Inflammatory bowel disease (IBD) – Research group Eduardo Villablanca

Inflammatory bowel disease (IBD), including Crohn’s disease (CD) and ulcerative colitis (UC), is a manifestation of an inappropriate inflammatory response to intestinal microorganisms in genetically susceptible individuals. IBD is a multifactorial complex disease, which is believed to originate from anomalous balance between tolerogenic and inflammatory immune responses against “self” antigens. Although substantial progress has been made over the last decade in defining the genetic architecture

Chiara Sorini, Chiara Zagami and Xinxin Luo in the lab

Picture above: Chiara Sorini, Chiara Zagami and Xinxin Luo in the lab. Photo: Eduardo Villablanca.
 

Research interests

Mucosal Immunology, Oral tolerance, Inflammatory Bowel Diseases.

Inflammatory bowel disease (IBD), including Crohn’s disease (CD) and ulcerative colitis (UC), is a manifestation of an inappropriate inflammatory response to intestinal microorganisms in genetically susceptible individuals. IBD is a multifactorial complex disease, which is believed to originate from anomalous balance between tolerogenic and inflammatory immune responses against “self” antigens. Although substantial progress has been made over the last decade in defining the genetic architecture of IBD, there is currently no cure likely due to a yet incomplete understanding of the causes leading to IBD.

Clockwise starting from the baby: Rebeca Cardoso, Francisca Castillo, Rodrigo Morales, Chiara Zagami, Gustavo Monasterio, Xinxin Luo, Chiara Sorini, Jennifer Fransson, Sanghita Benerjee, Srustidhar Das, Oscar Diaz, Eduardo Villablanca.
Villablanca research group - clockwise starting from the baby: Rebeca Cardoso, Francisca Castillo, Rodrigo Morales, Chiara Zagami, Gustavo Monasterio, Xinxin Luo, Chiara Sorini, Jennifer Fransson, Sanghita Benerjee, Srustidhar Das, Oscar Diaz, Eduardo Villablanca. Photo: Eduardo Villablanca

Research focus

Our lab that lies at the interface of immunology, human health, biological engineering, and systems biology, is seeking to define the complex dynamics of host-environment interactions required to sustain intestinal homeostasis, how breakdown in these interactions may lead to intestinal inflammatory disorders, and how we can promote mucosal healing to reverse the intestinal damage caused by inflammation. 

The main focus of our lab is to gain insights into the mechanisms that underlie the initiation and resolution of inflammatory bowel disease (IBD) to eventually develop therapeutics to treat intestinal autoimmune diseases.To accomplish these goals, we have built an interdisciplinary research program that combines the generation of novel experimental models of IBD (zebrafish and mouse), traditional molecular and cellular approaches (e.g. ex vivoimmune cell- intestinal organoid co-culture), cutting-edge technologies (scRNA-seq and spatial transcriptomics), systems biology, and the use of clinical samples. Thus, we are working to provide insights that may lead to novel, rational-based strategies to prevent the initiation of IBD by intervening during its preclinical phase and/or to accelerate and promote tissue regeneration upon damage.

Mission statement

Mission Statement

Our mission is to understand the genetic, cellular and environmental contribution towards IBD susceptibility.

Publications

Selected publications

Members and contact

Group leader

All members of the group


Former members

  • Sara Fernandez, Research tech (2015)
  • Paulo Czarnewski, PhD / Postdoc (2015)
  • Suvi Karvinen, Master student (2017)
  • Muksheed Shaik, Research tech (2017)
  • Anders Appelblom, Master student (2017)
  • Shuangjia Xue, Master student (2017)
  • Cristian Doñas, PhD / Postdoc (2019)
  • Martina Parigi, PhD student (2020)
  • Annika Frede, PhD / Postdoc (2020)
  • Roham Parsa, PhD / Postdoc (2020)
  • Santoshnisikranth Inampudi, Research tech (2020)
  • Oscar Diaz Perez, PhD student (2016- )
  • Kumar P. Tripathi, PhD / Postdoc (2018- )
  • Chiara Sorini, PhD / Postdoc (2016- )
  • Francisca Castillo, Research assistant (2020-  )
  • Chira Zagami, Student (2020-  )
  • Sanghita Benerjee, Postdoc (2020-  )

Collaborations

Our research program is also energized and diversified through international collaborations with leading scientists in the field. These include Dr. Samuel Huber and Dr. Nicola Gagliani at the Universitätsklinikum Hamburg-Eppenddorf (UKE, Hamburg, Germany).

In addition, I collaborate closely with Professor Miguel Allende (Universidad de Chile, Chile) and Dr. Pedro Hernandez (Institut Curie, Paris, France), who contribute with expertise on zebrafish-specific methodologies and reporters; Dr. Ana-Maria Lennon (Institut Curie, Paris, France), Dr. Matteo Iannacone (San Raffaele, Italy) who are expert in imaging and cell migration; Dr. Jan H. Niess (Univ. Bern, Switzerland), Professor Yasmine Belkaid (NIH, Bethesda, USA) and Professor Dennis L. Kasper (Harvard Medical School, Boston, USA) who are experts in mucosal immunology and interaction with the environment (e.g. dietary compounds and microbiota); Dr Moshe Biton (Weizmann institutet, Israel), Dr. Andreas Schlitzer (University of Bonn, Germany), who are experts in immunology and systems biology, and Professor Ramnik Xavier (Broad Institute, Boston, USA) who is an expert in IBD and systems immunology.

Videos

Villablanca lab Intro: Studying the initiation and resolution of inflammatory bowel diseases (IBD)

Our lab is trying to understand the molecular and cellular mechanisms involved in the initiation of inflammatory bowel diseases (IBD) and also try to identify novel genes and pathways that promote mucosal healing after intestinal damage. Our final goal is to identify new therapeutic target to treat IBD. 

B cell hinders the stroma-epithelium regenerative crosstalk during mucosal healing

The cellular mechanisms controlling mucosal healing (MH) following injury are largely unknown. Using unbiased multi-parameter analysis, Frede, Czarnewski, Monasterio, and colleagues identified that B cells accumulate in the colonic damaged areas during MH.  Surprisingly, B cells played detrimental roles during MH as their presence hindered the interaction between epithelium and stroma. This is the papervids summarizing the work of Frede, Czarnewski, Monasterio, et al, published in Immunity, 2022