Jeffrey Weiser
New York University, NY·Microbiology & Immunology
Before a bacterium can cause disease, it usually has to live quietly on a body surface first. For Streptococcus pneumoniae, a leading cause of pneumonia, ear infections and bloodstream infection, that surface is the lining of the nose and throat.
- Fields
Microbiology & Immunology
Medicine & Clinical Research
Biology
- Topics
Streptococcus pneumoniae
pneumococcus
nasopharyngeal colonization
- Grants
- 1 known grant, through Jun 2029
What they work on
- Determine how IL-1 and IL-17 signaling, two immune messenger pathways, recruit and activate the cells that take up and clear Streptococcus pneumoniae from the upper airway, using mice lacking the IL-1 or IL-17 receptor.
- Define how early IL-1 signaling influences the later, IL-17-dependent clearance of pneumococcal colonization, and test why infant mice show delayed IL-17 responses that may explain prolonged carriage in the young.
- Test how changes in the amount and physical properties of airway mucus, altered by bacterial enzymes such as neuraminidase, prevent clearance by mucociliary flow and stabilize colonization.
- Determine how pneumococcal retention in firm versus loose mucus governs shedding from the upper airway, the limiting step in host-to-host transmission, in mouse transmission models.
- Examine how co-infection with influenza virus, which also uses neuraminidase to modify mucus, synergistically increases pneumococcal colonization density, shedding and transmission.
More about the research
Colonization there is harmless in most people but is the starting point for every pneumococcal disease and the route by which the bacterium passes from person to person. This program, which has studied the organism for thirty years, asks two linked questions: how the immune system eventually clears the bacterium from the upper airway, and how the bacterium manipulates the mucus layer it lives in to stay put and to get shed onto a new host. The work uses bacterial genetics together with mucosal immunology in mouse models chosen because they reproduce key features seen in people: colonization lasting weeks to months, longer and denser colonization in infancy, host-to-host transmission, worse colonization and transmission during influenza co-infection, and pneumonia or bloodstream infection depending on bacterial serotype and host age.
Why it matters
Streptococcus pneumoniae colonization of the nose and throat precedes all pneumococcal disease and is how the bacterium spreads between people, including the heavy carriage seen in infants and the worsening that accompanies influenza. Defining the immune signals that clear it and the mucus changes that let it persist and be shed could point toward ways to shorten carriage or interrupt transmission, with lessons for other pathogens that start on mucosal surfaces.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Amali Samarasinghe
University of Wisconsin-Madison, WI·Microbiology & Immunology
Determine how eosinophils, allergy-associated white blood cells, take up and kill Streptococcus pneumoniae inside and outside the cell, and how taking up the bacteria changes the eosinophils' physiology and features.
Daren Knoell
University of Nebraska Medical Center, NE·Microbiology & Immunology
Determine how loss of the zinc transporter ZIP8 alters the makeup of myeloid immune cells in the lung in mice, and what that means for clearing Streptococcus pneumoniae and for survival.
Caitlyn Holmes
University of Minnesota, MN·Microbiology & Immunology·Early-career
Define how macrophages in the spleen, immune cells that engulf bacteria, restrict Klebsiella pneumoniae during bloodstream infection, a site rarely studied in Gram-negative disease.
The school
New York University: 72 labs on PI Pages, $1.5B a year on research, 540 research doctorates a year.
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