Publication

CD14 is a key organizer of microglial responses to CNS infection and injury

Janova, H., Boettcher, C., Holtman, I. R., Regen, T., van Rossum, D., Goetz, A., Ernst, A-S., Fritsche, C., Gertig, U., Saiepour, N., Gronke, K., Wrzos, C., Ribes, S., Rolfes, S., Weinstein, J., Ehrenreich, H., Pukrop, T., Kopatz, J., Stadelmann, C., Salinas-Riester, G., Weber, M. S., Prinz, M., Brueck, W., Eggen, B. J. L., Boddeke, H. W. G. M., Priller, J. & Hanisch, U-K., Apr-2016, In : Glia. 64, 4, p. 635-649 15 p.

Research output: Contribution to journalArticleAcademicpeer-review

APA

Janova, H., Boettcher, C., Holtman, I. R., Regen, T., van Rossum, D., Goetz, A., ... Hanisch, U-K. (2016). CD14 is a key organizer of microglial responses to CNS infection and injury. Glia, 64(4), 635-649. https://doi.org/10.1002/glia.22955

Author

Janova, Hana ; Boettcher, Chotima ; Holtman, Inge R. ; Regen, Tommy ; van Rossum, Denise ; Goetz, Alexander ; Ernst, Anne-Sophie ; Fritsche, Christin ; Gertig, Ulla ; Saiepour, Nasrin ; Gronke, Konrad ; Wrzos, Claudia ; Ribes, Sandra ; Rolfes, Simone ; Weinstein, Jonathan ; Ehrenreich, Hannelore ; Pukrop, Tobias ; Kopatz, Jens ; Stadelmann, Christine ; Salinas-Riester, Gabriela ; Weber, Martin S. ; Prinz, Marco ; Brueck, Wolfgang ; Eggen, Bart J. L. ; Boddeke, Hendrikus W. G. M. ; Priller, Josef ; Hanisch, Uwe-Karsten. / CD14 is a key organizer of microglial responses to CNS infection and injury. In: Glia. 2016 ; Vol. 64, No. 4. pp. 635-649.

Harvard

Janova, H, Boettcher, C, Holtman, IR, Regen, T, van Rossum, D, Goetz, A, Ernst, A-S, Fritsche, C, Gertig, U, Saiepour, N, Gronke, K, Wrzos, C, Ribes, S, Rolfes, S, Weinstein, J, Ehrenreich, H, Pukrop, T, Kopatz, J, Stadelmann, C, Salinas-Riester, G, Weber, MS, Prinz, M, Brueck, W, Eggen, BJL, Boddeke, HWGM, Priller, J & Hanisch, U-K 2016, 'CD14 is a key organizer of microglial responses to CNS infection and injury', Glia, vol. 64, no. 4, pp. 635-649. https://doi.org/10.1002/glia.22955

Standard

CD14 is a key organizer of microglial responses to CNS infection and injury. / Janova, Hana; Boettcher, Chotima; Holtman, Inge R.; Regen, Tommy; van Rossum, Denise; Goetz, Alexander; Ernst, Anne-Sophie; Fritsche, Christin; Gertig, Ulla; Saiepour, Nasrin; Gronke, Konrad; Wrzos, Claudia; Ribes, Sandra; Rolfes, Simone; Weinstein, Jonathan; Ehrenreich, Hannelore; Pukrop, Tobias; Kopatz, Jens; Stadelmann, Christine; Salinas-Riester, Gabriela; Weber, Martin S.; Prinz, Marco; Brueck, Wolfgang; Eggen, Bart J. L.; Boddeke, Hendrikus W. G. M.; Priller, Josef; Hanisch, Uwe-Karsten.

In: Glia, Vol. 64, No. 4, 04.2016, p. 635-649.

Research output: Contribution to journalArticleAcademicpeer-review

Vancouver

Janova H, Boettcher C, Holtman IR, Regen T, van Rossum D, Goetz A et al. CD14 is a key organizer of microglial responses to CNS infection and injury. Glia. 2016 Apr;64(4):635-649. https://doi.org/10.1002/glia.22955


BibTeX

@article{9483dc0cf2bd4071a5510b28ae387d5c,
title = "CD14 is a key organizer of microglial responses to CNS infection and injury",
abstract = "Microglia, innate immune cells of the CNS, sense infection and damage through overlapping receptor sets. Toll-like receptor (TLR) 4 recognizes bacterial lipopolysaccharide (LPS) and multiple injury-associated factors. We show that its co-receptor CD14 serves three non-redundant functions in microglia. First, it confers an up to 100-fold higher LPS sensitivity compared to peripheral macrophages to enable efficient proinflammatory cytokine induction. Second, CD14 prevents excessive responses to massive LPS challenges via an interferon -mediated feedback. Third, CD14 is mandatory for microglial reactions to tissue damage-associated signals. In mice, these functions are essential for balanced CNS responses to bacterial infection, traumatic and ischemic injuries, since CD14 deficiency causes either hypo- or hyperinflammation, insufficient or exaggerated immune cell recruitment or worsened stroke outcomes. While CD14 orchestrates functions of TLR4 and related immune receptors, it is itself regulated by TLR and non-TLR systems to thereby fine-tune microglial damage-sensing capacity upon infectious and non-infectious CNS challenges.",
keywords = "chemokines, cytokines, inflammation, monocytes, neutrophils, Toll-like receptor, damage, RECEPTOR 4, I INTERFERON, BRAIN, CELLS, LPS, INFLAMMATION, ACTIVATION, LIPOPOLYSACCHARIDE, RECRUITMENT, MACROPHAGES",
author = "Hana Janova and Chotima Boettcher and Holtman, {Inge R.} and Tommy Regen and {van Rossum}, Denise and Alexander Goetz and Anne-Sophie Ernst and Christin Fritsche and Ulla Gertig and Nasrin Saiepour and Konrad Gronke and Claudia Wrzos and Sandra Ribes and Simone Rolfes and Jonathan Weinstein and Hannelore Ehrenreich and Tobias Pukrop and Jens Kopatz and Christine Stadelmann and Gabriela Salinas-Riester and Weber, {Martin S.} and Marco Prinz and Wolfgang Brueck and Eggen, {Bart J. L.} and Boddeke, {Hendrikus W. G. M.} and Josef Priller and Uwe-Karsten Hanisch",
note = "{\circledC} 2015 Wiley Periodicals, Inc.",
year = "2016",
month = "4",
doi = "10.1002/glia.22955",
language = "English",
volume = "64",
pages = "635--649",
journal = "Glia",
issn = "0894-1491",
publisher = "WILEY",
number = "4",

}

RIS

TY - JOUR

T1 - CD14 is a key organizer of microglial responses to CNS infection and injury

AU - Janova, Hana

AU - Boettcher, Chotima

AU - Holtman, Inge R.

AU - Regen, Tommy

AU - van Rossum, Denise

AU - Goetz, Alexander

AU - Ernst, Anne-Sophie

AU - Fritsche, Christin

AU - Gertig, Ulla

AU - Saiepour, Nasrin

AU - Gronke, Konrad

AU - Wrzos, Claudia

AU - Ribes, Sandra

AU - Rolfes, Simone

AU - Weinstein, Jonathan

AU - Ehrenreich, Hannelore

AU - Pukrop, Tobias

AU - Kopatz, Jens

AU - Stadelmann, Christine

AU - Salinas-Riester, Gabriela

AU - Weber, Martin S.

AU - Prinz, Marco

AU - Brueck, Wolfgang

AU - Eggen, Bart J. L.

AU - Boddeke, Hendrikus W. G. M.

AU - Priller, Josef

AU - Hanisch, Uwe-Karsten

N1 - © 2015 Wiley Periodicals, Inc.

PY - 2016/4

Y1 - 2016/4

N2 - Microglia, innate immune cells of the CNS, sense infection and damage through overlapping receptor sets. Toll-like receptor (TLR) 4 recognizes bacterial lipopolysaccharide (LPS) and multiple injury-associated factors. We show that its co-receptor CD14 serves three non-redundant functions in microglia. First, it confers an up to 100-fold higher LPS sensitivity compared to peripheral macrophages to enable efficient proinflammatory cytokine induction. Second, CD14 prevents excessive responses to massive LPS challenges via an interferon -mediated feedback. Third, CD14 is mandatory for microglial reactions to tissue damage-associated signals. In mice, these functions are essential for balanced CNS responses to bacterial infection, traumatic and ischemic injuries, since CD14 deficiency causes either hypo- or hyperinflammation, insufficient or exaggerated immune cell recruitment or worsened stroke outcomes. While CD14 orchestrates functions of TLR4 and related immune receptors, it is itself regulated by TLR and non-TLR systems to thereby fine-tune microglial damage-sensing capacity upon infectious and non-infectious CNS challenges.

AB - Microglia, innate immune cells of the CNS, sense infection and damage through overlapping receptor sets. Toll-like receptor (TLR) 4 recognizes bacterial lipopolysaccharide (LPS) and multiple injury-associated factors. We show that its co-receptor CD14 serves three non-redundant functions in microglia. First, it confers an up to 100-fold higher LPS sensitivity compared to peripheral macrophages to enable efficient proinflammatory cytokine induction. Second, CD14 prevents excessive responses to massive LPS challenges via an interferon -mediated feedback. Third, CD14 is mandatory for microglial reactions to tissue damage-associated signals. In mice, these functions are essential for balanced CNS responses to bacterial infection, traumatic and ischemic injuries, since CD14 deficiency causes either hypo- or hyperinflammation, insufficient or exaggerated immune cell recruitment or worsened stroke outcomes. While CD14 orchestrates functions of TLR4 and related immune receptors, it is itself regulated by TLR and non-TLR systems to thereby fine-tune microglial damage-sensing capacity upon infectious and non-infectious CNS challenges.

KW - chemokines

KW - cytokines

KW - inflammation

KW - monocytes

KW - neutrophils

KW - Toll-like receptor

KW - damage

KW - RECEPTOR 4

KW - I INTERFERON

KW - BRAIN

KW - CELLS

KW - LPS

KW - INFLAMMATION

KW - ACTIVATION

KW - LIPOPOLYSACCHARIDE

KW - RECRUITMENT

KW - MACROPHAGES

U2 - 10.1002/glia.22955

DO - 10.1002/glia.22955

M3 - Article

VL - 64

SP - 635

EP - 649

JO - Glia

JF - Glia

SN - 0894-1491

IS - 4

ER -

ID: 27600259