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| 1 | Neutrophils in chronic inflammatory diseases显示文摘Chronic inflammation is a component of many disease conditions that affect a large group of individuals worldwide.Chronic inflammation is characterized by persistent,low-grade inflammation and is increased in the aging population.Neutrophils are normally the first responders to acute inflammation and contribute to the resolution of inflammation.However,in chronic inflammation,the role of neutrophils is less well understood and has been described as either beneficial or detrimental,causing tissue damage and enhancing the immune response.Emerging evidence suggests that neutrophils are important players in several chronic diseases,such as atherosclerosis,diabetes mellitus,nonalcoholic fatty liver disease and autoimmune disorders.This review will highlight the interaction of neutrophils with other cells in the context of chronic inflammation,the contribution of neutrophils to selected chronic inflammatory diseases,and possible future therapeutic strategies. | Andrea Herrero-Cervera Oliver Soehnlein Ellinor Kenne | 2022 | Cellular & Molecular Immunology2022，19，2： | 7 |
| 2 | Therapeutic ACPA inhibits NET formation: a potential therapy for neutrophil-mediated inflammatory diseases显示文摘Excessive release of neutrophil extracellular traps(NETs)is associated with disease severity and contributes to tissue injury,followed by severe organ damage.Pharmacological or genetic inhibition of NET release reduces pathology in multiple inflammatory disease models,indicating that NETs are potential therapeutic targets.Here,we demonstrate using a preclinical basket approach that our therapeutic anti-citrullinated protein antibody(tACPA)has broad therapeutic potential.Treatment with tACPA prevents disease symptoms in various mouse models with plausible NET-mediated pathology,including inflammatory arthritis(IA),pulmonary fibrosis,inflammatory bowel disease and sepsis.We show that citrulline residues in the N-termini of histones 2A and 4 are specific targets for therapeutic intervention,whereas antibodies against other N-terminal post-translational histone modifications have no therapeutic effects.Because citrullinated histones are generated during NET release,we investigated the ability of tACPA to inhibit NET formation.tACPA suppressed NET release from human neutrophils triggered with physiologically relevant human disease-related stimuli.Moreover,tACPA diminished NET release and potentially initiated NET uptake by macrophages in vivo,which was associated with reduced tissue damage in the joints of a chronic arthritis mouse model of IA.To our knowledge,we are the first to describe an antibody with NET-inhibiting properties and thereby propose tACPA as a drug candidate for NET-mediated inflammatory diseases,as it eliminates the noxious triggers that lead to continued inflammation and tissue damage in a multidimensional manner. | Renato G.S.Chirivi Jos W.Gvan Rosmalen Maarten van der Linden Maximilien Euler Gonny Schmets Galina Bogatkevich Konstantinos Kambas Jonas Hahn Quinte Braster Oliver Soehnlein Markus H.Hoffmann Helmuth H.Gvan Es Jos M.H.Raats | 2021 | Cellular & Molecular Immunology2021，18，6： | 5 |
| 3 | Trilateral interaction between innervation,leukocyte,and adventitia:a new driver of atherosclerotic plaque formation显示文摘A recent study by Mohanta et al.describes a new understanding of neuroimmune interactions in atherosclerosis.While atherosclerotic plaques are not innervated,ablating the sympathetic innervation to these regions attenuated atherosclerosis,suggesting a potential novel therapeutic strategy.Atherosclerosis continues to be the leading cause of death in industrialized countries due to its complications such as acute myocardial infarction or stroke.The disease is the result of a complex process,consisting of sub-endothelial lipid retention,immune cell migration,proteolytic injury,altogether leading to a chronic inflammatory responses in the wall of large arteries and ultimately plaque development.2 The inner layer of the blood vessels is not innervated and hence the nervous system connects with the vessel through its most outer layer,the lamina adventitia,hereby controlling important functions including arterial blood pressure.Beyond such homeostatic control of vessel function,increasing evidence demonstrates that activation of the sympathetic nervous system can modulate the degree of arterial inflammation. | Yahya Sohrabi Holger Reinecke Oliver Soehnlein | 2022 | Signal Transduction and Targeted Therapy2022，7，8： | 2 |
| 4 | Neutrophil gra-nule proteins tune monocytic cell function 显示文摘 | Soehnlein 0 Weber C Lindbom L | 2009 | TrendsImmunol2009，30，11： | 1 |
| 5 | Phagocyte partnership during the onset and resolution of inflammation显示文摘 | Soehnlein O Lindbom L | 2010 | Nature Reviews Immunology2010，10，6： | 1 |
| 6 | Neutro- phil secretion products pave the way for inflammatory monocytes 显示文摘 | SOEHNLEIN O ZERNECKE A ERIKSSON E E | 2008 | Blood2008，112，4： | 1 |
| 7 | Rolesofheparin-bindingproteininbacterialinfections显示文摘 | LINDER A SOEHNLEIN O AKESSON P | 2010 | Jour-nalofinnateimmunity2010，2，5： | 1 |
| 8 | Neutrophil secretion products pave the way for inflammatory monocytes显示文摘 | Oliver Soehnlein Alma Zernecke Einar E.Eriksson | | 0，，04： | 1 |
| 9 | Neutrophil-derivedheparin-binding protein (HBP/CAP37) deposited on en-dothelium enhances monocyte arrest under flow condi-tions显示文摘 | Soehnlein 0 Xie X Ulbrich H | 2005 | J Immunol2005，174，10： | 1 |
| 10 | Neulrophil secretion products rcgnlate anti-bacterial activity in monocytes and macrophages显示文摘 | SOEHNLEIN O KENNE E ROTZIUS P ~t al | 2008 | Clin Exp Immunol2008，151，1： | 1 |
| 11 | Mechanisms underlying neutro- phil-mediated monoeyte recruitment 显示文摘 | Soehnlein O Lindbom L Weber C | 2009 | Blood2009，114，21： | 1 |
| 12 | Roles of heparin-binding pro- tein in bacterial infections显示文摘 | Linder A Soehnlein O Akesson P | 2010 | J Innate Immun2010，2，5： | 1 |
| 13 | Multiple roles for neutrophils in atherosclerosis显示文摘 | Soehnlein O | 2012 | Circ Res2012，110，6： | 1 |
| 14 | Contribution of neutrophils to a- cute lung injury显示文摘 | GROMMES J SOEHNLEIN O | 2011 | Mol Med2011，17，34： | 1 |
| 15 | Neutrophil degranulation medi- ates severe lung damage triggered by streptococcal M 1 protein显示文摘 | Soehnlein O Oehmeke S Ma X | 2008 | Eur Respir J2008，32，2： | 1 |
| 16 | Phagocyte partnership during the onset and resolution of inflammation显示文摘 | SOEHNLEIN O LINDBOM L | 2010 | Nat Rev Immunol2010，10，： | 1 |
| 17 | Contribution of neutrophils to acute lung injury 显示文摘 | Grommes J Soehnlein O | 2011 | Mol Med2011，17，34： | 1 |
| 18 | Regulated release and functional modulation of junctional adhesion molecule A by disintegrin metalloproteinases 显示文摘 | Koenen R R Pruessmeyer J Soehnlein O | 2009 | Blood2009，113，19： | 1 |
| 19 | Distinct infiltrationof neutrophils in lesion shoulders in ApoE-/- mice显示文摘 | Rotzius P* Thams S Soehnlein 0 | 2010 | Am JPathol2010，177，1： | 1 |
| 20 | Myeloid cells in atherosclerosis:initiators and decision shapers显示文摘 | SOEHNLEIN O WEBER C | 2009 | Semin Immunopathol2009，31，： | 1 |
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