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Mice deficient in NKLAM have attenuated inflammatory cytokine production in a Sendai virus pneumonia model
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Mice deficient in NKLAM have attenuated inflammatory cytokine production in a Sendai virus pneumonia model
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Mice deficient in NKLAM have attenuated inflammatory cytokine production in a Sendai virus pneumonia model
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Journal Article
Mice deficient in NKLAM have attenuated inflammatory cytokine production in a Sendai virus pneumonia model
2019
Overview
Recent studies have begun to elucidate a role for E3 ubiquitin ligases as important mediators of the innate immune response. Our previous work defined a role for the ubiquitin ligase natural killer lytic-associated molecule (NKLAM/RNF19b) in mouse and human innate immunity. Here, we present novel data describing a role for NKLAM in regulating the immune response to Sendai virus (SeV), a murine model of paramyxoviral pneumonia. NKLAM expression was significantly upregulated by SeV infection. SeV-infected mice that are deficient in NKLAM demonstrated significantly less weight loss than wild type mice. In vivo, Sendai virus replication was attenuated in NKLAM-/- mice. Autophagic flux and the expression of autophagy markers LC3 and p62/SQSTM1 were also less in NKLAM-/- mice. Using flow cytometry, we observed less neutrophils and macrophages in the lungs of NKLAM-/- mice during SeV infection. Additionally, phosphorylation of STAT1 and NFκB p65 was lower in NKLAM-/- than wild type mice. The dysregulated phosphorylation profile of STAT1 and NFκB in NKLAM-/- mice correlated with decreased expression of numerous proinflammatory cytokines that are regulated by STAT1 and/or NFκB. The lack of NKLAM and the resulting attenuated immune response is favorable to NKLAM-/- mice receiving a low dose of SeV; however, at a high dose of virus, NKLAM-/- mice succumbed to the infection faster than wild type mice. In conclusion, our novel results indicate that NKLAM plays a role in regulating the production of pro-inflammatory cytokines during viral infection.
Publisher
Public Library of Science,Public Library of Science (PLoS)
Subject
/ Animals
/ Humans
/ Inflammation Mediators - metabolism
/ Ligases
/ Medicine
/ Medicine and Health Sciences
/ Membrane Proteins - deficiency
/ Membrane Proteins - genetics
/ Mice
/ Novels
/ Proteins
/ Research and Analysis Methods
/ Respirovirus Infections - genetics
/ Respirovirus Infections - metabolism
/ Respirovirus Infections - virology
/ Sequestosome-1 Protein - genetics
/ Sequestosome-1 Protein - metabolism
/ Transcription Factor RelA - genetics
/ Transcription Factor RelA - metabolism
/ Viruses
