Prc contributes to Escherichia coli evasion of classical complement-mediated serum killing
Escherichia coli is a common Gram-negative organism that causes bacteremia. Prc, a bacterial periplasmic protease, and its homologues are known to be involved in the pathogenesis of Gram-negative bacterial infections. The present study examined the role of Prc in E. coli bacteremia and characterized the ability of the prc mutant of the pathogenic E. coli strain RS218 to cause bacteremia and survive in human serum. The prc mutant of RS218 exhibited a decreased ability to cause a high level of bacteremia and was more sensitive to serum killing than strain RS218. This sensitivity was due to the mutant's decreased ability to avoid the activation of the antibody-dependent and -independent classical complement cascades as well as its decreased resistance to killing mediated by the membrane attack complex, the end product of complement system activation. The demonstration of Prc in the evasion of classical complement-mediated serum killing of pathogenic E. coli makes this factor a potential target for the development of therapeutic and preventive measures against E. coli bacteremia.
| Medienart: |
E-Artikel |
|---|
| Erscheinungsjahr: |
2012 |
|---|---|
| Erschienen: |
2012 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:80 |
|---|---|
| Enthalten in: |
Infection and immunity - 80(2012), 10 vom: 17. Okt., Seite 3399-409 |
| Sprache: |
Englisch |
|---|
| Beteiligte Personen: |
Wang, Chin-Ya [VerfasserIn] |
|---|
| Links: |
|---|
| Anmerkungen: |
Date Completed 03.12.2012 Date Revised 21.10.2021 published: Print-Electronic Citation Status MEDLINE |
|---|
| doi: |
10.1128/IAI.00321-12 |
|---|
| funding: |
|
|---|---|
| Förderinstitution / Projekttitel: |
|
| PPN (Katalog-ID): |
NLM219667837 |
|---|
| LEADER | 01000naa a22002652 4500 | ||
|---|---|---|---|
| 001 | NLM219667837 | ||
| 003 | DE-627 | ||
| 005 | 20231224043500.0 | ||
| 007 | cr uuu---uuuuu | ||
| 008 | 231224s2012 xx |||||o 00| ||eng c | ||
| 024 | 7 | |a 10.1128/IAI.00321-12 |2 doi | |
| 028 | 5 | 2 | |a pubmed24n0732.xml |
| 035 | |a (DE-627)NLM219667837 | ||
| 035 | |a (NLM)22825444 | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 041 | |a eng | ||
| 100 | 1 | |a Wang, Chin-Ya |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Prc contributes to Escherichia coli evasion of classical complement-mediated serum killing |
| 264 | 1 | |c 2012 | |
| 336 | |a Text |b txt |2 rdacontent | ||
| 337 | |a ƒaComputermedien |b c |2 rdamedia | ||
| 338 | |a ƒa Online-Ressource |b cr |2 rdacarrier | ||
| 500 | |a Date Completed 03.12.2012 | ||
| 500 | |a Date Revised 21.10.2021 | ||
| 500 | |a published: Print-Electronic | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a Escherichia coli is a common Gram-negative organism that causes bacteremia. Prc, a bacterial periplasmic protease, and its homologues are known to be involved in the pathogenesis of Gram-negative bacterial infections. The present study examined the role of Prc in E. coli bacteremia and characterized the ability of the prc mutant of the pathogenic E. coli strain RS218 to cause bacteremia and survive in human serum. The prc mutant of RS218 exhibited a decreased ability to cause a high level of bacteremia and was more sensitive to serum killing than strain RS218. This sensitivity was due to the mutant's decreased ability to avoid the activation of the antibody-dependent and -independent classical complement cascades as well as its decreased resistance to killing mediated by the membrane attack complex, the end product of complement system activation. The demonstration of Prc in the evasion of classical complement-mediated serum killing of pathogenic E. coli makes this factor a potential target for the development of therapeutic and preventive measures against E. coli bacteremia | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a Research Support, Non-U.S. Gov't | |
| 650 | 7 | |a Bacterial Outer Membrane Proteins |2 NLM | |
| 650 | 7 | |a Immunoglobulin G |2 NLM | |
| 650 | 7 | |a Complement System Proteins |2 NLM | |
| 650 | 7 | |a 9007-36-7 |2 NLM | |
| 650 | 7 | |a Endopeptidases |2 NLM | |
| 650 | 7 | |a EC 3.4.- |2 NLM | |
| 650 | 7 | |a C-terminal processing peptidase |2 NLM | |
| 650 | 7 | |a EC 3.4.21.102 |2 NLM | |
| 700 | 1 | |a Wang, Shainn-Wei |e verfasserin |4 aut | |
| 700 | 1 | |a Huang, Wen-Chun |e verfasserin |4 aut | |
| 700 | 1 | |a Kim, Kwang Sik |e verfasserin |4 aut | |
| 700 | 1 | |a Chang, Nan-Shan |e verfasserin |4 aut | |
| 700 | 1 | |a Wang, Ying-Hsiang |e verfasserin |4 aut | |
| 700 | 1 | |a Wu, Meng-Hsing |e verfasserin |4 aut | |
| 700 | 1 | |a Teng, Ching-Hao |e verfasserin |4 aut | |
| 773 | 0 | 8 | |i Enthalten in |t Infection and immunity |d 1970 |g 80(2012), 10 vom: 17. Okt., Seite 3399-409 |w (DE-627)NLM000004278 |x 0019-9567 |7 nnns |
| 773 | 1 | 8 | |g volume:80 |g year:2012 |g number:10 |g day:17 |g month:10 |g pages:3399-409 |
| 856 | 4 | 0 | |u http://dx.doi.org/10.1128/IAI.00321-12 |3 Volltext |
| 912 | |a GBV_USEFLAG_A | ||
| 912 | |a GBV_NLM | ||
| 951 | |a AR | ||
| 952 | |d 80 |j 2012 |e 10 |b 17 |c 10 |h 3399-409 | ||