Rabindra Mandal
CUNY Hunter College, NY·Microbiology & Immunology
Malaria still causes more than 200 million illnesses and 600,000 deaths a year, with young children in sub-Saharan Africa bearing most of the burden. Drugs are losing effectiveness as parasites become resistant, and vaccines protect only partially, so new ways to stop mild malaria from turning severe are needed.
- Fields
Microbiology & Immunology
Biology
Public Health & Epidemiology
- Topics
malaria
Plasmodium yoelii
gut microbiome
- Grants
- 1 known grant, through Jun 2028
What they work on
- Determine how the makeup of the gut bacterial community affects intestinal levels of sphingosine 1-phosphate (S1P), a lipid signaling molecule, and how those levels track with parasite burden in mice infected with Plasmodium yoelii 17XNL.
- Identify which gut bacteria metabolize S1P, using a click chemistry labeling strategy that tracks a chemically tagged lipid to the organisms consuming it, together with metagenomic sequencing of the microbial community.
- Test whether S1P signaling causally controls malaria severity by treating infected mice with selective S1P receptor blockers such as fingolimod (FTY720) and with inhibitors of S1P-metabolizing enzymes, then measuring parasite load and survival.
- Test the hypothesis that Bacteroides species worsen malaria by depleting intestinal S1P, comparing infection outcomes in mice whose Bacteroides are cleared by oral vancomycin with untreated controls.
More about the research
One underexplored lead is the community of bacteria living in the intestine, which appears to influence how badly a person is affected.
Why it matters
Severe malaria kills hundreds of thousands of children each year, and existing drugs and vaccines are losing ground. If gut bacteria worsen malaria by consuming the signaling lipid S1P, the gut microbiome becomes a target: altering bacterial communities or supporting S1P signaling could become a way to keep infections from becoming life-threatening. The findings may also apply to other infectious and inflammatory conditions shaped by microbial control of host lipid signaling.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Bumsuk Hahm
University of Missouri-Columbia, MO·Microbiology & Immunology
Determine how influenza virus lowers S1P lyase (SPL), the enzyme that degrades the lipid messenger S1P, and raises sphingosine kinase 2 (SK2), which makes it, and how these shifts speed viral replication in infected cells.
Jennifer DuBois
Montana State University, MT·Biochemistry
Determine the structure, function, regulation and molecular interactions of the heme utilization (hmu) pathway in the gut bacterium Bacteroides thetaiotaomicron, and identify its metabolic end products.
Geoffrey Hart
University of Minnesota, MN·Microbiology & Immunology
Test whether human NK cells, immune cells that kill antibody-coated targets, clear blood-stage Plasmodium in vivo by transferring them with human anti-merozoite antibodies into immunodeficient mice.
The school
CUNY Hunter College: 2 labs on PI Pages, $45M a year on research, 5 research doctorates a year.
Reach out
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