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Group B streptococcus (GBS) modifies macrophage phosphatidylserine metabolism during induction of apoptosis

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Title: Group B streptococcus (GBS) modifies macrophage phosphatidylserine metabolism during induction of apoptosis
Authors: Buratta, Sandra1, Fettucciari, Katia2, Mambrini, Raffaela1, Fetriconi, Ilaria2, Marconi, Pierfrancesco2, Mozzi, Rita1 mozzi@unipg.it
Source: FEBS Letters. Jun2002, Vol. 520 Issue 1-3, p68. 5p.
Subjects: Streptococcus, Phosphatidylserines, Macrophages
Abstract: Group B streptococcus (GBS) induced macrophage apoptosis by which it could avoid host defence mechanisms. Macrophages, which constitutively express phosphatidylserine (PtdSer) on the outer leaflet of plasma membrane, increased PtdSer exposure during GBS-induced apoptosis. Induction of apoptosis decreased PtdSer radioactivity of macrophages incubated with [3H]serine. The effect appeared not due to increasing conversion of PtdSer to phosphatidylethanolamine or phosphatidylcholine nor to the release of radioactive membrane vesicles. The radioactivity in lysoPtdSer was also reduced. These results confirm that induction of apoptosis involves a modification of PtdSer metabolism and point out the typical features of the GBS-induced apoptosis with respect to other models of apoptosis. [Copyright &y& Elsevier]
Copyright of FEBS Letters is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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DbLabel: Engineering Source
An: 7818435
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  Data: Group B streptococcus (GBS) modifies macrophage phosphatidylserine metabolism during induction of apoptosis
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  Data: <searchLink fieldCode="AR" term="%22Buratta%2C+Sandra%22">Buratta, Sandra</searchLink><relatesTo>1</relatesTo><br /><searchLink fieldCode="AR" term="%22Fettucciari%2C+Katia%22">Fettucciari, Katia</searchLink><relatesTo>2</relatesTo><br /><searchLink fieldCode="AR" term="%22Mambrini%2C+Raffaela%22">Mambrini, Raffaela</searchLink><relatesTo>1</relatesTo><br /><searchLink fieldCode="AR" term="%22Fetriconi%2C+Ilaria%22">Fetriconi, Ilaria</searchLink><relatesTo>2</relatesTo><br /><searchLink fieldCode="AR" term="%22Marconi%2C+Pierfrancesco%22">Marconi, Pierfrancesco</searchLink><relatesTo>2</relatesTo><br /><searchLink fieldCode="AR" term="%22Mozzi%2C+Rita%22">Mozzi, Rita</searchLink><relatesTo>1</relatesTo><i> mozzi@unipg.it</i>
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  Data: <searchLink fieldCode="JN" term="%22FEBS+Letters%22">FEBS Letters</searchLink>. Jun2002, Vol. 520 Issue 1-3, p68. 5p.
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  Data: <searchLink fieldCode="DE" term="%22Streptococcus%22">Streptococcus</searchLink><br /><searchLink fieldCode="DE" term="%22Phosphatidylserines%22">Phosphatidylserines</searchLink><br /><searchLink fieldCode="DE" term="%22Macrophages%22">Macrophages</searchLink>
– Name: Abstract
  Label: Abstract
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  Data: Group B streptococcus (GBS) induced macrophage apoptosis by which it could avoid host defence mechanisms. Macrophages, which constitutively express phosphatidylserine (PtdSer) on the outer leaflet of plasma membrane, increased PtdSer exposure during GBS-induced apoptosis. Induction of apoptosis decreased PtdSer radioactivity of macrophages incubated with [3H]serine. The effect appeared not due to increasing conversion of PtdSer to phosphatidylethanolamine or phosphatidylcholine nor to the release of radioactive membrane vesicles. The radioactivity in lysoPtdSer was also reduced. These results confirm that induction of apoptosis involves a modification of PtdSer metabolism and point out the typical features of the GBS-induced apoptosis with respect to other models of apoptosis. [Copyright &y& Elsevier]
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  Label:
  Group: Ab
  Data: <i>Copyright of FEBS Letters is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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        Value: 10.1016/S0014-5793(02)02769-2
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        Text: English
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              Text: Jun2002
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              Y: 2002
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