期刊
JOURNAL OF BACTERIOLOGY
卷 186, 期 2, 页码 575-579出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/JB.186.2.575-579.2004
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资金
- NHLBI NIH HHS [K08 HL067903-03, K08 HL067903, K08 HL067903-02, K08 HL067903-01, K08 HL67903] Funding Source: Medline
- NIAID NIH HHS [R01 AI047938] Funding Source: Medline
- NICHD NIH HHS [HD043376, K12 HD043376] Funding Source: Medline
- PHS HHS [K12] Funding Source: Medline
- EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT [K12HD043376] Funding Source: NIH RePORTER
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [K08HL067903] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI047938] Funding Source: NIH RePORTER
Spontaneous polymyxin-resistant mutants of Pseudomonas aeruginosa were isolated. The mutations responsible for this phenotype were mapped to a two-component signal transduction system similar to PmrAB of Salmonella enterica serovar Typhimurium. Lipid A of these mutants contained aminoarabinose, an inducible modification that is associated with polymyxin resistance. Thus, P. aeruginosa possesses a mechanism that induces resistance to cationic antimicrobial peptides in response to environmental conditions.
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