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Interleukin 6 trans‐signaling is a critical driver of lung allograft fibrosis

dc.contributor.authorWheeler, David S.
dc.contributor.authorMisumi, Keizo
dc.contributor.authorWalker, Natalie M.
dc.contributor.authorVittal, Ragini
dc.contributor.authorCombs, Michael P.
dc.contributor.authorAoki, Yoshiro
dc.contributor.authorBraeuer, Russell R.
dc.contributor.authorLama, Vibha N.
dc.date.accessioned2021-07-01T20:14:24Z
dc.date.available2022-08-01 16:14:23en
dc.date.available2021-07-01T20:14:24Z
dc.date.issued2021-07
dc.identifier.citationWheeler, David S.; Misumi, Keizo; Walker, Natalie M.; Vittal, Ragini; Combs, Michael P.; Aoki, Yoshiro; Braeuer, Russell R.; Lama, Vibha N. (2021). "Interleukin 6 trans‐signaling is a critical driver of lung allograft fibrosis." American Journal of Transplantation (7): 2360-2371.
dc.identifier.issn1600-6135
dc.identifier.issn1600-6143
dc.identifier.urihttps://hdl.handle.net/2027.42/168372
dc.publisherWiley Periodicals, Inc.
dc.subject.otheranimal models: murine
dc.subject.otherbasic (laboratory) research / science
dc.subject.otherbronchiolitis obliterans (BOS)
dc.subject.othercellular biology
dc.subject.othercytokines / cytokine receptors
dc.subject.otherfibrosis
dc.subject.otherlung transplantation / pulmonology
dc.subject.othertranslational research / science
dc.titleInterleukin 6 trans‐signaling is a critical driver of lung allograft fibrosis
dc.typeArticle
dc.rights.robotsIndexNoFollow
dc.subject.hlbsecondlevelMedicine (General)
dc.subject.hlbtoplevelHealth Sciences
dc.description.peerreviewedPeer Reviewed
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/168372/1/ajt16417.pdf
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/168372/2/ajt16417_am.pdf
dc.identifier.doi10.1111/ajt.16417
dc.identifier.sourceAmerican Journal of Transplantation
dc.identifier.citedreferencePeters M, Blinn G, Solem F, et al. In vivo and in vitro activities of the gp130‐stimulating designer cytokine Hyper‐IL‐6. J Immunol. 1998; 161 ( 7 ): 3575 ‐ 3581.
dc.identifier.citedreferenceJarnicki A, Putoczki T, Ernst M. Stat3: linking inflammation to epithelial cancer ‐ more than a "gut" feeling? Cell Div. 2010; 5: 14.
dc.identifier.citedreferenceWhitehead BF, Stoehr C, Wu CJ, et al. Cytokine gene expression in human lung transplant recipients. Transplantation. 1993; 56 ( 4 ): 956 ‐ 961.
dc.identifier.citedreferenceIacono A, Dauber J, Keenan R, et al. Interleukin 6 and interferon‐gamma gene expression in lung transplant recipients with refractory acute cellular rejection: implications for monitoring and inhibition by treatment with aerosolized cyclosporine. Transplantation. 1997; 64 ( 2 ): 263 ‐ 269.
dc.identifier.citedreferenceRizzo M, SivaSai KSR, Smith MA, et al. Increased expression of inflammatory cytokines and adhesion molecules by alveolar macrophages of human lung allograft recipients with acute rejection: decline with resolution of rejection. J Heart Lung Transplant. 2000; 19 ( 9 ): 858 ‐ 865.
dc.identifier.citedreferenceYoshida Y, Iwaki Y, Pham SI, et al. Benefits of posttransplantation monitoring of interleukin 6 in lung transplantation. Ann Thorac Surg. 1993; 55 ( 1 ): 89 ‐ 93.
dc.identifier.citedreferenceLu KC, Jaramillo A, Lecha RL, et al. Interleukin‐6 and interferon‐gamma gene polymorphisms in the development of bronchiolitis obliterans syndrome after lung transplantation. Transplantation. 2002; 74 ( 9 ): 1297 ‐ 1302.
dc.identifier.citedreferenceSnyder LD, Hartwig MG, Ganous T, et al. Cytokine gene polymorphisms are not associated with bronchiolitis obliterans syndrome or survival after lung transplant. J Heart Lung Transplant. 2006; 25 ( 11 ): 1330 ‐ 1335.
dc.identifier.citedreferenceScholma J, Slebos D‐J, Marike boezen H, et al. Eosinophilic granulocytes and interleukin‐6 level in bronchoalveolar lavage fluid are associated with the development of obliterative bronchiolitis after lung transplantation. Am J Respir Crit Care Med. 2000; 162 ( 6 ): 2221 ‐ 2225.
dc.identifier.citedreferenceLama VN, Smith L, Badri L, et al. Evidence for tissue‐resident mesenchymal stem cells in human adult lung from studies of transplanted allografts. J Clin Invest. 2007; 117 ( 4 ): 989 ‐ 996.
dc.identifier.citedreferenceBoyum A. Isolation of mononuclear cells and granulocytes from human blood. Isolation of monuclear cells by one centrifugation, and of granulocytes by combining centrifugation and sedimentation at 1 g. Scand J Clin Lab Invest Suppl. 1968; 97: 77 ‐ 89.
dc.identifier.citedreferenceMimura T, Walker N, Aoki Y, et al. Local origin of mesenchymal cells in a murine orthotopic lung transplantation model of bronchiolitis obliterans. Am J Pathol. 2015; 185 ( 6 ): 1564 ‐ 1574.
dc.identifier.citedreferenceMi F, Gong L. Secretion of interleukin‐6 by bone marrow mesenchymal stem cells promotes metastasis in hepatocellular carcinoma. Biosci Rep. 2017; 37 ( 4 ).
dc.identifier.citedreferenceMcFarland‐Mancini MM, Funk HM, Paluch AM, et al. Differences in wound healing in mice with deficiency of IL‐6 versus IL‐6 receptor. J Immunol. 2010; 184 ( 12 ): 7219 ‐ 7228.
dc.identifier.citedreferenceMisumi K, Wheeler DS, Aoki Y, et al. Humoral immune responses mediate the development of a restrictive phenotype of chronic lung allograft dysfunction. JCI Insight. 2020; 5 ( 23 ): e136533.
dc.identifier.citedreferencePolgar A, Brozik M, Toth S, et al. Soluble interleukin‐6 receptor in plasma and in lymphocyte culture supernatants of healthy individuals and patients with systemic lupus erythematosus and rheumatoid arthritis. Med Sci Monit. 2000; 6 ( 1 ): 13 ‐ 18.
dc.identifier.citedreferenceHasegawa M, Sato S, Ihn H, Takehara K. Enhanced production of interleukin‐6 (IL‐6), oncostatin M and soluble IL‐6 receptor by cultured peripheral blood mononuclear cells from patients with systemic sclerosis. Rheumatology (Oxford). 1999; 38 ( 7 ): 612 ‐ 617.
dc.identifier.citedreferenceYokoyama A, Kohno N, Sakai K, Kondo K, Hirasawa Y, Hiwada K. Circulating levels of soluble interleukin‐6 receptor in patients with bronchial asthma. Am J Respir Crit Care Med. 1997; 156 ( 5 ): 1688 ‐ 1691.
dc.identifier.citedreferenceRavi AK, Khurana S, Lemon J, et al. Increased levels of soluble interleukin‐6 receptor and CCL3 in COPD sputum. Respir Res. 2014; 15: 103.
dc.identifier.citedreferenceYokoyama A, Kohno N, Hirasawa Y, et al. Evaluation of soluble IL‐6 receptor concentration in serum and epithelial lining fluid from patients with interstitial lung diseases. Clin Exp Immunol. 1995; 100 ( 2 ): 325 ‐ 329.
dc.identifier.citedreferenceEggenhofer E, Hoogduijn MJ. Mesenchymal stem cell‐educated macrophages. Transplant Res. 2012; 1 ( 1 ): 12.
dc.identifier.citedreferenceKim J, Hematti P. Mesenchymal stem cell‐educated macrophages: a novel type of alternatively activated macrophages. Exp Hematol. 2009; 37 ( 12 ): 1445 ‐ 1453.
dc.identifier.citedreferenceChen L, Tredget EE, Wu PY, Wu Y. Paracrine factors of mesenchymal stem cells recruit macrophages and endothelial lineage cells and enhance wound healing. PLoS One. 2008; 3 ( 4 ): e1886.
dc.identifier.citedreferenceMoodley YP, Misso NL, Scaffidi AK, et al. Inverse effects of interleukin‐6 on apoptosis of fibroblasts from pulmonary fibrosis and normal lungs. Am J Respir Cell Mol Biol. 2003; 29 ( 4 ): 490 ‐ 498.
dc.identifier.citedreferenceWillis RA, Nussler AK, Fries KM, Geller DA, Phipps RP. Induction of nitric oxide synthase in subsets of murine pulmonary fibroblasts: effect on fibroblast interleukin‐6 production. Clin Immunol Immunopathol. 1994; 71 ( 2 ): 231 ‐ 239.
dc.identifier.citedreferenceEickelberg O, Pansky A, Mussmann R, et al. Transforming growth factor‐beta1 induces interleukin‐6 expression via activating protein‐1 consisting of JunD homodimers in primary human lung fibroblasts. J Biol Chem. 1999; 274 ( 18 ): 12933 ‐ 12938.
dc.identifier.citedreferenceFries KM, Felch ME, Phipps RP. Interleukin‐6 is an autocrine growth factor for murine lung fibroblast subsets. Am J Respir Cell Mol Biol. 1994; 11 ( 5 ): 552 ‐ 560.
dc.identifier.citedreferenceCifaldi L, Prencipe G, Caiello I, et al. Inhibition of natural killer cell cytotoxicity by interleukin‐6: implications for the pathogenesis of macrophage activation syndrome. Arthritis Rheumatol. 2015; 67 ( 11 ): 3037 ‐ 3046.
dc.identifier.citedreferenceMacDonald KP, Blazar BR, Hill GR. Cytokine mediators of chronic graft‐versus‐host disease. J Clin Invest. 2017; 127 ( 7 ): 2452 ‐ 2463.
dc.identifier.citedreferenceTvedt THA, Skaarud KJ, Tjonnfjord GE, Gedde‐Dahl T, Iversen PO, Bruserud O. The Systemic Metabolic Profile Early after Allogeneic Stem Cell Transplantation: Effects of Adequate Energy Support Administered through Enteral Feeding Tube. Biol Blood Marrow Transplant. 2020; 26 ( 2 ): 380 ‐ 391.
dc.identifier.citedreferenceGroner B. Determinants of the extent and duration of STAT3 signaling. JAKSTAT. 2012; 1 ( 3 ): 211 ‐ 215.
dc.identifier.citedreferenceVerleden GM, Glanville AR, Lease ED, et al. Chronic lung allograft dysfunction: Definition, diagnostic criteria, and approaches to treatment‐A consensus report from the Pulmonary Council of the ISHLT. J Heart Lung Transplant. 2019; 38 ( 5 ): 493 ‐ 503.
dc.identifier.citedreferencevon der Thusen JH, Vandermeulen E, Vos R, Weynand B, Verbeken EK, Verleden SE. The histomorphological spectrum of restrictive chronic lung allograft dysfunction and implications for prognosis. Mod Pathol. 2018; 31 ( 5 ): 780 ‐ 790.
dc.identifier.citedreferenceMartinu T, Howell DN, Davis RD, Steele MP, Palmer SM. Pathologic correlates of bronchiolitis obliterans syndrome in pulmonary retransplant recipients. Chest. 2006; 129 ( 4 ): 1016 ‐ 1023.
dc.identifier.citedreferenceHeng D, Sharples LD, McNeil K, Stewart S, Wreghitt T, Wallwork J. Bronchiolitis obliterans syndrome: incidence, natural history, prognosis, and risk factors. J Heart Lung Transplant. 1998; 17 ( 12 ): 1255 ‐ 1263.
dc.identifier.citedreferenceSharples LD, McNeil K, Stewart S, Wallwork J. Risk factors for bronchiolitis obliterans: a systematic review of recent publications. J Heart Lung Transplant. 2002; 21 ( 2 ): 271 ‐ 281.
dc.identifier.citedreferenceElssner A, Jaumann F, Dobmann S, et al. Elevated levels of interleukin‐8 and transforming growth factor‐beta in bronchoalveolar lavage fluid from patients with bronchiolitis obliterans syndrome: proinflammatory role of bronchial epithelial cells. Munich Lung Transplant Group. Transplantation. 2000; 70 ( 2 ): 362 ‐ 367.
dc.identifier.citedreferenceMagnan A, Mege JL, Escallier JC, et al. Balance between alveolar macrophage IL‐6 and TGF‐beta in lung‐transplant recipients. Marseille and Montreal Lung Transplantation Group. Am J Respir Crit Care Med. 1996; 153 ( 4 Pt 1 ): 1431 ‐ 1436.
dc.identifier.citedreferenceCao P, Aoki Y, Badri L, et al. Autocrine lysophosphatidic acid signaling activates beta‐catenin and promotes lung allograft fibrosis. J Clin Invest. 2017; 127 ( 4 ): 1517 ‐ 1530.
dc.identifier.citedreferenceWalker NM, Mazzoni SM, Vittal R, Fingar DC, Lama VN. c‐Jun N‐terminal kinase (JNK)‐mediated induction of mSin1 expression and mTORC2 activation in mesenchymal cells during fibrosis. J Biol Chem. 2018; 293 ( 44 ): 17229 ‐ 17239.
dc.identifier.citedreferenceWalker NM, Belloli EA, Stuckey L, et al. Mechanistic Target of Rapamycin Complex 1 (mTORC1) and mTORC2 as Key Signaling Intermediates in Mesenchymal Cell Activation. J Biol Chem. 2016; 291 ( 12 ): 6262 ‐ 6271.
dc.identifier.citedreferenceBadri L, Murray S, Liu LX, et al. Mesenchymal stromal cells in bronchoalveolar lavage as predictors of bronchiolitis obliterans syndrome. Am J Respir Crit Care Med. 2011; 183 ( 8 ): 1062 ‐ 1070.
dc.identifier.citedreferenceWalker N, Badri L, Wettlaufer S, et al. Resident tissue‐specific mesenchymal progenitor cells contribute to fibrogenesis in human lung allografts. Am J Pathol. 2011; 178 ( 6 ): 2461 ‐ 2469.
dc.identifier.citedreferenceRose‐John S, Winthrop K, Calabrese L. The role of IL‐6 in host defence against infections: immunobiology and clinical implications. Nat Rev Rheumatol. 2017; 13 ( 7 ): 399 ‐ 409.
dc.identifier.citedreferenceTanaka T, Narazaki M, Kishimoto T. IL‐6 in inflammation, immunity, and disease. Cold Spring Harb Perspect Biol. 2014; 6 ( 10 ): a016295.
dc.identifier.citedreferenceHoriuchi S, Koyanagiu Y, Zhouu Y, et al. Soluble interleukin‐6 receptors released from T cell or granulocyte/macrophage cell lines and human peripheral blood mononuclear cells are generated through an alternative splicing mechanism. Eur J Immunol. 1994; 24 ( 8 ): 1945 ‐ 1948.
dc.identifier.citedreferenceLust JA, Donovan KA, Kline MP, Greipp PR, Kyle RA, Maihle NJ. Isolation of an mRNA encoding a soluble form of the human interleukin‐6 receptor. Cytokine. 1992; 4 ( 2 ): 96 ‐ 100.
dc.identifier.citedreferenceMullberg J, Oberthur W, Lottspeich F, et al. The soluble human IL‐6 receptor. Mutational characterization of the proteolytic cleavage site. J Immunol. 1994; 152 ( 10 ): 4958 ‐ 4968.
dc.identifier.citedreferenceSchindler C, Levy DE, Decker T. JAK‐STAT signaling: from interferons to cytokines. J Biol Chem. 2007; 282 ( 28 ): 20059 ‐ 20063.
dc.identifier.citedreferenceTormo AJ, Letellier MC, Sharma M, Elson G, Crabe S, Gauchat JF. IL‐6 activates STAT5 in T cells. Cytokine. 2012; 60 ( 2 ): 575 ‐ 582.
dc.identifier.citedreferenceHuynh J, Chand A, Gough D, Ernst M. Therapeutically exploiting STAT3 activity in cancer ‐ using tissue repair as a road map. Nat Rev Cancer. 2019; 19 ( 2 ): 82 ‐ 96.
dc.identifier.citedreferenceChakraborty D, Šumová B, Mallano T, et al. Activation of STAT3 integrates common profibrotic pathways to promote fibroblast activation and tissue fibrosis. Nat Commun. 2017; 8 ( 1 ): 1130.
dc.working.doiNOen
dc.owningcollnameInterdisciplinary and Peer-Reviewed


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