Correction
for Mehrad et al., J Immunol 176 (5) 3233-3239.
The Journal of Immunology, 2006, 176: 7788.
Copyright © 2006 by The American Association of Immunologists
The lupus-susceptibility locus, Sle3, mediates enhanced resistance to bacterial infections
B. Mehrad,
S. J. Park,
G. Akangire,
T. J. Standiford,
T. Wu,
J. Zhu and
C. Mohan
Mehrad, B., S. J. Park, G. Akangire, T. J. Standiford, T. Wu, J. Zhu, and C. Mohan. 2006. The lupus-susceptibility locus, Sle3, mediates enhanced resistance to bacterial infections. J. Immunol. 176: 3233–3239.
In Results, in the second paragraph under the heading Role of delayed neutrophil apoptosis, reference to supplemental data and the respective footnote (4) are incorrect. The corrected sentence and data added as Figure 7 are shown below.
We also examined the role of this locus in another bacterial infection: in a model of intra-abdominal sepsis, we found greater number of i.p. neutrophils in B6.Sle3 as compared with B6 mice associated with fewer viable bacteria in the peritoneal cavity and bloodstream on day 1 of infection (Fig. 7), suggesting that the microbicidal and neutrophil phenotype conferred by the Sle3 locus is not restricted to a single organ or pathogen.
View larger version (20K):
[in this window]
[in a new window]
|
FIGURE 7. Effect of Sle3 locus in intra-abdominal sepsis. a and b, Bacterial burden and number of intra-peritoneal neutrophils on day 1 after cecal ligation and puncture, performed as described (1). Data represent mean ± SEM (n = 6–9 mice/group; representative of 2 experiments). CFU, colony-forming unit; ND, none detected; *, p < 0.05 compared to wildtypes. c, Survival in mice with cecal ligation and puncture (n = 10 mice/group); representative of 2 experiments).
|
|
