Microbiology & Immunology | Faculty | Peter H. Dube, Ph.D.
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Microbiology & Immunology Faculty

  Research | Publications | Lab Members | Biosketch


Peter H. Dube, Ph.D.
Associate Professor

STRF - Room 289.4
Tel: (210) 562-4181
Fax: (210) 562-4191
Email: dube@uthscsa.edu
 

Research

The research in the Dube laboratory is focused on inflammation and how inflammation leads to disease. In particular, we investigate how bacterial pathogens and their products influence inflammatory responses. The three major areas of interest are pulmonary infections leading to asthma or the exacerbation of asthma, acute infections of the lungs by biodefense-related pathogens and infectious gastroenteritis caused by invasive bacterial pathogens.

Our interests in asthma revolve around Mycoplasma pneumoniae and a toxin produced by this pathogen called the Community Acquired Respiratory Distress Syndrome toxin (CARDS toxin). Mycoplasma pneumoniae is often associated with acute exacerbations of asthma in children and adults and recent data suggests that CARDS toxin might be linked to a subset of asthma exacerbations. We are currently investigating how the CARDS toxin influences the immune system to promote asthma-like responses. Using a variety of animal models we have been able to show that exposure to purified CARDS toxin or low dose infection with M. pneumoiniae leads to the development of asthma-like inflammation in naive animals or exacerbation of asthma-like inflammation in animals with experimental asthma. We are using these models to dissect the immunological mechanisms responsible for generation of M. pneumoniae and CARDS toxin-associated asthma responses.

In addition to studying asthma we are also interested in understanding the acute pneumonia that develops during pneumonic plague (pulmonary infection with Yersinia pestis). Pneumonic plague is one of the most feared infections because it rapidly leads to death. We have discovered that one of the mechanisms used by Y. pestis to cause such an aggressive pneumonia is that inflammatory responses are blocked for the first 24hrs following initial infection. This delay in the inflammatory response provides a significant advantage to the pathogens. Studies investigate the virulence factors responsible for this delay in inflammatory responses.

Our interests in invasive bacterial pathogens of the gut are directed at understanding how Yersinia enterocolitica, a common food borne pathogen, avoids initial recognition and inflammatory responses. We are investigating the bacterial factors responsible for both activating and inhibiting the inflammasome. The inflammasome is the cellular machinery responsible for generating inflammatory responses and Y. enterocolitica regulates these responses at various stages. An important aspect of Y. enterocolitica virulence is the ability to elaborate a Type Three Secretion System (TTSS). TTSS allow bacterial pathogens to directly inject virulence factors into the host cell cytoplasm. We are interested in bacterial factors that make the cell permissive for performing TTS as these represent a novel group of virulence proteins that could be targeted for therapeutic intervention.

Biodefense research: We have initiated studies looking at the host response to Yersinia pestis infection. Y. pestis is the causative agent of plague. We employ models of both bubonic and primary pneumonic plague to look at gene expression in response to infection.


 

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Publications

Affiliations

American Society For Microbiology
American Association of Immunologists
Editorial board member for Infection and Immunity
Frontiers in Cellular Microbiology
 

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Lab Members

  Lab Rooms: STRF - 279.1 C-H Phone: (210) 562-4175

  • Angelene Cantwell, Senior Research Associate

Graduate Students

  • Josephine Thinwa
  • Jorge Medina

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