Recent Publications

Researchers at Fundación Ciencia & Vida have recently published the following scientific articles and book chapters:

 

Mario Rosemblatt (Cellular and Molecular Immunology Lab):

  • Doñas C, Carrasco M, Fritz M, Prado C, Tejón G, Osorio-Barrios F, Manríquez V, Pacheco R, Reyes P, Bono MR, Loyola A, Rosemblatt M. GSK-J4 limits inflammation through the induction of a tolerogenic phenotype on DCs. J Autoimmun 75:105-117. doi:10.1016/j.jaut.2016.07.011 (2016).
    In collaboration with Drs. Loyola and Pacheco (FCV) and Dr. Bono (Faculty of Sciences – University of Chile), we demonstrated that treatment of mice with the epigenetic drug GSK-J4 inhibited the development of a form of Multiple Sclerosis, opening the way for a new treatment for autoimmune diseases.
  • Bono MR, Tejon G, Flores-Santibañez F, Fernandez D, Rosemblatt M, Sauma D. Retinoic acid as a modulator of T cell immunity. Nutrients 8(6): 349. doi:10.3390/nu8060349 (2016).
    In this Review, we summarized the role of Retinoic Acid, a derivative of Vitamin A, in the fine-tuning of the immune system and the balance between immunity and tolerance.

Nicole Tischler (Molecular Virology Lab):

  • Albornoz A, Hoffmann AB, Lozach PY, Tischler ND. Early Bunyavirus-host cell interactions. Viruses 8(5), pii: E143. doi: 10.3390/v8050143 (2016).
    In this review we highlight cellular and viral factors that mediate the entry pathway of bunyaviruses into diverse host cells.
  • Barriga GP, Villalón-Letelier F, Márquez CL, Bignon EA, Acuña R, Ross BH, Monasterio O, Mardones GA, Vidal SE, Tischler ND. Inhibition of the hantavirus fusion process by predicted domain III and stem peptides from glycoprotein Gc. PLoS Negl Trop Dis 10(7), e0004799. doi: 10.1371/journal.pntd.0004799 (2016).
    Here we identify peptides that block hantavirus entry into cells and describe the molecular mechanism of inhibition. 

Tomás Perez-Acle (Computational Biology Lab):

  • Escalona Y, Garate JA, Araya-Secchi R, Huynh T, Zhou R, Perez-Acle T. Exploring the membrane potential of simple dual-membrane systems as models for gap-junction channels. Biophys J 110 (12), 2678-2688. doi: 10.1016/j.bpj.2016.05.005 (2016).
    In this article we provide insights at the atomic scale on the effects of charge distributions over ionic transport, constituting a step forward into a better understanding of gap-junction channels.

David Holmes (Bioinformatics and Genome Biology Lab):

  • Ullrich SR, González C, Poehlein A, Tischler JS, Daniel R, Schlömann M, Holmes DS, Mühling M. Gene loss and horizontal gene transfer contributed to the genome evolution of the extreme acidophile “Ferrovum”. Front Microbiol 7, 797. doi: 10.3389/fmicb.2016.00797 (2016).
    In collaboration with Dr. Ullrich (Technical University, Freiberg, Germany), advances were made regarding the phylogeny and evolution of an important group of microorganisms involved in biomining and acid mine drainage.
  • Ullrich SR, Poehlein A, Tischler JS, González C, Ossandon FJ, Daniel R, Holmes DS, Schlömann M, Mühling M. Genome analysis of the biotechnologically relevant acidophilic iron oxidising strain JA12 indicates phylogenetic and metabolic diversity within the novel genus “Ferrovum”. PLoS One 11 (1), doi: 10.1371/journal.pone.0146832 (2016).
    In collaboration with Dr. Ullrich (Technical University, Freiberg, Germany), we advanced our understanding the genetics and physiology of an important biomining microorganism.
  • Cárdenas JP, Quatrini R, Holmes DS. Progress in Acidophile Genomics. In: Acidophiles: Life in Extremely Acidic Environments. Chapter 11 (pp 179–198). Eds Quatrini R and Johnson DB. Caister Academic Press. UK (2016).
    In this review, we summarize the information available from a compilation of all the genomes of extreme acidophiles.

Alejandra Loyola (Epigenetics and Chromatin Lab):

  • Alarcon V, Hernández S, Rubio L, Alvarez F, Flores Y, Varas-GodoyM, De Ferrari GV, Kann M, Villanueva RA, Loyola A. The enzymes LSD1 and Set1A cooperate with the viral protein HBx to establish an active hepatitis B viral chromatin state. Sci Rep 6, 25901. doi: 10.1038/srep25901 (2016)
    In this article we shed light on the mechanisms that regulate the hepatitis B viral replication mediated by the viral chromatin structure.

Rodrigo Pacheco (Neuroimmunology Lab):

  • Pardo E, Cárcamo C, Uribe-San Martín R, Ciampi E, Segovia-Miranda F, Curkovic C, Montecino F, Holmes C, Tichauer JE, Acuña E, Osorio-Barrios F, Castro M, Cortes P, Oyanadel C, Valenzuela D, Pacheco R, Naves R, Soza A, González A. Galectin-8 as an immunosuppressor in experimental autoimmune encephalomyelitis and a target of human early prognostic antibodies in multiple sclerosis. PLoS ONE. Accepted (2017)
    In collaboration with Dr. Alfonso González and Dr. Andrea Soza, in this study we found how galectine 8 attenuates the inflammatory response of Th17 cells. Accordingly, we found the mechanism of how the presence of anti-galectin 8 antibodies in multiple sclerosis patients predicts a stronger severity of clinical manifestation.
  • Pacheco R. Targeting dopamine receptor D3 signalling in inflammation. Oncotarget 8(5):7224-7225 (2017).
    In this comment, I summarize how the inhibition of dopamine receptor D3 attenuates the inflammatory response mediated by CD4+ T-cells in inflammatory disorders that involve the reduction of dopamine levels in the target tissue, such as Parkinson’s disease and inflammatory bowel diseases.
  • Figueroa C, Gálvez-Cancino F, Oyarce C, Contreras F, Prado C, Valeria C, Cruz S, Lladser A, Pacheco R. Inhibition of dopamine receptor D3 signaling in dendritic cells increases antigen cross-presentation to CD8+ T-cells favoring anti-tumor immunity. J Neuroimmunol 303: 99-107 (2017).
    In collaboration with Dr. Lladser’s team, in this study we found how dopamine receptor D3 signalling in dendritic cells attenuates the antigen-cross-presentation to CD8+ T-cells. Accordingly, we found that targeting the inhibition of dopamine receptor D3 in dendritic cells strongly potentiates cytotoxic T-lymphocytes mediated response and thereby the anti-tumour immunity.
  • Elgueta D, Aymerich MS, Contreras F, Montoya A, Celorrio M, Rojo-Bustamante E, Riquelme E, González H, Vásquez M, Franco R, Pacheco R. Pharmacologic antagonism of dopamine receptor D3 attenuates neurodegeneration and motor impairment in a mouse model of Parkinson’s disease. Neuropharmacology 113: 110-123 (2017).
    In this study, we found how the pharmacological inhibition of dopamine receptor D3 exerts a significant therapeutic effect in an animal model of Parkinson’s disease attenuating both, the motor impairment and the neurodegeneration of dopaminergic neurons in the nigrostriatal pathway.

Raquel Quatrini (Microbial Ecophysiology Lab):

  • Nuñez H, Covarrubias PC, Moya-Beltrán A, Issotta F, Atavales J, Acuña LG, Johnson DB, Quatrini R. Detection, identification and typing of Acidithiobacillus species and strains: a review. Res Microbiol S0923-2508(16)30046-8. doi: 10.1016/j.resmic.2016.05.006 (2016).
    In this review we provide an overview of techniques used in molecular detection, identification and typing of Acidithiobacillus spp. and discuss each method in the context of their contribution to the general and specific understanding of the role of the acidithiobacilli in microbial ecology and industrial biotechnology.
  • Issotta F, Galleguillos P, Moya-Beltrán A, Davis-Belmar CS, Rautenbach G, Covarrubias PC, Acosta-Grinok M, Ossandon FJ, Contador Y, Holmes DS, Marín-Eliantonio S, Quatrini R, Demergasso C. Draft genome sequence of chloride-tolerant Leptospirillum ferriphilum Sp-Cl from industrial bioleaching operations in northern Chile. Stand Genomic Sci 11:19. doi: 10.1186/s40793-016-0142-1 (2016).
    In this paper we describe the basic microbiological features and genomic properties of the biotechnologically relevant strain Leptospirillum ferriphilum Sp-Cl aiming to provide further understanding of the mechanisms used by acidophilic bacteria to endure high osmotic stress and high chloride levels.
  • Johnson DB, Quatrini R. Acidophile Microbiology in Space and Time. In: Acidophiles: Life in Extremely Acidic Environments. Chapter 1 (pp 3-16). Eds Quatrini R and Johnson DB. Caister Academic Press. UK (2016).
    This chapter introduces the subject of acidophile microbiology, tracing its origins to the current status quo, and provides the reader of this textbook with general information which provides a backdrop to the more specific topics described in subsequent chapters.
  • Quatrini R, Ossandon FJ, Rawlings DE. The Flexible Genome of Acidophilic Prokaryotes. In: Acidophiles: Life in Extremely Acidic Environments. Chapter 12 (pp 199-220). Eds Quatrini R and Johnson DB. Caister Academic Press. UK (2016).
    In this chapter, current knowledge gathered on mobile genetic elements that favour horizontal gene transfer in extreme acidic econiches and the strategies used by acidophiles to contain their dispersal, are explored. Also, major lacunae in our understanding of the mobilome of acidophilic prokaryotes and topics for further investigations are identified.

Álvaro Lladser (Gene Immunotherapy Lab):

  • Ligtenberg MA, Witt K, Galvez-Cancino P, Sette A, Lundqvist A, Lladser A, Kiessling R. Cripto-1 vaccination elicits protective immunity against metastatic melanoma. Oncoimmunology 5(5):e1128613. doi: 10.1080/2162402X.2015.1128613 (2016)
    In this work, we described that vaccination against cripto-1, a tumor-associated antigen up-regulated in “cancer-stem cells”, represents a novel strategy to target metastatic melanoma in mouse models.
  • Ligtenberg MA, Mougiakakos D, Mukhopadhyay M, Witt K, Lladser A, Chmielewski M, Riet T, Abken H, Kiessling R. Coexpressed catalase protects chimeric antigen receptor-redirected T cells as well as bystander cells from oxidative stress-induced loss of antitumor activity. J Immunol 196(2),759-766. doi: 10.4049/jimmunol.1401710 (2016)
    In this study, we demonstrated that by co-expressing tumor-specific chimeric antigen receptors along with catalase, we can both redirect specificity of human T cells against tumors and protect T cells and bystander cells from tumor-induced oxidative stress-mediated suppression.