Abstract
Insights into the host factors and mechanisms mediating the primary host responses after pathogen presentation remain limited, due in part to the complexity and genetic intractability of host systems. Here, we employ the model Drosophila melanogaster to dissect and identify early host responses that function in the initiation and progression of Pseudomonas aeruginosa pathogenesis. First, we use immune potentiation and genetic studies to demonstrate that flies mount a heightened defense against the highly virulent P. aeruginosa strain PA14 when first inoculated with strain CF5, which is avirulent in flies; this effect is mediated via the Imd and Toll signaling pathways. Second, we use whole-genome expression profiling to assess and compare the Drosophila early defense responses triggered by the PA14 vs. CF5 strains to identify genes whose expression patterns are different in susceptible vs. resistant host-pathogen interactions, respectively. Our results identify pathogenesis- and defense-specific genes and uncover a previously undescribed mechanism used by P. aeruginosa in the initial stages of its host interaction: suppression of Drosophila defense responses by limiting antimicrobial peptide gene expression. These results provide insights into the genetic factors that mediate or restrict pathogenesis during the early stages of the bacterial-host interaction to advance our understanding of P. aeruginosa-human infections.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 2573-2578 |
| Number of pages | 6 |
| Journal | Proceedings of the National Academy of Sciences of the United States of America |
| Volume | 102 |
| Issue number | 7 |
| DOIs | |
| State | Published - Feb 15 2005 |
| Externally published | Yes |
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Keywords
- Drosophila melanogaster
- Immune potentiation
- Innate immunity
- Pathogenesis
ASJC Scopus subject areas
- General
Cite this
Profiling early infection responses : Pseudomonas aeruginosa eludes host defenses by suppressing antimocrobial peptide gene expression. / Apidianakis, Yiorgos; Mindrinos, Michael N.; Xiao, Wenzhong; Lau, Gee W.; Baldini, Regina L.; Davis, Ronald W.; Rahme, Laurence G.
In: Proceedings of the National Academy of Sciences of the United States of America, Vol. 102, No. 7, 15.02.2005, p. 2573-2578.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Profiling early infection responses
T2 - Pseudomonas aeruginosa eludes host defenses by suppressing antimocrobial peptide gene expression
AU - Apidianakis, Yiorgos
AU - Mindrinos, Michael N.
AU - Xiao, Wenzhong
AU - Lau, Gee W.
AU - Baldini, Regina L.
AU - Davis, Ronald W.
AU - Rahme, Laurence G.
PY - 2005/2/15
Y1 - 2005/2/15
N2 - Insights into the host factors and mechanisms mediating the primary host responses after pathogen presentation remain limited, due in part to the complexity and genetic intractability of host systems. Here, we employ the model Drosophila melanogaster to dissect and identify early host responses that function in the initiation and progression of Pseudomonas aeruginosa pathogenesis. First, we use immune potentiation and genetic studies to demonstrate that flies mount a heightened defense against the highly virulent P. aeruginosa strain PA14 when first inoculated with strain CF5, which is avirulent in flies; this effect is mediated via the Imd and Toll signaling pathways. Second, we use whole-genome expression profiling to assess and compare the Drosophila early defense responses triggered by the PA14 vs. CF5 strains to identify genes whose expression patterns are different in susceptible vs. resistant host-pathogen interactions, respectively. Our results identify pathogenesis- and defense-specific genes and uncover a previously undescribed mechanism used by P. aeruginosa in the initial stages of its host interaction: suppression of Drosophila defense responses by limiting antimicrobial peptide gene expression. These results provide insights into the genetic factors that mediate or restrict pathogenesis during the early stages of the bacterial-host interaction to advance our understanding of P. aeruginosa-human infections.
AB - Insights into the host factors and mechanisms mediating the primary host responses after pathogen presentation remain limited, due in part to the complexity and genetic intractability of host systems. Here, we employ the model Drosophila melanogaster to dissect and identify early host responses that function in the initiation and progression of Pseudomonas aeruginosa pathogenesis. First, we use immune potentiation and genetic studies to demonstrate that flies mount a heightened defense against the highly virulent P. aeruginosa strain PA14 when first inoculated with strain CF5, which is avirulent in flies; this effect is mediated via the Imd and Toll signaling pathways. Second, we use whole-genome expression profiling to assess and compare the Drosophila early defense responses triggered by the PA14 vs. CF5 strains to identify genes whose expression patterns are different in susceptible vs. resistant host-pathogen interactions, respectively. Our results identify pathogenesis- and defense-specific genes and uncover a previously undescribed mechanism used by P. aeruginosa in the initial stages of its host interaction: suppression of Drosophila defense responses by limiting antimicrobial peptide gene expression. These results provide insights into the genetic factors that mediate or restrict pathogenesis during the early stages of the bacterial-host interaction to advance our understanding of P. aeruginosa-human infections.
KW - Drosophila melanogaster
KW - Immune potentiation
KW - Innate immunity
KW - Pathogenesis
UR - http://www.scopus.com/inward/record.url?scp=14044277610&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=14044277610&partnerID=8YFLogxK
U2 - 10.1073/pnas.0409588102
DO - 10.1073/pnas.0409588102
M3 - Article
C2 - 15695583
AN - SCOPUS:14044277610
VL - 102
SP - 2573
EP - 2578
JO - Proceedings of the National Academy of Sciences of the United States of America
JF - Proceedings of the National Academy of Sciences of the United States of America
SN - 0027-8424
IS - 7
ER -