| Id |
Subject |
Object |
Predicate |
Lexical cue |
| T1 |
172-276 |
DRI_Challenge |
denotes |
Little is known about how organisms exposed to recurrent infections adapt their innate immune responses. |
| T2 |
277-528 |
DRI_Outcome |
denotes |
Here, we report that planarians display a form of instructed immunity to primo-infection by Staphylococcus aureus that consists of a transient state of heightened resistance to re-infection that persists for approximately 30days after primo-infection. |
| T3 |
529-567 |
DRI_Approach |
denotes |
We established the involvement of stem |
| T4 |
588-741 |
DRI_Approach |
denotes |
in this instructed immunity using the complementary approaches of RNA-interference-mediated cell depletion and tissue grafting-mediated gain of function. |
| T5 |
742-967 |
DRI_Background |
denotes |
Mechanistically, primo-infection leads to expression of the peptidoglycan receptor Smed-PGRP-2, which in turn promotes Smed-setd8-1 histone methyltransferase expression and increases levels of lysine methylation in neoblasts. |
| T6 |
968-1168 |
DRI_Outcome |
denotes |
Depletion of neoblasts did not affect S. aureus clearance in primo-infection but, in re-infection, abrogated the heightened elimination of bacteria and reduced Smed-PGRP-2 and Smed-setd8-1 expression. |
| T7 |
1169-1334 |
DRI_Background |
denotes |
Smed-PGRP-2 and Smed-setd8-1 sensitize animals to heightened expression of Smed-p38 MAPK and Smed-morn2, which are downstream components of anti-bacterial responses. |
| T8 |
1335-1541 |
DRI_Outcome |
denotes |
Our study reveals a central role of neoblasts in innate immunity against S. aureus to establish a resistance state facilitating Smed-sted8-1-dependent expression of anti-bacterial genes during re-infection. |
