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Article ; Online: Mechanical adaptation of brachiopod shells via hydration-induced structural changes.

Ihli, Johannes / Schenk, Anna S / Rosenfeldt, Sabine / Wakonig, Klaus / Holler, Mirko / Falini, Giuseppe / Pasquini, Luca / Delacou, Eugénia / Buckman, Jim / Glen, Thomas S / Kress, Thomas / Tsai, Esther H R / Reid, David G / Duer, Melinda J / Cusack, Maggie / Nudelman, Fabio

Nature communications

2021 Volume 12, Issue 1, Page(s) 5383

Abstract: The function-optimized properties of biominerals arise from the hierarchical organization of primary building blocks. Alteration of properties in response to environmental stresses generally involves time-intensive processes of resorption and ... ...

Abstract	The function-optimized properties of biominerals arise from the hierarchical organization of primary building blocks. Alteration of properties in response to environmental stresses generally involves time-intensive processes of resorption and reprecipitation of mineral in the underlying organic scaffold. Here, we report that the load-bearing shells of the brachiopod Discinisca tenuis are an exception to this process. These shells can dynamically modulate their mechanical properties in response to a change in environment, switching from hard and stiff when dry to malleable when hydrated within minutes. Using ptychographic X-ray tomography, electron microscopy and spectroscopy, we describe their hierarchical structure and composition as a function of hydration to understand the structural motifs that generate this adaptability. Key is a complementary set of structural modifications, starting with the swelling of an organic matrix on the micron level via nanocrystal reorganization and ending in an intercalation process on the molecular level in response to hydration.
MeSH term(s)	Adaptation, Physiological ; Animal Shells/anatomy & histology ; Animal Shells/physiology ; Animal Shells/ultrastructure ; Animals ; Invertebrates/anatomy & histology ; Invertebrates/physiology ; Invertebrates/ultrastructure ; Microscopy, Electron ; Organism Hydration Status/physiology
Language	English
Publishing date	2021-09-10
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-021-25613-4
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Article ; Online: Mechanical adaptation of brachiopod shells via hydration-induced structural changes

Johannes Ihli / Anna S. Schenk / Sabine Rosenfeldt / Klaus Wakonig / Mirko Holler / Giuseppe Falini / Luca Pasquini / Eugénia Delacou / Jim Buckman / Thomas S. Glen / Thomas Kress / Esther H. R. Tsai / David G. Reid / Melinda J. Duer / Maggie Cusack / Fabio Nudelman

Nature Communications, Vol 12, Iss 1, Pp 1-

2021 Volume 12

Abstract: Bioinspired materials require an understanding of how biomaterials achieve the materials properties. Here, the authors report on the load-bearing shell of Discinisca tenuis and explore how hydration changes the dry shell from hard and stiff to soft and ... ...

Abstract	Bioinspired materials require an understanding of how biomaterials achieve the materials properties. Here, the authors report on the load-bearing shell of Discinisca tenuis and explore how hydration changes the dry shell from hard and stiff to soft and flexible within minutes by reorganisation caused by organic matrix swelling.
Keywords	Science ; Q
Language	English
Publishing date	2021-09-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
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Article ; Online: Lack of chemokine (C-C motif) ligand 3 leads to decreased survival and reduced immune response after bacterial meningitis.

Aust, Vanessa / Kress, Eugenia / Abraham, Stephanie / Schröder, Nicole / Kipp, Markus / Stope, Matthias B / Pufe, Thomas / Tauber, Simone C / Brandenburg, Lars-Ove

Cytokine

2018 Volume 111, Page(s) 246–254

Abstract: Pneumococcal meningitis, caused by Streptococcus pneumoniae, is the most common type of bacterial meningitis. The clinical management of this disease has been challenged by the emergence of multidrug-resistant Streptococcus pneumoniae, requiring the ... ...

Abstract	Pneumococcal meningitis, caused by Streptococcus pneumoniae, is the most common type of bacterial meningitis. The clinical management of this disease has been challenged by the emergence of multidrug-resistant Streptococcus pneumoniae, requiring the urgent development of new therapeutic alternatives. Over the course of bacterial meningitis, pathogen invasion is accompanied by a massive recruitment of peripheral immune cells, especially neutrophil granulocytes, which are recruited under the coordination of several cytokines and chemokines. Here, we used chemokine (C-C motif) ligand 3 (Ccl3)-deficient mice to investigate the functional role of CCL3 in a mouse model of pneumococcal meningitis. Following intrathecal infection with Streptococcus pneumoniae Ccl3-deficient mice presented a significantly shorter survival and higher bacterial load than wildtype mice, paralleled by an ameliorated infiltration of neutrophil granulocytes into the CNS. Blood sample analysis revealed that infected Ccl3-deficient mice showed a significant decrease in erythrocytes, hemoglobin and hematocrit as well as in the number of banded neutrophils. Moreover, infected Ccl3-deficient mice showed an altered cytokine expression profile. Glial cell activation remained unchanged in both genotypes. In summary, this study demonstrates that CCL3 is beneficial in Streptococcus pneumoniae-induced meningitis. Pharmacological modulation of the CCL3 pathways might, therefore, represent a future therapeutic option to manage Streptococcus pneumoniae meningitis.
MeSH term(s)	Animals ; Chemokine CCL3/immunology ; Chemokines/immunology ; Cytokines/immunology ; Disease Models, Animal ; Immunity, Innate/immunology ; Meningitis, Bacterial/immunology ; Meningitis, Bacterial/microbiology ; Meningitis, Pneumococcal/immunology ; Meningitis, Pneumococcal/microbiology ; Mice ; Mice, Inbred C57BL ; Neutrophils/immunology ; Streptococcus pneumoniae/immunology
Chemical Substances	CCL3 protein, human ; Chemokine CCL3 ; Chemokines ; Cytokines
Language	English
Publishing date	2018-09-07
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1018055-2
ISSN	1096-0023 ; 1043-4666
ISSN (online)	1096-0023
ISSN	1043-4666
DOI	10.1016/j.cyto.2018.09.001
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Article ; Online: Lack of Toll-like receptor 2 results in higher mortality of bacterial meningitis by impaired host resistance.

Böhland, Martin / Kress, Eugenia / Stope, Matthias B / Pufe, Thomas / Tauber, Simone C / Brandenburg, Lars-Ove

Journal of neuroimmunology

2016 Volume 299, Page(s) 90–97

Abstract: Bacterial meningitis is - despite therapeutical progress during the last decades - still characterized by high mortality and severe permanent neurogical sequelae. The brain is protected from penetrating pathogens by both the blood-brain barrier and the ... ...

Abstract	Bacterial meningitis is - despite therapeutical progress during the last decades - still characterized by high mortality and severe permanent neurogical sequelae. The brain is protected from penetrating pathogens by both the blood-brain barrier and the innate immune system. Invading pathogens are recognized by so-called pattern recognition receptors including the Toll-like receptors (TLR) which are expressed by glial immune cells in the central nervous system. Among these, TLR2 is responsible for the detection of Gram-positive bacteria such as the meningitis-causing pathogen Streptococcus pneumoniae. Here, we used TLR2-deficient mice to investigate the effects on mortality, bacterial growth and inflammation in a mouse model of pneumococcal meningitis. Our results revealed a significantly increased mortality rate and higher bacterial burden in TLR2-deficient mice with pneumococcal meningitis. Furthermore, infected TLR2-deficient mice suffered from a significantly increased pro-inflammatory cytokine tumor necrosis factor-α (TNF-α) and Chemokine (C-C motif) ligand 2 (CCL2) or CCL3 chemokine expression and decreased expression of anti-inflammatory cytokines and antimicrobial peptides. In contrast, glial cell activation assessed by glial cell marker expression was comparable to wildtype mice. Taken together, the results suggest that TLR2 is essential for an efficient immune response against Streptococcus pneumoniae meningitis since lack of the receptor led to a worse outcome by higher mortality due to increased bacterial burden, weakened innate immune response and reduced expression of antimicrobial peptides.
MeSH term(s)	Animals ; Immunity, Innate/physiology ; Meningitis, Pneumococcal/immunology ; Meningitis, Pneumococcal/metabolism ; Meningitis, Pneumococcal/mortality ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mortality/trends ; Neuroglia/immunology ; Neuroglia/metabolism ; Toll-Like Receptor 2/deficiency ; Toll-Like Receptor 2/immunology
Chemical Substances	Tlr2 protein, mouse ; Toll-Like Receptor 2
Language	English
Publishing date	2016--15
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	8335-5
ISSN	1872-8421 ; 0165-5728
ISSN (online)	1872-8421
ISSN	0165-5728
DOI	10.1016/j.jneuroim.2016.09.003
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Zs.A 1646: Show issues

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Article ; Online: Intrathecal application of the antimicrobial peptide CRAMP reduced mortality and neuroinflammation in an experimental model of pneumococcal meningitis.

Dörr, Arndt / Kress, Eugenia / Podschun, Rainer / Pufe, Thomas / Tauber, Simone C / Brandenburg, Lars-Ove

The Journal of infection

2015 Volume 71, Issue 2, Page(s) 188–199

Abstract: Antimicrobial peptides (AP) are important components of the innate immune system. Our previous work revealed a higher mortality rate and up-regulation of proinflammatory gene expression as well as glial cell activation in cathelicidin-related ... ...

Abstract	Antimicrobial peptides (AP) are important components of the innate immune system. Our previous work revealed a higher mortality rate and up-regulation of proinflammatory gene expression as well as glial cell activation in cathelicidin-related antimicrobial peptide (CRAMP)-deficient mice after bacterial meningitis. However, the influence of CRAMP application on the progression of inflammation and its impact on mortality after bacterial meningitis remains unknown. To assess the effects of continuous CRAMP exposure in the brain, C57BL/6 wildtype mice were given intracerebroventricular infusion of CRAMP to investigate the effects on mortality, glial cell activation and inflammation in a mouse model of pneumococcal meningitis using immunohistochemistry and realtime RT-PCR. Our results revealed a decrease of mortality after CRAMP infusion. The intrathecal CRAMP infusion after pneumococcal meningitis resulted in a decreased mRNA expression of pro-inflammatory cytokines, whereas the immune responses including the expression of pattern recognition receptors and chemokines were increased in bacterial meningitis. Taken together, the results support the important role of CRAMP as part of the innate immune response against pathogens in bacterial CNS infections. The APs may be a promising approach for the development of an adjuvant therapy for bacterial meningitis.
MeSH term(s)	Animals ; Antimicrobial Cationic Peptides/therapeutic use ; Brain/pathology ; Cytokines/biosynthesis ; Disease Models, Animal ; Immunohistochemistry ; Male ; Meningitis, Pneumococcal/drug therapy ; Mice, Inbred C57BL ; Real-Time Polymerase Chain Reaction ; Survival Analysis ; Treatment Outcome
Chemical Substances	Antimicrobial Cationic Peptides ; Cytokines
Language	English
Publishing date	2015-08
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	424417-5
ISSN	1532-2742 ; 0163-4453
ISSN (online)	1532-2742
ISSN	0163-4453
DOI	10.1016/j.jinf.2015.04.006
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Zs.A 1501: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Formyl Peptide Receptor 1-Mediated Glial Cell Activation in a Mouse Model of Cuprizone-Induced Demyelination.

Bihler, Kai / Kress, Eugenia / Esser, Stefan / Nyamoya, Stella / Tauber, Simone C / Clarner, Tim / Stope, Matthias B / Pufe, Thomas / Brandenburg, Lars-Ove

Journal of molecular neuroscience : MN

2017 Volume 62, Issue 2, Page(s) 232–243

Abstract: Multiple sclerosis (MS) is a chronic degenerative disease of the central nervous system that is characterized by myelin abnormalities, oligodendrocyte pathology, and concomitant glia activation. Unclear are the factors triggering gliosis and ... ...

Abstract	Multiple sclerosis (MS) is a chronic degenerative disease of the central nervous system that is characterized by myelin abnormalities, oligodendrocyte pathology, and concomitant glia activation. Unclear are the factors triggering gliosis and demyelination. New findings suggest an important role of the innate immune response in the initiation and progression of active demyelinating lesions. The innate immune response is induced by pathogen-associated or danger-associated molecular patterns, which are identified by pattern recognition receptors (PRRs), including the G-protein coupled with formyl peptide receptors (FPRs). Glial cells, the immune cells of the central nervous system, also express the PRRs. In this study, we used the cuprizone mice model to investigate the expression of the FPR1 in the course of cuprizone-induced demyelination In addition, we used FPR1-deficient mice to analyze glial cell activation through immunohistochemistry and real-time RT-PCR in cuprizone model. Our results revealed a significantly increased expression of FPR1 in the cortex of cuprizone-treated mice. FPR1-deficient mice showed a slight but significant decrease of demyelination in the corpus callosum compared to the wild-type mice. Furthermore, FPR1 deficiency resulted in reduced glial cell activation and mRNA expression of microglia/macrophages markers, as well as pro- and anti-inflammatory cytokines in the cortex, compared to wild-type mice after cuprizone-induced demyelination. Combined together, these results suggest that the FPR1 is an important part of the innate immune response in the course of cuprizone-induced demyelination.
Language	English
Publishing date	2017-06
Publishing country	United States
Document type	Journal Article
ZDB-ID	1043392-2
ISSN	1559-1166 ; 0895-8696
ISSN (online)	1559-1166
ISSN	0895-8696
DOI	10.1007/s12031-017-0924-y
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Zs.A 3006: Show issues

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Article ; Online: CRAMP deficiency leads to a pro-inflammatory phenotype and impaired phagocytosis after exposure to bacterial meningitis pathogens.

Kress, Eugenia / Merres, Julika / Albrecht, Lea-Jessica / Hammerschmidt, Sven / Pufe, Thomas / Tauber, Simone C / Brandenburg, Lars-Ove

Cell communication and signaling : CCS

2017 Volume 15, Issue 1, Page(s) 32

Abstract: Background: Antimicrobial peptides are important components of the host defence with a broad range of functions including direct antimicrobial activity and modulation of inflammation. Lack of cathelin-related antimicrobial peptide (CRAMP) was associated ...

Abstract	Background: Antimicrobial peptides are important components of the host defence with a broad range of functions including direct antimicrobial activity and modulation of inflammation. Lack of cathelin-related antimicrobial peptide (CRAMP) was associated with higher mortality and bacterial burden and impaired neutrophil granulocyte infiltration in a model of pneumococcal meningitis. The present study was designed to characterize the effects of CRAMP deficiency on glial response and phagocytosis after exposure to bacterial stimuli. Methods: CRAMP-knock out and wildtype glial cells were exposed to bacterial supernatants from Streptococcus pneumoniae and Neisseria meningitides or the bacterial cell wall components lipopolysaccharide and peptidoglycan. Cell viability, expression of pro- and anti-inflammatory mediators and activation of signal transduction pathways, phagocytosis rate and glial cell phenotype were investigated by means of cell viability assays, immunohistochemistry, real-time RT-PCR and Western blot. Results: CRAMP-deficiency was associated with stronger expression of pro-inflammatory and weakened expression of anti-inflammatory cytokines indicating a higher degree of glial cell activation even under resting-state conditions. Furthermore, increased translocation of nuclear factor 'kappa-light-chain-enhancer' of activated B-cells was observed and phagocytosis of S. pneumoniae was reduced in CRAMP-deficient microglia indicating impaired antimicrobial activity. Conclusions: In conclusion, the present study detected severe alterations of the glial immune response due to lack of CRAMP. The results indicate the importance of CRAMP to maintain and regulate the delicate balance between beneficial and harmful immune response in the brain.
MeSH term(s)	Animals ; Antimicrobial Cationic Peptides ; Cathelicidins/deficiency ; Cathelicidins/genetics ; Cathelicidins/metabolism ; Cells, Cultured ; Mice ; Microglia/metabolism ; Microglia/microbiology ; Neisseria meningitidis/pathogenicity ; Phagocytosis ; Phenotype ; Streptococcus pneumoniae/pathogenicity
Chemical Substances	Antimicrobial Cationic Peptides ; Cathelicidins ; ropocamptide (3DD771JO2H)
Language	English
Publishing date	2017-09-16
Publishing country	England
Document type	Journal Article
ISSN	1478-811X
ISSN (online)	1478-811X
DOI	10.1186/s12964-017-0190-1
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Article ; Online: Präimplantationsdiagnostik, Ungelöste Fragen angesichts des neuen Gesetzes.

Kress, H

Bundesgesundheitsblatt, Gesundheitsforschung, Gesundheitsschutz

2012 Volume 55, Issue 3, Page(s) 427–430

Title translation	Preimplantation genetic diagnosis. Unanswered questions in light of the new law.
MeSH term(s)	Abortion, Eugenic/legislation & jurisprudence ; Cytogenetic Analysis ; Embryonic Development ; Ethics ; Ethics Committees/legislation & jurisprudence ; Female ; Fertilization in Vitro/legislation & jurisprudence ; Genetic Testing/legislation & jurisprudence ; Germany ; Gestational Age ; Humans ; Infant, Newborn ; National Health Programs/legislation & jurisprudence ; Personal Autonomy ; Pregnancy ; Pregnancy Reduction, Multifetal/legislation & jurisprudence ; Preimplantation Diagnosis ; Religion and Medicine ; Stem Cell Research/legislation & jurisprudence
Language	German
Publishing date	2012-03
Publishing country	Germany
Document type	Journal Article
ZDB-ID	1461973-8
ISSN	1437-1588 ; 1436-9990
ISSN (online)	1437-1588
ISSN	1436-9990
DOI	10.1007/s00103-012-1465-8
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Article ; Online: CRAMP deficiency leads to a pro-inflammatory phenotype and impaired phagocytosis after exposure to bacterial meningitis pathogens

Eugenia Kress / Julika Merres / Lea-Jessica Albrecht / Sven Hammerschmidt / Thomas Pufe / Simone C. Tauber / Lars-Ove Brandenburg

Cell Communication and Signaling, Vol 15, Iss 1, Pp 1-

2017 Volume 15

Abstract: Abstract Background Antimicrobial peptides are important components of the host defence with a broad range of functions including direct antimicrobial activity and modulation of inflammation. Lack of cathelin-related antimicrobial peptide (CRAMP) was ... ...

Abstract	Abstract Background Antimicrobial peptides are important components of the host defence with a broad range of functions including direct antimicrobial activity and modulation of inflammation. Lack of cathelin-related antimicrobial peptide (CRAMP) was associated with higher mortality and bacterial burden and impaired neutrophil granulocyte infiltration in a model of pneumococcal meningitis. The present study was designed to characterize the effects of CRAMP deficiency on glial response and phagocytosis after exposure to bacterial stimuli. Methods CRAMP-knock out and wildtype glial cells were exposed to bacterial supernatants from Streptococcus pneumoniae and Neisseria meningitides or the bacterial cell wall components lipopolysaccharide and peptidoglycan. Cell viability, expression of pro- and anti-inflammatory mediators and activation of signal transduction pathways, phagocytosis rate and glial cell phenotype were investigated by means of cell viability assays, immunohistochemistry, real-time RT-PCR and Western blot. Results CRAMP-deficiency was associated with stronger expression of pro-inflammatory and weakened expression of anti-inflammatory cytokines indicating a higher degree of glial cell activation even under resting-state conditions. Furthermore, increased translocation of nuclear factor ‘kappa-light-chain-enhancer’ of activated B-cells was observed and phagocytosis of S. pneumoniae was reduced in CRAMP-deficient microglia indicating impaired antimicrobial activity. Conclusions In conclusion, the present study detected severe alterations of the glial immune response due to lack of CRAMP. The results indicate the importance of CRAMP to maintain and regulate the delicate balance between beneficial and harmful immune response in the brain.
Keywords	Antimicrobial peptide ; Cathelicidin ; Cramp ; Glial cell ; Innate immunity ; Signal transduction ; Medicine ; R ; Cytology ; QH573-671
Subject code	571
Language	English
Publishing date	2017-09-01T00:00:00Z
Publisher	BMC
Document type	Article ; Online
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Article ; Online: Lack of Proinflammatory Cytokine Interleukin-6 or Tumor Necrosis Factor Receptor-1 Results in a Failure of the Innate Immune Response after Bacterial Meningitis.

Albrecht, Lea-Jessica / Tauber, Simone C / Merres, Julika / Kress, Eugenia / Stope, Matthias B / Jansen, Sandra / Pufe, Thomas / Brandenburg, Lars-Ove

Mediators of inflammation

2016 Volume 2016, Page(s) 7678542

Abstract: The most frequent pathogen that causes bacterial meningitis is the Gram-positive bacterium Streptococcus pneumoniae. By entering the brain, host cells will be activated and proinflammatory cytokines like interleukin-6 (IL-6) and tumor necrosis factor-α ( ... ...

Abstract	The most frequent pathogen that causes bacterial meningitis is the Gram-positive bacterium Streptococcus pneumoniae. By entering the brain, host cells will be activated and proinflammatory cytokines like interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) are released. The goal of the current study was to examine the interaction between IL-6 and TNFR1 as receptor for TNF-α and the innate immune response in vivo in a model of Streptococcus pneumoniae-induced meningitis. For the experiments IL-6(-/-), TNFR1(-/-), and TNFR1-IL-6(-/-) KO mice were used. Our results revealed higher mortality rates and bacterial burden after infection in TNFR1(-/-), IL-6(-/-), and TNFR1-IL-6(-/-) mice and a decreased immune response including lower neutrophil infiltration in the meninges of TNFR1(-/-) and TNFR1-IL-6(-/-) mice in contrast to IL-6(-/-) and wild type mice. Furthermore, the increased mortality of TNFR1(-/-) and TNFR1-IL-6(-/-) mice correlated with decreased glial cell activation compared to IL-6(-/-) or wild type mice after pneumococcal meningitis. Altogether, the results show the importance of TNFR1 and IL-6 in the regulation of the innate immune response. The lack of TNFR1 and IL-6 results in higher mortality by weakened immune defence, whereas the lack of TNFR1 results in more severe impairment of the innate immune response than the lack of IL-6 alone.
MeSH term(s)	Animals ; Immunity, Innate/genetics ; Immunity, Innate/immunology ; Interleukin-6/deficiency ; Interleukin-6/genetics ; Male ; Meningitis, Bacterial/immunology ; Meningitis, Bacterial/metabolism ; Mice ; Mice, Knockout ; Pneumococcal Infections/immunology ; Pneumococcal Infections/metabolism ; Receptors, Tumor Necrosis Factor, Type I/deficiency ; Receptors, Tumor Necrosis Factor, Type I/genetics ; Streptococcus pneumoniae/immunology ; Streptococcus pneumoniae/pathogenicity
Chemical Substances	Interleukin-6 ; Receptors, Tumor Necrosis Factor, Type I
Language	English
Publishing date	2016
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1137605-3
ISSN	1466-1861 ; 0962-9351
ISSN (online)	1466-1861
ISSN	0962-9351
DOI	10.1155/2016/7678542
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