Daniel Wozniak

About

Daniel Wozniak, PhD, is the Samuel Saslaw Professor of Infectious Diseases at Ohio State College of Medicine, where he also serves as Vice Chair of Microbial Infection and Immunity, Professor in the Microbiology Program, and Co-Director of the Microbial Communities Program Area at the Infectious Diseases Institute. His laboratory focuses on understanding the molecular biology and pathogenesis of important human pathogens such as Pseudomonas aeruginosa, Acinetobacter baumannii, and Staphylococcus aureus. His research centers on the regulation of virulence gene expression, biofilm formation and pathogenesis, experimental therapeutics to combat infections, animal models of chronic infection, and the evolution of bacteria during infection. Dr. Wozniak's work aims to address the challenges posed by biofilms, which are involved in many chronic and recurrent bacterial infections and contribute significantly to healthcare costs. His collaborative efforts include exploiting enzyme activity to break down biofilm matrices, developing human monoclonal antibodies targeting biofilm components, and implementing therapies to disrupt biofilms in patients with chronic wounds. He is recognized as a 2022 OSU Distinguished Scholar and is actively involved in advancing infectious disease research and treatment.

Research topics

• Cell biology
• Biology
• Pathology
• Chemistry
• Medicine
• Immunology
• Biochemistry
• Genetics
• Microbiology

Selected publications

• Role of Cardiac Macrophages on Cardiac Inflammation, Fibrosis and Tissue Repair

  Cells · 2020 · 388 citations

  The immune system plays a pivotal role in the initiation, development and resolution of inflammation following insult or damage to organs. The heart is a vital organ which supplies nutrients and oxygen to all parts of the body. Heart failure (HF) has been conventionally described as a disease associated with cardiac tissue damage caused by systemic inflammation, arrhythmia and conduction defects. Cardiac inflammation and subsequent tissue damage is orchestrated by the infiltration and activation…

  DOI

• Sequential ubiquitination of NLRP3 by RNF125 and Cbl-b limits inflammasome activation and endotoxemia

  The Journal of Experimental Medicine · 2020 · 193 citations

  Aberrant NLRP3 inflammasome activation contributes to the development of endotoxemia. The importance of negative regulation of NLRP3 inflammasomes remains poorly understood. Here, we show that the E3 ubiquitin ligase Cbl-b is essential for preventing endotoxemia induced by a sub-lethal dose of LPS via a caspase-11/NLRP3-dependent manner. Further studies show that NLRP3 undergoes both K63- and K48-linked polyubiquitination. Cbl-b binds to the K63-ubiquitin chains attached to the NLRP3 leucine-ric…

  DOI

• Pseudomonas aeruginosa aggregates in cystic fibrosis sputum produce exopolysaccharides that likely impede current therapies

  Cell Reports · 2021 · 170 citations

  In cystic fibrosis (CF) airways, Pseudomonas aeruginosa forms cellular aggregates called biofilms that are thought to contribute to chronic infection. To form aggregates, P. aeruginosa can use different mechanisms, each with its own pathogenic implications. However, how they form in vivo is controversial and unclear. One mechanism involves a bacterially produced extracellular matrix that holds the aggregates together. Pel and Psl exopolysaccharides are structural and protective components of thi…

  DOI

• The surface interface and swimming motility influence surface-sensing responses in <i>Pseudomonas aeruginosa</i>

  Proceedings of the National Academy of Sciences · 2024-09-16 · 16 citations

  articleOpen access

  Bacterial biofilms have been implicated in several chronic infections. After initial attachment, a critical first step in biofilm formation is a cell inducing a surface-sensing response. In the Gram-negative opportunistic pathogen Pseudomonas aeruginosa , two second messengers, cyclic diguanylate monophosphate (c-di-GMP) and cyclic adenosine monophosphate (cAMP), are produced by different surface-sensing mechanisms. However, given the disparate cellular behaviors regulated by these second messen…

  PublisherOA PDFDOI

• Quorum sensing regulation of Psl polysaccharide production by <i>Pseudomonas aeruginosa</i>

  Journal of Bacteriology · 2024-11-12 · 8 citations

  articleOpen access

  ABSTRACT Pseudomonas aeruginosa is a common opportunistic pathogen and a model organism for studying bacterial sociality. A social behavior of P. aeruginosa that is critical for its success as a pathogen is its ability to form protective biofilms. Many of P. aeruginosa ’s social phenotypes are regulated by quorum sensing—a type of cell-cell communication that allows bacteria to respond to population density. Although biofilm formation is known to be affected by quorum sensing, evidence for direc…

  PublisherOA PDFDOI

Recent grants

• Revisiting alginate paradigms

  NIH · $2.5M · 2017–2023

• Pseudomonas biofilms and immunity

  NIH · $1.9M · 2013–2018

• The biofilm matrix of P. aeruginosa

  NIH · $2.9M · 2019–2025

Frequent coauthors

• Matthew R. Parsek

  University of Washington

  62 shared

• P. Lynne Howell

  43 shared

• Sashwati Roy

  40 shared

• Chandan K. Sen

  Indiana University School of Medicine

  40 shared

• Paul Stoodley

  The Ohio State University Wexner Medical Center

  37 shared

• Oleg Derzhko

  National Academy of Sciences of Ukraine

  35 shared

• Preston J. Hill

  The Ohio State University

  34 shared

• Z. Luyan

  Chinese Academy of Sciences

  30 shared

Labs

• Microbial Infection and ImmunityPI

Education

• Ph.D., Microbiology

  Ohio State University

  2000

• M.S., Microbiology and Immunology

  University of California, San Francisco

  1995

• B.S., Microbiology

  University of California, Berkeley

  1993

Awards & honors

• 2022 OSU Distinguished Scholar

Similar researchers at Ohio State University

• Michael Baileyh-132
• Zihai Lih-70
• Benjamin Segalh-65