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The Cardiac Microenvironment Instructs Divergent Monocyte Fates and Functions in Myocarditis

Hou, X;Chen, G;Bracamonte-Baran, W;Choi, HS;Diny, NL;Sung, J;Hughes, D;Won, T;Wood, MK;Talor, MV;Hackam, DJ;Klingel, K;Davogustto, G;Taegtmeyer, H;Coppens, I;Barin, JG;Čiháková, D;
Product: Pertussis Toxin from B. pertussis, Lyophilized (Salt-Free)

Two types of monocytes, Ly6Chi and Ly6Clo, infiltrate the heart in murine experimental autoimmune myocarditis (EAM). We discovered a role for cardiac fibroblasts in facilitating monocyte-to-macrophage differentiation of both Ly6Chi and Ly6Clo cells, allowing these macrophages to perform divergent functions in myocarditis progression. During the acute phase of EAM, IL-17A is highly abundant. It signals through cardiac fibroblasts to attenuate efferocytosis of Ly6Chi monocyte-derived macrophages (MDMs) and simultaneously prevents Ly6Clo monocyte-to-macrophage differentiation. We demonstrated an inverse clinical correlation between heart IL-17A levels and efferocytic receptor expressions in humans with heart failure (HF). In the absence of IL-17A signaling, Ly6Chi MDMs act as robust phagocytes and are less pro-inflammatory, whereas Ly6Clo monocytes resume their differentiation into MHCII+ macrophages. We propose that MHCII+Ly6Clo MDMs are associated with the reduction of cardiac fibrosis and prevention of the myocarditis sequalae. Copyright © 2019 The Author(s). Published by Elsevier Inc. All rights reserved.

PubMed ID: 31269438
360836082019-07-152019-07-1516:21:5216:21:522019-07-252019-07-2512:13:0112:13:01Hou, X;Chen, G;Bracamonte-Baran, W;Choi, HS;Diny, NL;Sung, J;Hughes, D;Won, T;Wood, MK;Talor, MV;Hackam, DJ;Klingel, K;Davogustto, G;Taegtmeyer, H;Coppens, I;Barin, JG;Čiháková, D;Hou, X;Chen, G;Bracamonte-Baran, W;Choi, HS;Diny, NL;Sung, J;Hughes, D;Won, T;Wood, MK;Talor, MV;Hackam, DJ;Klingel, K;Davogustto, G;Taegtmeyer, H;Coppens, I;Barin, JG;Čiháková, D;20192019The Cardiac Microenvironment Instructs Divergent Monocyte Fates and Functions in MyocarditisThe Cardiac Microenvironment Instructs Divergent Monocyte Fates and Functions in MyocarditisCell ReportsCell Reports172-189.e7172-189.e72828113126943831269438

Two types of monocytes, Ly6Chi and Ly6Clo, infiltrate the heart in murine experimental autoimmune myocarditis (EAM). We discovered a role for cardiac fibroblasts in facilitating monocyte-to-macrophage differentiation of both Ly6Chi and Ly6Clo cells, allowing these macrophages to perform divergent functions in myocarditis progression. During the acute phase of EAM, IL-17A is highly abundant. It signals through cardiac fibroblasts to attenuate efferocytosis of Ly6Chi monocyte-derived macrophages (MDMs) and simultaneously prevents Ly6Clo monocyte-to-macrophage differentiation. We demonstrated an inverse clinical correlation between heart IL-17A levels and efferocytic receptor expressions in humans with heart failure (HF). In the absence of IL-17A signaling, Ly6Chi MDMs act as robust phagocytes and are less pro-inflammatory, whereas Ly6Clo monocytes resume their differentiation into MHCII+ macrophages. We propose that MHCII+Ly6Clo MDMs are associated with the reduction of cardiac fibrosis and prevention of the myocarditis sequalae. Copyright © 2019 The Author(s). Published by Elsevier Inc. All rights reserved.

Two types of monocytes, Ly6Chi and Ly6Clo, infiltrate the heart in murine experimental autoimmune myocarditis (EAM). We discovered a role for cardiac fibroblasts in facilitating monocyte-to-macrophage differentiation of both Ly6Chi and Ly6Clo cells, allowing these macrophages to perform divergent functions in myocarditis progression. During the acute phase of EAM, IL-17A is highly abundant. It signals through cardiac fibroblasts to attenuate efferocytosis of Ly6Chi monocyte-derived macrophages (MDMs) and simultaneously prevents Ly6Clo monocyte-to-macrophage differentiation. We demonstrated an inverse clinical correlation between heart IL-17A levels and efferocytic receptor expressions in humans with heart failure (HF). In the absence of IL-17A signaling, Ly6Chi MDMs act as robust phagocytes and are less pro-inflammatory, whereas Ly6Clo monocytes resume their differentiation into MHCII+ macrophages. We propose that MHCII+Ly6Clo MDMs are associated with the reduction of cardiac fibrosis and prevention of the myocarditis sequalae. Copyright © 2019 The Author(s). Published by Elsevier Inc. All rights reserved.

8.38.3

 EAM Induction

To induce EAM, we injected mice with 125 μg myosin heavy chain α peptide MyHCα614-629 (Ac-SLKLMATLFSTYASAD; Genscript) (Pummerer et al., 1996) emulsified in CFA (Sigma-Aldrich) supplemented with 5mg/mL heat-killed Mycobacterium tuberculosis strain H37Ra (Difco) on days 0 and 7. On the first day of immunization, mice also received a dose of 500 ng pertussis toxins intraperitoneally (List Biological Laboratories) (Ciháková et al., 2004).

... Pertussis Toxin from Bordetella pertussis List Biological Laboratories, Inc. Cat#180, #181 

Author did not specify which List Labs Pertussis Toxin was utilized.  List Labs provides Product #180 - Pertussis Toxin from B. pertussis, Lyophilized in Buffer and Product #181 - Pertussis Toxin from B. pertussis, Lyophilized (Salt-Free).

 EAM Induction

To induce EAM, we injected mice with 125 μg myosin heavy chain α peptide MyHCα614-629 (Ac-SLKLMATLFSTYASAD; Genscript) (Pummerer et al., 1996) emulsified in CFA (Sigma-Aldrich) supplemented with 5mg/mL heat-killed Mycobacterium tuberculosis strain H37Ra (Difco) on days 0 and 7. On the first day of immunization, mice also received a dose of 500 ng pertussis toxins intraperitoneally (List Biological Laboratories) (Ciháková et al., 2004).

... Pertussis Toxin from Bordetella pertussis List Biological Laboratories, Inc. Cat#180, #181 

Author did not specify which List Labs Pertussis Toxin was utilized.  List Labs provides Product #180 - Pertussis Toxin from B. pertussis, Lyophilized in Buffer and Product #181 - Pertussis Toxin from B. pertussis, Lyophilized (Salt-Free).

http://dx.doi.org/10.1016/j.celrep.2019.06.007http://dx.doi.org/10.1016/j.celrep.2019.06.0072019-07-022019-07-0210.1016/j.celrep.2019.06.00710.1016/j.celrep.2019.06.007Pertussis Toxin from B. pertussis, Lyophilized (Salt-Free)Pertussis Toxin from B. pertussis, Lyophilized (Salt-Free)cihakova@jhmi.educihakova@jhmi.edu180;181;ACT;Acute;Autoimmune;Biological;Bordetella pertussis;Clinical;Experimental;IL;Inflammatory;List;List Biological;Macrophage;Monocyte;Murine;Pertussis;Prevention;Protease;Receptor;Reduction;Toxin;Cell Reports180;181;ACT;Acute;Autoimmune;Biological;Bordetella pertussis;Clinical;Experimental;IL;Inflammatory;List;List Biological;Macrophage;Monocyte;Murine;Pertussis;Prevention;Protease;Receptor;Reduction;Toxin;Cell Reports181181the-cardiac-microenvironment-instructs-divergentthe-cardiac-microenvironment-instructs-divergent