Timothy Casselli
University of South Alabama, AL·Microbiology & Immunology
Lyme disease is caused by Borrelia burgdorferi, a corkscrew-shaped bacterium (a spirochete) spread by ticks. Besides joints and the heart, it can reach the nervous system and cause Lyme neuroborreliosis, which includes meningitis (inflammation of the membranes around the brain), nerve inflammation and brain dysfunction.
- Fields
Microbiology & Immunology
Neuroscience
Medicine & Clinical Research
- Topics
Lyme disease
Borrelia burgdorferi
spirochete
- Grants
- 1 known grant, through Mar 2027
What they work on
- Determine whether the blood-cerebrospinal fluid barrier, the cell layer separating blood from the fluid around the brain, is where Borrelia burgdorferi and immune cells enter the central nervous system in infected mice.
- Test whether inflammation during B. burgdorferi infection breaks down the blood-CSF barrier and so allows both bacteria and white blood cells to invade the meninges and cerebrospinal fluid.
- Identify host immune responses linked to greater central nervous system invasion by infecting mouse strains with altered immune responses, focusing on pathways tied to Lyme arthritis severity or barrier permeability.
More about the research
There is no vaccine and no effective way to control the ticks, so the disease remains a public health concern. How the bacterium gets into the brain and spinal cord has been hard to study, because mice were long thought not to develop nervous system disease.
Why it matters
Neurologic Lyme disease can cause meningitis and nerve damage, and there is no vaccine. Identifying where B. burgdorferi enters the central nervous system, and which immune responses help it get in, could reveal targets for drugs that prevent or treat Lyme neuroborreliosis. This could help people infected through tick bites.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Jenifer Coburn
Medical College of Wisconsin, WI·Microbiology & Immunology
Test whether the interaction between the Borrelia burgdorferi surface protein P66 and the macrophage receptor SIRPα weakens innate and adaptive immunity, comparing p66-deficient and gene-restored bacteria in mice over six infection time points.
Karen Cyndari
University of Iowa, IA·Microbiology & Immunology·Early-career
Measure whether Borrelia burgdorferi infection breaks down the tight-junction barrier formed by resident synovial macrophages, using infected human synovial explants imaged by confocal microscopy and histomorphometry.
Janakiram Seshu
University of Texas at San Antonio, TX·Microbiology & Immunology
Determine the correlates of protection from Purified Borrelial Lipoproteins by comparing antibody levels and bacteria-killing (borrelicidal) activity after oral versus injected dosing in C3H/HeN laboratory mice and white-footed mice (Peromyscus leucopus).
The school
University of South Alabama: 5 labs on PI Pages, $70M a year on research, 53 research doctorates a year.
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