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Anti-GBM glomerulonephritis involves IL-1 but is independent of NLRP3/ASC inflammasome-mediated activation of caspase-1

Standard

Anti-GBM glomerulonephritis involves IL-1 but is independent of NLRP3/ASC inflammasome-mediated activation of caspase-1. / Lichtnekert, Julia; Kulkarni, Onkar P; Mulay, Shrikant R; Rupanagudi, Khader Valli; Ryu, Mi; Allam, Ramanjaneyulu; Vielhauer, Volker; Muruve, Dan; Lindenmeyer, Maja T; Cohen, Clemens D; Anders, Hans-Joachim.

in: PLOS ONE, Jahrgang 6, Nr. 10, 2011, S. e26778.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Lichtnekert, J, Kulkarni, OP, Mulay, SR, Rupanagudi, KV, Ryu, M, Allam, R, Vielhauer, V, Muruve, D, Lindenmeyer, MT, Cohen, CD & Anders, H-J 2011, 'Anti-GBM glomerulonephritis involves IL-1 but is independent of NLRP3/ASC inflammasome-mediated activation of caspase-1', PLOS ONE, Jg. 6, Nr. 10, S. e26778. https://doi.org/10.1371/journal.pone.0026778

APA

Lichtnekert, J., Kulkarni, O. P., Mulay, S. R., Rupanagudi, K. V., Ryu, M., Allam, R., Vielhauer, V., Muruve, D., Lindenmeyer, M. T., Cohen, C. D., & Anders, H-J. (2011). Anti-GBM glomerulonephritis involves IL-1 but is independent of NLRP3/ASC inflammasome-mediated activation of caspase-1. PLOS ONE, 6(10), e26778. https://doi.org/10.1371/journal.pone.0026778

Vancouver

Lichtnekert J, Kulkarni OP, Mulay SR, Rupanagudi KV, Ryu M, Allam R et al. Anti-GBM glomerulonephritis involves IL-1 but is independent of NLRP3/ASC inflammasome-mediated activation of caspase-1. PLOS ONE. 2011;6(10):e26778. https://doi.org/10.1371/journal.pone.0026778

Bibtex

@article{c307bd3b57184b02b2c1568a21a8836a,
title = "Anti-GBM glomerulonephritis involves IL-1 but is independent of NLRP3/ASC inflammasome-mediated activation of caspase-1",
abstract = "IL-1β and IL-18 are proinflammatory cytokines that contribute to renal immune complex disease, but whether IL-1β and IL-18 are mediators of intrinsic glomerular inflammation is unknown. In contrast to other cytokines the secretion of IL-1β and IL-18 requires a second stimulus that activates the inflammasome-ASC-caspase-1 pathway to cleave pro-IL-1β and -IL-18 into their mature and secretable forms. As the NLRP3 inflammasome and caspase-1 were shown to contribute to postischemic and postobstructive tubulointerstitial inflammation, we hypothesized a similar role for NLRP3, ASC, and caspase-1 in glomerular immunopathology. This concept was supported by the finding that lack of IL-1R1 reduced antiserum-induced focal segmental necrosis, crescent formation, and tubular atrophy when compared to wildtype mice. Lack of IL-18 reduced tubular atrophy only. However, NLRP3-, ASC- or caspase-1-deficiency had no significant effect on renal histopathology or proteinuria of serum nephritis. In vitro studies with mouse glomeruli or mesangial cells, glomerular endothelial cells, and podocytes did not reveal any pro-IL-1β induction upon LPS stimulation and no caspase-1 activation after an additional exposure to the NLRP3 agonist ATP. Only renal dendritic cells, which reside mainly in the tubulointerstitium, expressed pro-IL-1β and were able to activate the NLRP3-caspase-1 axis and secrete mature IL-1β. Together, the NLRP3-ASC-caspase-1 axis does not contribute to intrinsic glomerular inflammation via glomerular parenchymal cells as these cannot produce IL-1β during sterile inflammation.",
keywords = "Animals, Autoantibodies, Carrier Proteins, Caspase 1, Cytokines, Enzyme Activation, Glomerulonephritis, Inflammasomes, Inflammation, Interleukin-1, Interleukin-1beta, Mice, NLR Family, Pyrin Domain-Containing 3 Protein, Journal Article, Research Support, Non-U.S. Gov't",
author = "Julia Lichtnekert and Kulkarni, {Onkar P} and Mulay, {Shrikant R} and Rupanagudi, {Khader Valli} and Mi Ryu and Ramanjaneyulu Allam and Volker Vielhauer and Dan Muruve and Lindenmeyer, {Maja T} and Cohen, {Clemens D} and Hans-Joachim Anders",
year = "2011",
doi = "10.1371/journal.pone.0026778",
language = "English",
volume = "6",
pages = "e26778",
journal = "PLOS ONE",
issn = "1932-6203",
publisher = "Public Library of Science",
number = "10",

}

RIS

TY - JOUR

T1 - Anti-GBM glomerulonephritis involves IL-1 but is independent of NLRP3/ASC inflammasome-mediated activation of caspase-1

AU - Lichtnekert, Julia

AU - Kulkarni, Onkar P

AU - Mulay, Shrikant R

AU - Rupanagudi, Khader Valli

AU - Ryu, Mi

AU - Allam, Ramanjaneyulu

AU - Vielhauer, Volker

AU - Muruve, Dan

AU - Lindenmeyer, Maja T

AU - Cohen, Clemens D

AU - Anders, Hans-Joachim

PY - 2011

Y1 - 2011

N2 - IL-1β and IL-18 are proinflammatory cytokines that contribute to renal immune complex disease, but whether IL-1β and IL-18 are mediators of intrinsic glomerular inflammation is unknown. In contrast to other cytokines the secretion of IL-1β and IL-18 requires a second stimulus that activates the inflammasome-ASC-caspase-1 pathway to cleave pro-IL-1β and -IL-18 into their mature and secretable forms. As the NLRP3 inflammasome and caspase-1 were shown to contribute to postischemic and postobstructive tubulointerstitial inflammation, we hypothesized a similar role for NLRP3, ASC, and caspase-1 in glomerular immunopathology. This concept was supported by the finding that lack of IL-1R1 reduced antiserum-induced focal segmental necrosis, crescent formation, and tubular atrophy when compared to wildtype mice. Lack of IL-18 reduced tubular atrophy only. However, NLRP3-, ASC- or caspase-1-deficiency had no significant effect on renal histopathology or proteinuria of serum nephritis. In vitro studies with mouse glomeruli or mesangial cells, glomerular endothelial cells, and podocytes did not reveal any pro-IL-1β induction upon LPS stimulation and no caspase-1 activation after an additional exposure to the NLRP3 agonist ATP. Only renal dendritic cells, which reside mainly in the tubulointerstitium, expressed pro-IL-1β and were able to activate the NLRP3-caspase-1 axis and secrete mature IL-1β. Together, the NLRP3-ASC-caspase-1 axis does not contribute to intrinsic glomerular inflammation via glomerular parenchymal cells as these cannot produce IL-1β during sterile inflammation.

AB - IL-1β and IL-18 are proinflammatory cytokines that contribute to renal immune complex disease, but whether IL-1β and IL-18 are mediators of intrinsic glomerular inflammation is unknown. In contrast to other cytokines the secretion of IL-1β and IL-18 requires a second stimulus that activates the inflammasome-ASC-caspase-1 pathway to cleave pro-IL-1β and -IL-18 into their mature and secretable forms. As the NLRP3 inflammasome and caspase-1 were shown to contribute to postischemic and postobstructive tubulointerstitial inflammation, we hypothesized a similar role for NLRP3, ASC, and caspase-1 in glomerular immunopathology. This concept was supported by the finding that lack of IL-1R1 reduced antiserum-induced focal segmental necrosis, crescent formation, and tubular atrophy when compared to wildtype mice. Lack of IL-18 reduced tubular atrophy only. However, NLRP3-, ASC- or caspase-1-deficiency had no significant effect on renal histopathology or proteinuria of serum nephritis. In vitro studies with mouse glomeruli or mesangial cells, glomerular endothelial cells, and podocytes did not reveal any pro-IL-1β induction upon LPS stimulation and no caspase-1 activation after an additional exposure to the NLRP3 agonist ATP. Only renal dendritic cells, which reside mainly in the tubulointerstitium, expressed pro-IL-1β and were able to activate the NLRP3-caspase-1 axis and secrete mature IL-1β. Together, the NLRP3-ASC-caspase-1 axis does not contribute to intrinsic glomerular inflammation via glomerular parenchymal cells as these cannot produce IL-1β during sterile inflammation.

KW - Animals

KW - Autoantibodies

KW - Carrier Proteins

KW - Caspase 1

KW - Cytokines

KW - Enzyme Activation

KW - Glomerulonephritis

KW - Inflammasomes

KW - Inflammation

KW - Interleukin-1

KW - Interleukin-1beta

KW - Mice

KW - NLR Family, Pyrin Domain-Containing 3 Protein

KW - Journal Article

KW - Research Support, Non-U.S. Gov't

U2 - 10.1371/journal.pone.0026778

DO - 10.1371/journal.pone.0026778

M3 - SCORING: Journal article

C2 - 22046355

VL - 6

SP - e26778

JO - PLOS ONE

JF - PLOS ONE

SN - 1932-6203

IS - 10

ER -