Role of CD14 in responses to clinical isolates of Escherichia coli: effects of K1 capsule expression.
Infect Immun
; 75(11): 5415-24, 2007 Nov.
Article
en En
| MEDLINE
| ID: mdl-17709409
ABSTRACT
Severe bacterial infections leading to sepsis or septic shock can be induced by bacteria that utilize different factors to drive pathogenicity and/or virulence, leading to disease in the host. One major factor expressed by all clinical isolates of gram-negative bacteria is lipopolysaccharide (LPS); a second factor expressed by some Escherichia coli strains is a K1 polysaccharide capsule. To determine the role of the CD14 LPS receptor in the pathogenic effects of naturally occurring E. coli, the responses of CD14-/- and CD14+/+ mice to three different isolates of E. coli obtained from sepsis patients were compared; two isolates express both smooth LPS and the K1 antigen, while the third isolate expresses only LPS and is negative for K1. An additional K1-positive isolate obtained from a newborn with meningitis and a K1-negative isogenic mutant of this strain were also used for these studies. CD14-/- mice were resistant to the lethal effects of the K1-negative isolates. This resistance was accompanied by significantly lower levels of systemic tumor necrosis factor alpha (TNF-alpha) and interleukin-6 (IL-6) in these mice than in CD14+/+ mice, enhanced clearance of the bacteria, and significantly fewer additional gross symptoms. In contrast, CD14-/- mice were as sensitive as CD14+/+ mice to the lethal effects of the K1-positive isolates, even though they had significantly lower levels of TNF-alpha and IL-6 than CD14+/+ mice. These studies show that different bacterial isolates can use distinctly different mechanisms to cause disease and suggest that new, nonantibiotic therapeutics need to be directed against multiple targets.
Texto completo:
1
Bases de datos:
MEDLINE
Asunto principal:
Polisacáridos Bacterianos
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Cápsulas Bacterianas
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Receptores de Lipopolisacáridos
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Escherichia coli
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Antígenos Bacterianos
Límite:
Animals
Idioma:
En
Revista:
Infect Immun
Año:
2007
Tipo del documento:
Article
País de afiliación:
Estados Unidos