Lack of formyl peptide receptor 1 and 2 leads to more severe inflammation and higher mortality in mice with of pneumococcal meningitis

Sandra Oldekamp; Sebastian Pscheidl; Eugenia Kress; Oliver Soehnlein; Sandra Jansen; Thomas Pufe; Ji Ming Wang; Simone C. Tauber; Lars‐Ove Brandenburg

doi:10.1111/imm.12324

journal article Oct 02, 2014

Lack of formyl peptide receptor 1 and 2 leads to more severe inflammation and higher mortality in mice with of pneumococcal meningitis

Sandra Oldekamp Sebastian Pscheidl Eugenia Kress Oliver Soehnlein

Sandra Jansen Thomas Pufe Ji Ming Wang

Simone C. Tauber Lars‐Ove Brandenburg

Immunology Vol. 143 No. 3 pp. 447-461 · Wiley

View at Publisher Save 10.1111/imm.12324

Abstract

SummaryBacterial meningitis is, despite progress in research and the development of new treatment strategies, still a cause of severe neuronal sequelae. The brain is protected from penetrating pathogens by both the blood–brain barrier and the innate immune system. The invading pathogens are recognized by pattern recognition receptors including the G‐protein coupled formyl peptide receptors (FPRs), which are expressed by immune cells of the central nervous system. The expression of FPRs is up‐regulated during bacterial meningitis, but the consequence on the progression of inflammation and impact on mortality are far from clear. Therefore, we used mFPR1 and mFPR2‐deficient mice to investigate the effects on inflammation, bacterial growth and mortality in a mouse model of pneumococcal meningitis. Our results revealed increased bacterial burden, increased neutrophil infiltration and higher mortality in mFPR1/2‐deficient mice in comparison to wild‐type mice. The mFPR1‐ or mFPR2‐deficient mice also showed significantly increased glial cell density, whereas the immune responses including the expression of anti‐inflammatory cytokines and antimicrobial peptides were decreased in bacterial meningitis. Taken together, the results suggest that FPR1 and FPR2 play an important role in the innate immune responses against Streptococcus pneumoniae within the central nervous system and the lack of the receptors leads to a dysregulation of the inflammatory response compared with wild‐type mice.

Topics

No keywords indexed for this article. Browse by subject →

References

49

[1]

10.1086/596498

[2]

10.1186/1471-2334-10-22

[3]

10.1056/nejm199710023371404

[4]

10.1097/qco.0b013e328337f49e

[5]

10.1007/s11481-009-9170-6

[6]

10.1111/j.1471-4159.2006.04076.x

[7]

DAMPs, PAMPs and alarmins: all we need to know about danger

Marco E Bianchi

Journal of Leukocyte Biology 10.1189/jlb.0306164

[8]

10.1084/jem.155.1.264

[9]

Circulating mitochondrial DAMPs cause inflammatory responses to injury

Qin Zhang, Mustafa Raoof, Yu Chen et al.

Nature 10.1038/nature08780

[10]

10.1006/geno.1998.5376

[11]

10.1124/mol.112.081315

[12]

10.1016/j.cytogfr.2006.09.009

[13]

10.1111/j.1471-4159.2010.06637.x

[14]

10.1007/s11064-010-0301-5

[15]

10.1038/srep00786

[16]

10.1084/jem.189.4.657

[17]

10.1186/1742-2094-8-11

[18]

10.4049/jimmunol.0903526

[19]

10.4049/jimmunol.0903022

[20]

10.1016/j.jneuroim.2009.10.004

[21]

Preparation of separate astroglial and oligodendroglial cell cultures from rat cerebral tissue.

K D McCarthy, J de Vellis

The Journal of cell biology 10.1083/jcb.85.3.890

[22]

10.1186/1750-1326-7-55

[23]

10.1007/s004010000326

[24]

10.1186/1742-2094-9-168

[25]

10.1097/01.jnen.0000178853.21799.88

[26]

10.1159/000353645

[27]

10.1016/j.jneuroim.2012.10.012

[28]

10.1007/s12031-012-9773-x

[29]

10.1152/physrev.00011.2010

[30]

10.3390/polym4010539

[31]

10.1074/jbc.272.20.13088

[32]

10.1042/cs20110164

[33]

10.1016/j.febslet.2006.10.061

[34]

10.2174/138161208783597407

[35]

10.1016/j.cca.2010.07.006

[36]

10.1160/th10-10-0662

[37]

10.3390/ijms14047193

[38]

10.1111/j.1471-4159.2006.04351.x

[39]

10.1016/s1471-4906(02)02316-5

[40]

10.1186/1471-2334-7-25

[41]

10.1128/iai.02008-06

[42]

Activation of Toll-like Receptor 2 on Microglia Promotes Cell Uptake of Alzheimer Disease-associated Amyloid β Peptide

Keqiang Chen, Pablo Iribarren, Jinyue Hu et al.

Journal of Biological Chemistry 10.1074/jbc.m508125200

[43]

10.1189/jlb.0907607

[44]

10.1016/j.bbrc.2009.01.068

[45]

10.1189/jlb.1008638

[46]

10.1074/jbc.m113.450635

[47]

10.1111/j.1365-2567.2009.03225.x

[48]

Innate immunity in the central nervous system

Richard M. Ransohoff, Melissa A. Brown

Journal of Clinical Investigation 10.1172/jci58644

[49]

10.1016/j.febslet.2011.05.030

Metrics

56

Citations

49

References

Details

Published: Oct 02, 2014
Vol/Issue: 143(3)
Pages: 447-461
License: View

Authors

S

Sandra Oldekamp

Department of Anatomy and Cell Biology RWTH Aachen University Aachen Germany

S

Sebastian Pscheidl

Department of Anatomy and Cell Biology RWTH Aachen University Aachen Germany

E

Eugenia Kress

Department of Anatomy and Cell Biology RWTH Aachen University Aachen Germany

O

Oliver Soehnlein

Institute for Cardiovascular Prevention LMU Munich Munich Germany

S

Sandra Jansen

Department of Anatomy and Cell Biology RWTH Aachen University Aachen Germany

T

Thomas Pufe

Department of Anatomy and Cell Biology RWTH Aachen University Aachen Germany

J

Ji Ming Wang

Laboratory of Molecular Immunoregulation Cancer and Inflammation Program Center for Cancer Research National Cancer Institute Frederick MD USA

S

Simone C. Tauber

Department of Neurology RWTH University Hospital Aachen Aachen Germany

L

Lars‐Ove Brandenburg

Department of Anatomy and Cell Biology RWTH Aachen University Aachen Germany

Cite This Article

Sandra Oldekamp, Sebastian Pscheidl, Eugenia Kress, et al. (2014). Lack of formyl peptide receptor 1 and 2 leads to more severe inflammation and higher mortality in mice with of pneumococcal meningitis. Immunology, 143(3), 447-461. https://doi.org/10.1111/imm.12324

Lack of formyl peptide receptor 1 and 2 leads to more severe inflammation and higher mortality in mice with of pneumococcal meningitis

You May Also Like