Human mannose-binding lectin inhibitor prevents Shiga toxin-induced renal injury

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Standard

Human mannose-binding lectin inhibitor prevents Shiga toxin-induced renal injury. / Ozaki, Masayuki; Kang, Yulin; Tan, Ying Siow; Pavlov, Vasile I; Liu, Bohan; Boyle, Daniel C; Kushak, Rafail I; Skjoedt, Mikkel-Ole; Grabowski, Eric F; Taira, Yasuhiko; Stahl, Gregory L.

I: Kidney International, Bind 90, Nr. 4, 10.2016, s. 774-782.

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt

Harvard

Ozaki, M, Kang, Y, Tan, YS, Pavlov, VI, Liu, B, Boyle, DC, Kushak, RI, Skjoedt, M-O, Grabowski, EF, Taira, Y & Stahl, GL 2016, 'Human mannose-binding lectin inhibitor prevents Shiga toxin-induced renal injury', Kidney International, bind 90, nr. 4, s. 774-782. https://doi.org/10.1016/j.kint.2016.05.011

APA

Ozaki, M., Kang, Y., Tan, Y. S., Pavlov, V. I., Liu, B., Boyle, D. C., Kushak, R. I., Skjoedt, M-O., Grabowski, E. F., Taira, Y., & Stahl, G. L. (2016). Human mannose-binding lectin inhibitor prevents Shiga toxin-induced renal injury. Kidney International, 90(4), 774-782. https://doi.org/10.1016/j.kint.2016.05.011

Vancouver

Ozaki M, Kang Y, Tan YS, Pavlov VI, Liu B, Boyle DC o.a. Human mannose-binding lectin inhibitor prevents Shiga toxin-induced renal injury. Kidney International. 2016 okt.;90(4):774-782. https://doi.org/10.1016/j.kint.2016.05.011

Author

Ozaki, Masayuki ; Kang, Yulin ; Tan, Ying Siow ; Pavlov, Vasile I ; Liu, Bohan ; Boyle, Daniel C ; Kushak, Rafail I ; Skjoedt, Mikkel-Ole ; Grabowski, Eric F ; Taira, Yasuhiko ; Stahl, Gregory L. / Human mannose-binding lectin inhibitor prevents Shiga toxin-induced renal injury. I: Kidney International. 2016 ; Bind 90, Nr. 4. s. 774-782.

Bibtex

@article{4174e05260a74af795b564b03fbd50b1,
title = "Human mannose-binding lectin inhibitor prevents Shiga toxin-induced renal injury",
abstract = "Hemolytic uremic syndrome caused by Shiga toxin-producing Escherichia coli (STEC HUS) is a worldwide endemic problem, and its pathophysiology is not fully elucidated. Here we tested whether the mannose-binding lectin (MBL2), an initiating factor of lectin complement pathway activation, plays a crucial role in STEC HUS. Using novel human MBL2-expressing mice (MBL2 KI) that lack murine Mbls (MBL2(+/+)Mbl1(-/-)Mbl2(-/-)), a novel STEC HUS model consisted of an intraperitoneal injection with Shiga toxin-2 (Stx-2) with or without anti-MBL2 antibody (3F8, intraperitoneal). Stx-2 induced weight loss, anemia, and thrombocytopenia and increased serum creatinine, free serum hemoglobin, and cystatin C levels, but a significantly decreased glomerular filtration rate compared with control/sham mice. Immunohistochemical staining revealed renal C3d deposition and fibrin deposition in glomeruli in Stx-2-injected mice. Treatment with 3F8 completely inhibited serum MBL2 levels and significantly attenuated Stx-2 induced-renal injury, free serum hemoglobin levels, renal C3d, and fibrin deposition and preserved the glomerular filtration rate. Thus, MBL2 inhibition significantly protected against complement activation and renal injury induced by Stx-2. This novel mouse model can be used to study the role of complement, particularly lectin pathway-mediated complement activation, in Stx-2-induced renal injury.",
author = "Masayuki Ozaki and Yulin Kang and Tan, {Ying Siow} and Pavlov, {Vasile I} and Bohan Liu and Boyle, {Daniel C} and Kushak, {Rafail I} and Mikkel-Ole Skjoedt and Grabowski, {Eric F} and Yasuhiko Taira and Stahl, {Gregory L}",
note = "Copyright {\textcopyright} 2016 International Society of Nephrology. Published by Elsevier Inc. All rights reserved.",
year = "2016",
month = oct,
doi = "10.1016/j.kint.2016.05.011",
language = "English",
volume = "90",
pages = "774--782",
journal = "Kidney International",
issn = "0085-2538",
publisher = "Elsevier",
number = "4",

}

RIS

TY - JOUR

T1 - Human mannose-binding lectin inhibitor prevents Shiga toxin-induced renal injury

AU - Ozaki, Masayuki

AU - Kang, Yulin

AU - Tan, Ying Siow

AU - Pavlov, Vasile I

AU - Liu, Bohan

AU - Boyle, Daniel C

AU - Kushak, Rafail I

AU - Skjoedt, Mikkel-Ole

AU - Grabowski, Eric F

AU - Taira, Yasuhiko

AU - Stahl, Gregory L

N1 - Copyright © 2016 International Society of Nephrology. Published by Elsevier Inc. All rights reserved.

PY - 2016/10

Y1 - 2016/10

N2 - Hemolytic uremic syndrome caused by Shiga toxin-producing Escherichia coli (STEC HUS) is a worldwide endemic problem, and its pathophysiology is not fully elucidated. Here we tested whether the mannose-binding lectin (MBL2), an initiating factor of lectin complement pathway activation, plays a crucial role in STEC HUS. Using novel human MBL2-expressing mice (MBL2 KI) that lack murine Mbls (MBL2(+/+)Mbl1(-/-)Mbl2(-/-)), a novel STEC HUS model consisted of an intraperitoneal injection with Shiga toxin-2 (Stx-2) with or without anti-MBL2 antibody (3F8, intraperitoneal). Stx-2 induced weight loss, anemia, and thrombocytopenia and increased serum creatinine, free serum hemoglobin, and cystatin C levels, but a significantly decreased glomerular filtration rate compared with control/sham mice. Immunohistochemical staining revealed renal C3d deposition and fibrin deposition in glomeruli in Stx-2-injected mice. Treatment with 3F8 completely inhibited serum MBL2 levels and significantly attenuated Stx-2 induced-renal injury, free serum hemoglobin levels, renal C3d, and fibrin deposition and preserved the glomerular filtration rate. Thus, MBL2 inhibition significantly protected against complement activation and renal injury induced by Stx-2. This novel mouse model can be used to study the role of complement, particularly lectin pathway-mediated complement activation, in Stx-2-induced renal injury.

AB - Hemolytic uremic syndrome caused by Shiga toxin-producing Escherichia coli (STEC HUS) is a worldwide endemic problem, and its pathophysiology is not fully elucidated. Here we tested whether the mannose-binding lectin (MBL2), an initiating factor of lectin complement pathway activation, plays a crucial role in STEC HUS. Using novel human MBL2-expressing mice (MBL2 KI) that lack murine Mbls (MBL2(+/+)Mbl1(-/-)Mbl2(-/-)), a novel STEC HUS model consisted of an intraperitoneal injection with Shiga toxin-2 (Stx-2) with or without anti-MBL2 antibody (3F8, intraperitoneal). Stx-2 induced weight loss, anemia, and thrombocytopenia and increased serum creatinine, free serum hemoglobin, and cystatin C levels, but a significantly decreased glomerular filtration rate compared with control/sham mice. Immunohistochemical staining revealed renal C3d deposition and fibrin deposition in glomeruli in Stx-2-injected mice. Treatment with 3F8 completely inhibited serum MBL2 levels and significantly attenuated Stx-2 induced-renal injury, free serum hemoglobin levels, renal C3d, and fibrin deposition and preserved the glomerular filtration rate. Thus, MBL2 inhibition significantly protected against complement activation and renal injury induced by Stx-2. This novel mouse model can be used to study the role of complement, particularly lectin pathway-mediated complement activation, in Stx-2-induced renal injury.

U2 - 10.1016/j.kint.2016.05.011

DO - 10.1016/j.kint.2016.05.011

M3 - Journal article

C2 - 27378476

VL - 90

SP - 774

EP - 782

JO - Kidney International

JF - Kidney International

SN - 0085-2538

IS - 4

ER -

ID: 172399001