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Clemente Britto-Leon, MD

Assistant Professor of Medicine (Pulmonary, Critical Care and Sleep Medicine)
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Contact Info

Pulmonary, Critical Care & Sleep Medicine

PO Box 208057

New Haven, CT 06520-8057

United States

About

Titles

Assistant Professor of Medicine (Pulmonary, Critical Care and Sleep Medicine)

Biography

Dr. Britto received his medical degree from the Luis Razetti School of Medicine at the Universidad Central de Venezuela in Caracas, Venezuela. He completed his Internal Medicine residency training at Albert Einstein Medical Center in Philadelphia.

Dr. Britto completed his fellowship training in Pulmonary & Critical Care Medicine at Yale, followed by a Fellowship in Adult Cystic Fibrosis sponsored by the Cystic Fibrosis Foundation. During his fellowship, Dr. Britto became involved in research focused on the pathogenesis of airway diseases in the laboratory of his mentor, Lauren Cohn, M.D.

Dr. Britto joined the faculty at Yale in 2013, where his clinical responsibilities include being a member of the Adult Cystic Fibrosis Program and attending in the Medical Intensive Care Unit. These activities complement his research program focused on understanding the role of the airway epithelium in the development of airway diseases such as asthma and cystic fibrosis.

Appointments

Other Departments & Organizations

Education & Training

Fellowship
Yale-New Haven Hospital (2013)
Fellowship
Yale-New Haven Hospital (2013)
Residency
Albert Einstein Medical Center (2008)
Residency
Albert Einstein Medical Center (2007)
Internship
Albert Einstein Medical Center (2005)
MD
Universidad Central de Venezuela (2002)

Research

Overview

Short Palate Lung and Nasal epithelium Clone 1 (SPLUNC1) is an abundant airway protein with host protective functions relevant to cystic fibrosis (CF), the most common fatal genetic disease in the United States. The antimicrobial defense, mucociliary clearance and ion tranport regulation properties of SPLUNC1 may be important in the development of CF lung disease, the main cause of mortality in these patients. Persistent pulmonary inflammation and neutrophilic infiltration are hallmarks of CF lung disease. Work in our laboratory suggests that SPLUNC1 may have a novel role in regulating neutrophilic airway inflammation, as SPLUNC1-deficient (splunc1-/-) mice have dramatically decreased airway neutrophils during acute inflammation induced by LPS compared to wild type (WT) littermates.

SPLUNC1 is decreased in the airways of patients during allergic inflammation and we have shown that SPLUNC1 is decreased by common respiratory pathogens in animal models of airway inflammation in vivo, and by interferon gamma in vitro. Interestingly, this suppression of SPLUNC1 appears to be impaired in lung explants of severe CF patients undergoing lung transplantation, where SPLUNC1 is increased despite chronic inflammation and infection. In preliminary work, we determined that the suppression of SPLUNC1 is also impaired in the bronchoalveolar lavage fluid (BALF) of unstimulated CFTR-deficient (cftr-/-) and F508del homozygous (F508del) mice, two animal models of CF indicating that these animal models may be useful to study the regulation of SPLUNC1 in CF.

Despite the apparent paradox between the pathological and protective role of SPLUNC1, little is known about the mechanisms that regulate its activity, the role that SPLUNC1 plays in neutrophilic inflammation and its sigificance in the development of CF lung disease. We believe that the suppression of SPLUNC1 is a protective mechanism to limit neutrophilic inflammation and subsequent airway injury and so, high SPLUNC1 in CF may be detrimental by promoting neutrophilic inflammation, a fundamental part of CF lung disease pathogenesis. The objective of our research program is to understand how SPLUNC1 influences neutrophilic airway inflammation and if the modulation of SPLUNC1 can limit airway inflammation in CF.

Regulation of SPLUNC1 expression by the airway epithelium: identification of mechanisms by which pathogens, PAMPs and cytokines modulate SPLUNC1 expression.

Mechanisms of neutrophilic inflammation control by SPLUNC1: characterization of the role of SPLUNC1 in neutrophil recruitment to the lungs during acute airway inflammation.

Role of SPLUNC1 in immune responses in CF: defining mechanisms by which SPLUNC1 is increased in CF and what effect this increase has in neutrophilic immune responses.

Medical Subject Headings (MeSH)

Airway Management; Bacterial Infections and Mycoses; Cystic Fibrosis; Epithelium; Immune System Diseases; Lung; Pulmonary Medicine; Respiratory Tract Diseases

Research at a Glance

Yale Co-Authors

Frequent collaborators of Clemente Britto-Leon's published research.

Publications

Featured Publications

2024

2023

2022

Clinical Trials

Current Trials

Clinical Care

Overview

Clinical Specialties

Pulmonology & Sleep Medicine; Pulmonary Critical Care

Fact Sheets

Board Certifications

  • Critical Care Medicine (Internal Medicine)

    Certification Organization
    AB of Internal Medicine
    Latest Certification Date
    2021
    Original Certification Date
    2011
  • Pulmonary Disease

    Certification Organization
    AB of Internal Medicine
    Latest Certification Date
    2020
    Original Certification Date
    2010

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Contacts

Appointment Number
Clinic Fax Number
Mailing Address

Pulmonary, Critical Care & Sleep Medicine

PO Box 208057

New Haven, CT 06520-8057

United States

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