcus aureus

Dinges

Orwin

Schlievert

2000

Clinical Microbiology Reviews

1,090

619

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Section: Beta-hemolysin (Sphingomyelinase C)mentioning

confidence: 99%

Exotoxins of Staphylococcus aureus

Dinges

Orwin

Schlievert

2000

Clinical Microbiology Reviews

1,090

619

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“…Toxin-producing bacteria may also target host sphingolipids. For example, ␤-toxin from Staphylococcus aureus or ␣-toxin produced by Clostridium perfringens can hydrolyze host sphingomyelin (23,67,98). Also, cholera toxin and botulinum neurotoxin can bind to glycosphingolipids such as the ganglioside GM1 (15,96,135,149).…”

Section: The Sphingolipid-infection Connection: Model Systems For Sphmentioning

confidence: 99%

Role of Sphingolipids in Microbial Pathogenesis

Heung¹,

Luberto²,

2006

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“…SMase C hydrolyzes sphingomyelin to phosphocholine and ceramide (25) rather than to choline and ceramide-1-phosphate (Fig. 5A).…”

Section: Discovery and Identification Of Cftr-inhibiting Activity In mentioning

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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A Phospholipase in Staphylococcal Toxin which hydrolyses Sphingomyelin

Cited by 92 publications

References 1 publication

Exotoxins of Staphylococcus aureus

Exotoxins of Staphylococcus aureus

Role of Sphingolipids in Microbial Pathogenesis

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

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A Phospholipase in Staphylococcal Toxin which hydrolyses Sphingomyelin

Cited by 92 publications

References 1 publication

Exotoxins of Staphylococcus aureus

Exotoxins of Staphylococcus aureus

Role of Sphingolipids in Microbial Pathogenesis

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

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