PubMed:28456423 JSONTXT

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aureus Promotes Smed-PGRP-2/Smed-setd8-1 Methyltransferase Signalling in Planarian Neoblasts to Sensitize Anti-bacterial Gene Responses During Re-infection.\nLittle is known about how organisms exposed to recurrent infections adapt their innate immune responses. 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. We established the involvement of stem cell-like neoblasts in this instructed immunity using the complementary approaches of RNA-interference-mediated cell depletion and tissue grafting-mediated gain of function. 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. 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. 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. 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."}

{"project":"PubMed_ArguminSci","denotations":[{"id":"T1","span":{"begin":172,"end":276},"obj":"DRI_Challenge"},{"id":"T2","span":{"begin":277,"end":528},"obj":"DRI_Outcome"},{"id":"T3","span":{"begin":529,"end":567},"obj":"DRI_Approach"},{"id":"T4","span":{"begin":588,"end":741},"obj":"DRI_Approach"},{"id":"T5","span":{"begin":742,"end":967},"obj":"DRI_Background"},{"id":"T6","span":{"begin":968,"end":1168},"obj":"DRI_Outcome"},{"id":"T7","span":{"begin":1169,"end":1334},"obj":"DRI_Background"},{"id":"T8","span":{"begin":1335,"end":1541},"obj":"DRI_Outcome"}],"text":"Staphylococcus aureus Promotes Smed-PGRP-2/Smed-setd8-1 Methyltransferase Signalling in Planarian Neoblasts to Sensitize Anti-bacterial Gene Responses During Re-infection.\nLittle is known about how organisms exposed to recurrent infections adapt their innate immune responses. 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. We established the involvement of stem cell-like neoblasts in this instructed immunity using the complementary approaches of RNA-interference-mediated cell depletion and tissue grafting-mediated gain of function. 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. 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. 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. 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."}

{"project":"Goldhamster2_Cellosaurus","denotations":[{"id":"T1","span":{"begin":158,"end":160},"obj":"CVCL_U263|Spontaneously_immortalized_cell_line|Labeo rohita"},{"id":"T2","span":{"begin":283,"end":285},"obj":"CVCL_5M23|Cancer_cell_line|Mesocricetus auratus"},{"id":"T3","span":{"begin":317,"end":318},"obj":"CVCL_6479|Finite_cell_line|Mus musculus"},{"id":"T4","span":{"begin":408,"end":409},"obj":"CVCL_6479|Finite_cell_line|Mus musculus"},{"id":"T5","span":{"begin":454,"end":456},"obj":"CVCL_U263|Spontaneously_immortalized_cell_line|Labeo rohita"},{"id":"T6","span":{"begin":529,"end":531},"obj":"CVCL_5M23|Cancer_cell_line|Mesocricetus auratus"},{"id":"T7","span":{"begin":1053,"end":1055},"obj":"CVCL_U263|Spontaneously_immortalized_cell_line|Labeo rohita"},{"id":"T8","span":{"begin":1353,"end":1354},"obj":"CVCL_6479|Finite_cell_line|Mus musculus"},{"id":"T9","span":{"begin":1431,"end":1432},"obj":"CVCL_6479|Finite_cell_line|Mus musculus"},{"id":"T10","span":{"begin":1528,"end":1530},"obj":"CVCL_U263|Spontaneously_immortalized_cell_line|Labeo rohita"}],"text":"Staphylococcus aureus Promotes Smed-PGRP-2/Smed-setd8-1 Methyltransferase Signalling in Planarian Neoblasts to Sensitize Anti-bacterial Gene Responses During Re-infection.\nLittle is known about how organisms exposed to recurrent infections adapt their innate immune responses. 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. We established the involvement of stem cell-like neoblasts in this instructed immunity using the complementary approaches of RNA-interference-mediated cell depletion and tissue grafting-mediated gain of function. 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. 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. 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. 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."}