current research depict specif mode immun energi metabol be interrel molecular cellular organ organ level henc wherea alternativelyactiv macrophag domin insulinsensit adipos tissu lean m1skew classicallyactiv macrophag accumul parallel adipos obes promot inflamm insulin resist metainflamm the latest frontier immunometabol explor coregul energi metabol immun function within hematopoiet cell m1skew macrophag sustain edemat hypox tissu anaerob glycolysi wherea mitochondri biogenesi respir domin cell review under mechan consequ transit from predomin adipos tissu well extracellular signal transcript factor control macrophag phenotyp impos distinct metabol mode

Haim Shapiro

Aviv Lutaty

Amiram Ariel

Macrophages, Meta-Inflammation, and Immuno-Metabolism

the 13 kda heparinbind growth factor midkin origin identifi molecul involv orchestr embryon develop recent studi provid evid new role acut chronic inflammatori process accord sever inflammatori diseas includ nephriti arthriti atherosclerosi coliti autoimmun enceph have been shown allevi absenc anim model reduc leukocyt recruit site inflamm found one import mechan attenu chronic inflamm when absent furthermor found modul express proinflammatori cytokin expans regulatori tcell here review current understand role differ inflammatori disord summar knowledg biolog

Ludwig T. Weckbach

Takashi Muramatsu

Barbara Walzog

Midkine in Inflammation

dietari supplement larginin shown improv immun respons various inflammatori model howev molecular mechan under larginin effect immun cell remain unrecogn herein test hypothesi limit larginin could lead uncoupl state murin macrophag induc nitric oxid synthas therefor increas induc nitricoxidesynthasederiv superoxid anion format important demonstr larginin dose time depend potenti superoxid anion product bacteri endotoxinstimul macrophag although did influenc nadph oxidas express activ detail analysi macrophag activ show time depend between lpsinduc inos express increas format moreov downregul macrophag inos express well inhibit inos activ nos inhibitor unveil import role enzym control peroxynitrit format dure macrophag stimul conclus our data demonstr simultan induct nadph oxidas togeth inos enzym can result uncoupl state inos result product function import level soon after macrophag activ lps moreov demonstr first time increas concentr larginin further potenti inosdepend format inflammatori macrophag

Michaela Pekarova

Antonin Lojek

Hana Martiskova

Ondrej Vasicek

Lucia Bino

A. Klinke

D. Lau

Radek Kuchta

Jaroslav Kadlec

Radimir Vrba

Lukas Kubala

New Role for L-Arginine in Regulation of Inducible Nitric-Oxide-Synthase-Derived Superoxide Anion Production in Raw 264.7 Macrophages

the role apoptosisassoci specklik protein asc assembl inflammasom complex within macrophag has been elucid sever studi particular role asc function adaptor protein link nodlik receptor nlrs procaspase1 therebi lead activ caspase1 cleav inflammatori cytokin il1 il18 induc pyroptosi has been note asc maintain inflammasomeindepend role includ limit control express dock2 mitogenactiv protein kinas mapk erk2 regul pathway this paper emphas major role asc dure pathogen infect mechan which mediat inflamm discuss it more recent discov function

Hoda Hassan

Amal O. Amer

Cell Intrinsic Roles of Apoptosis-Associated Speck-Like Protein in Regulating Innate and Adaptive Immune Responses

recombin escherichia coli k12 strain transform modifi bacteri luciferas gene luxabcde from photorhabdus luminescen construct order monitor activ various antimicrobi agent realtim basi this coli lux emit without ani addit substrat constitut bioluminesc which correl number viabl bacteri cell the decreas signal correl number kill bacteri cell antimicrobi activ hydrogen peroxid 2 2 myeloperoxidas mpo assess high concentr 2 2 alon had bacteriocid function mpo enhanc kill form hypochlor acid hocl taurin known hocl scaveng block kill mpo when coli lux incub neutrophil similar kill kinet record 2 2 mpo experi the opson bacteria enhanc kill maximum rate mpo releas from lysosom coincid onset kill

J. T. Atosuo

E.-M. Lilius

The Real-Time-Based Assessment of the Microbial Killing by the Antimicrobial Compounds of Neutrophils

macrophag termin differenti cell mononuclear phagocyt system also encompass dendrit cell circul blood monocyt commit myeloid progenitor cell bone marrow both macrophag monocyt precursor can chang function state respons microenvironment cue exhibit mark heterogen howev still uncertainti regard distinct express pattern surfac marker clear defin macrophag subset particular case human macrophag addit tissu distribut macrophag can function polar proinflammatori altern activ well regulatori cell respons both exogen infect solid tumor well system biolog approach

Luca Cassetta

Edana Cassol

Guido Poli

Macrophage Polarization in Health and Disease

phagocyt special cell immun system design engulf destroy harm microorgan insid newli form phagosom the latter intracellular organell transform toxic environ within minut disappear onc pathogen destroy reactiv oxygen speci reactiv nitrogen speci produc insid phagosom intracellular granul lysosom phagocyt fuse phagosom liber destruct enzym this process phagocytosi effici protect against most infect howev some microorgan avoid destruct caus sever damag understand failur phagosom kill need learn more about actual destruct process phagosom this paper summar method investig biochemistri phagosom discuss some limit accord natur phagosom issu local tempor dynam emphas recent develop highlight

Oliver Nüsse

Biochemistry of the Phagosome: The Challenge to Study a Transient Organelle

recent have report addit macrophag also neutrophil granulocyt can phagocytos apoptot neutrophil base find hypothes cannibalist neutrophil site acut infect inflamm play major role clearanc apoptot neutrophil sinc site infect inflamm neutrophil expos microbi constitu proinflammatori cytokin present studi analyz effect tlrligand cytokin abil neutrophil phagocytos apoptot cell vitro observ exposur ligand tlr2 malp2 pam3csk4 tlr4 lps tlr7 tlr8 r848 tlr9 odn 2006 led increas phagocytosi apoptot cell neutrophil addit proinflammatori cytokin tnf gmcsf strong enhanc uptak apoptot cell neutrophil these result support hypothesi neutrophil acquir abil phagocytos apoptot cell site acut infect inflamm therebi can contribut resolut inflamm

Lars Hellberg

Sabrina Fuchs

Christoph Gericke

Arup Sarkar

Martina Behnen

Werner Solbach

Tamás Laskay

Proinflammatory Stimuli Enhance Phagocytosis of Apoptotic Cells by Neutrophil Granulocytes

the cd40 ligand cd40l cd40 two molecul belong tnf tnf receptor superfamili role adapt immun system has wide been explor howev wide rang express molecul hematopoiet well nonhematopoiet cell has reveal multipl function cd40 cd40l interact differ cell type process granulopoiesi cd40 trigger stromal cell has been document enhanc express granulopoiesi growth factor granulocytecolonystimul factor gcsf granulocyt monocytecolonystimul factor gmcsf upon disrupt cd40 cd40lsignal pathway case xlink hyperimmunoglobulin igm syndrom xhigm can lead neutropenia chronic idiopath neutropenia cin adult howev under influenc inflammatori microenviron cd40l play role granulocyt progenitor cell deplet provid thus pathogenet caus cin

Irene Mavroudi

Helen A. Papadaki

The Role of CD40/CD40 Ligand Interactions in Bone Marrow Granulopoiesis

neutrophil granulocyt have shortest lifespan among leukocyt circul die via apoptosi site infect tissu injuri prolong neutrophil lifespan critic effect host defens apoptosi inflammatori neutrophil clearanc critic control point termin inflammatori respons evasion neutrophil apoptosi aggrav local injuri lead persist tissu damag the shortliv prosurviv bcl2 famili protein mcl1 myeloid cell leukemia1 instrument control apoptosi consequ neutrophil lifespan respons rapid chang environment cue dure inflamm this paper focus multipl level control mcl1 express function discuss target mcl1 potenti therapeut strategi enhanc resolut inflamm through acceler neutrophil apoptosi

Eric Milot

János G. Filep

Regulation of Neutrophil Survival/Apoptosis by Mcl-1

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