Mast Cells Are Critical Regulators of Bone Fracture-Induced Inflammation and Osteoclast Formation and Activity.
AuthorsKroner J, Kovtun A, Kemmler J, Messmann JJ, Strauss G, Seitz S, Schinke T, Amling M, Kotrba J, Froebel J, Dudeck J, Dudeck A, Ignatius A
JournalJ Bone Miner Res
PubMed ID28777474
'Mast cells, important sensor and effector cells of the immune system, may influence bone metabolism as their number is increased in osteoporotic patients. They are also present during bone fracture healing with currently unknown functions. Using a novel c-Kit-independent mouse model of mast cell deficiency, we demonstrated that mast cells ... More
Small Heterodimer Partner Deficiency Increases Inflammatory Liver Injury Through C-X-C motif chemokine ligand 2-Driven Neutrophil Recruitment in Mice.
AuthorsNoh JR, Kim YH, Kim DK, Hwang JH, Kim KS, Choi DH, Lee SJ, Lee HG, Lee TG, Weng HL, Dooley S, Choi HS, Lee CH
JournalToxicol Sci
PubMed ID29409050
'Although detailed pathophysiological mechanisms of fulminant hepatitis remain elusive, immune cell recruitment with excessive cytokine production is a well-recognized hallmark of the disease. We determined the function of orphan nuclear receptor small heterodimer partner (SHP) in concanavalin A (ConA)-induced hepatitis model. Male C57BL/6 J mice were injected intravenously with either ... More
Ventilator-induced lung injury is aggravated by antibiotic mediated microbiota depletion in mice.
AuthorsWienhold SM, Macrì M, Nouailles G, Dietert K, Gurtner C, Gruber AD, Heimesaat MM, Lienau J, Schumacher F, Kleuser B, Opitz B, Suttorp N, Witzenrath M, Müller-Redetzky HC
JournalCrit Care
PubMed ID30373626
'Antibiotic exposure alters the microbiota, which can impact the inflammatory immune responses. Critically ill patients frequently receive antibiotic treatment and are often subjected to mechanical ventilation, which may induce local and systemic inflammatory responses and development of ventilator-induced lung injury (VILI). The aim of this study was to investigate whether ... More
Vaccination with Necroptotic Cancer Cells Induces Efficient Anti-tumor Immunity.
AuthorsAaes TL, Kaczmarek A, Delvaeye T, De Craene B, De Koker S, Heyndrickx L, Delrue I, Taminau J, Wiernicki B, De Groote P, Garg AD, Leybaert L, Grooten J, Bertrand MJ, Agostinis P, Berx G, Declercq W, Vandenabeele P, Krysko DV
JournalCell Rep
PubMed ID27050509
'Successful immunogenic apoptosis in experimental cancer therapy depends on the induction of strong host anti-tumor responses. Given that tumors are often resistant to apoptosis, it is important to identify alternative molecular mechanisms that elicit immunogenic cell death. We have developed a genetic model in which direct dimerization of FADD combined ... More
Alteration of Gut Microbiota and Inflammatory Cytokine/Chemokine Profiles in 5-Fluorouracil Induced Intestinal Mucositis.
AuthorsLi HL, Lu L, Wang XS, Qin LY, Wang P, Qiu SP, Wu H, Huang F, Zhang BB, Shi HL, Wu XJ
JournalFront Cell Infect Microbiol
PubMed ID29124041
Disturbed homeostasis of gut microbiota has been suggested to be closely associated with 5-fluorouracil (5-Fu) induced mucositis. However, current knowledge of the overall profiles of 5-Fu-disturbed gut microbiota is limited, and so far there is no direct convincing evidence proving the causality between 5-Fu-disturbed microbiota and colonic mucositis. In mice, ... More
Gelatinase B/matrix metalloproteinase-9 is a phase-specific effector molecule, independent from Fas, in experimental autoimmune encephalomyelitis.
AuthorsUgarte-Berzal E, Berghmans N, Boon L, Martens E, Vandooren J, Cauwe B, Thijs G, Proost P, Van Damme J, Opdenakker G
JournalPLoS One
PubMed ID30273366
Gelatinase B/matrix metalloproteinase-9 (MMP-9) triggers multiple sclerosis (MS) and the animal model of experimental autoimmune encephalomyelitis (EAE) by the breakdown of the blood-brain barrier. Interestingly, MMP-9 is beneficial in systemic autoimmunity caused by Fas-deficiency. Fas-deficient (faslpr) and Fas-ligand-deficient mice are protected against EAE. We here investigated the interaction between Fas ... More
Influence of Menopause on Inflammatory Cytokines during Murine and Human Bone Fracture Healing.
AuthorsFischer V, Kalbitz M, Müller-Graf F, Gebhard F, Ignatius A, Liedert A, Haffner-Luntzer M
JournalInt J Mol Sci
PubMed ID30013010
Postmenopausal females display a chronic inflammatory phenotype with higher levels of circulating pro-inflammatory cytokines. Furthermore, the inflammatory response to injury may be altered under estrogen-deficiency, because it was shown previously that estrogen-deficient mice displayed increased levels of the inflammatory cytokines Midkine (Mdk) and Interleukin-6 (IL-6) in the early fracture hematoma. ... More
3D Organotypic Spinal Cultures: Exploring Neuron and Neuroglia Responses Upon Prolonged Exposure to Graphene Oxide.
AuthorsMusto M, Rauti R, Rodrigues AF, Bonechi E, Ballerini C, Kostarelos K, Ballerini L
JournalFront Syst Neurosci
PubMed ID30733671
Graphene-based nanomaterials are increasingly engineered as components of biosensors, interfaces or drug delivery platforms in neuro-repair strategies. In these developments, the mostly used derivative of graphene is graphene oxide (GO). To tailor the safe development of GO nanosheets, we need to model ... More
Reduced Terminal Complement Complex Formation in Mice Manifests in Low Bone Mass and Impaired Fracture Healing.
AuthorsMödinger Y, Rapp AE, Vikman A, Ren Z, Fischer V, Bergdolt S, Haffner-Luntzer M, Song WC, Lambris JD, Huber-Lang M, Neidlinger-Wilke C, Brenner RE, Ignatius A
JournalAm J Pathol
PubMed ID30339839
The terminal complement complex (TCC) is formed on activation of the complement system, a crucial arm of innate immunity. TCC formation on cell membranes results in a transmembrane pore leading to cell lysis. In addition, sublytic TCC concentrations can modulate various cellular functions. TCC-induced effects may play a role in ... More