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231226s2023 xx |||||o 00| ||eng c |
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|a 10.1016/j.clim.2023.109819
|2 doi
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|a pubmed24n1371.xml
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|a (DE-627)NLM364103418
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|a (NLM)37918467
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|a (PII)S1521-6616(23)00582-X
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|a DE-627
|b ger
|c DE-627
|e rakwb
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|a eng
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| 100 |
1 |
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|a Lee, Unn Hwa
|e verfasserin
|4 aut
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| 245 |
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|a DRG2 in macrophages is crucial for initial inflammatory response and protection against Listeria monocytogenes infection
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|c 2023
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|a Text
|b txt
|2 rdacontent
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|a ƒaComputermedien
|b c
|2 rdamedia
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|a ƒa Online-Ressource
|b cr
|2 rdacarrier
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|a Date Completed 11.01.2024
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|a Date Revised 10.04.2024
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|a published: Print-Electronic
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|a Citation Status MEDLINE
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|a Copyright © 2023 Elsevier Inc. All rights reserved.
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|a Innate immune response is critical for the control of Listeria monocytogenes infection. Here, we identified developmentally regulated GTP-binding protein 2 (DRG2) in macrophages as a major regulator of the innate immune response against L. monocytogenes infection. Both whole-body DRG2 knockout (KO) mice and macrophage-specific DRG2 KO mice had low levels of IL-6 during early infection and increased susceptibility to L. monocytogenes infection. Following an initial impaired inflammatory response of macrophages upon i.p. L. monocytogenes infection, DRG2-/- mice showed delayed recruitment of neutrophils and monocytes into the peritoneal cavity, which led to elevated bacterial burden, inflammatory cytokine production at a late infection time point, and liver micro-abscesses. DRG2 deficiency decreased the transcriptional activity of NF-κB and impaired the inflammatory response of both bone marrow-derived and peritoneal macrophages upon L. monocytogenes stimulation. Our findings reveal that DRG2 in macrophages is critical for the initial inflammatory response and protection against L. monocytogenes infection
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|a Journal Article
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|a Research Support, Non-U.S. Gov't
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|a DRG2
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|a Inflammatory response
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|a L. monocytogenes
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|a NF-κB
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|a Tissue-resident macrophages
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|a developmentally regulated GTP-binding protein
|2 NLM
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|a 149371-72-2
|2 NLM
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|a GTP-Binding Proteins
|2 NLM
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| 650 |
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|a EC 3.6.1.-
|2 NLM
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| 700 |
1 |
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|a Park, Sang Jin
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Ju, Seong A
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Lee, Sang Chul
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Kim, Byung Sam
|e verfasserin
|4 aut
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| 700 |
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|a Ahn, Byungyong
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Yi, Jawoon
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Park, Jihwan
|e verfasserin
|4 aut
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1 |
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|a Won, Young-Wook
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Han, In Seob
|e verfasserin
|4 aut
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| 700 |
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|a Lee, Byung Ju
|e verfasserin
|4 aut
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|a Cho, Wha Ja
|e verfasserin
|4 aut
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| 700 |
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|a Park, Jeong Woo
|e verfasserin
|4 aut
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| 773 |
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|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 257(2023) vom: 02. Dez., Seite 109819
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnns
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| 773 |
1 |
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|g volume:257
|g year:2023
|g day:02
|g month:12
|g pages:109819
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|u http://dx.doi.org/10.1016/j.clim.2023.109819
|3 Volltext
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