Ben Blumberg

I am a PhD student in the Department of Molecular Microbiology and Immunology (MMI) at the Johns Hopkins Bloomberg School of Public Health (JHSPH). I graduated with a B.S. degree in Biology from the University of Vermont in 2006 and then spent three as a research technician prior to joining the Dimopoulos group. My research project is focusing on bacteria-independent activation of anti-Plasmodium immunity in the dissecting the Anopheles mosquito. VIDEO PRESENTATION /  Contact: bblumber@jhsph.edu

Bio - current research - cv - links

Bio:
I am a PhD student in the Department of Molecular Microbiology and Immunology (MMI) at the Johns Hopkins Bloomberg School of Public Health (JHSPH). I graduated with a B.S. degree in Biology from the University of Vermont in 2006. My current research project broadly focuses on the dissection of the Anopheles gambiae mosquito’s immune response to bacteria and the human malaria parasite Plasmodium falciparum. Previous studies have shown that the immune signaling pathway IMD is implicated in defenses against P. falciparum, and that the activation of this pathway required the presence of bacteria in the mosquito midgut. My project is looking at bacteria-independent anti-Plasmodium defense reactions. Towards this I have used a microarray gene expression approach with infections of aseptic mosquitoes, in conjunction with RNAi-based gene silencing assays of discovered immune factors.
 

 

Current research:

 Dissecting the Anopheles gambiae anti-Plasmodium & anti-bacterial defenses: Characterizing differentially regulated genes in response to Plasmodium infection of septic and aseptic mosquitoes.

The mosquito Anopheles gambiae is the primary vector of Plasmodium falciparum, the most dangerous human malaria parasite. Knowledge of the molecular interactions between the parasite and the mosquito is fundamental for efficacious drug design, effective transmission blocking vaccines, and the creation of transgenic mosquitoes refractory to Plasmodium infection. The Dimopoulos Group is very interested in the mosquito’s immune response to P. falciparum. The lab has shown that A. gambiae midgut microbiota stimulate basal immunity (Dong et al. 2009). Antibiotic treatment of mosquitoes results in increased susceptibility to Plasmodium infection (Figure 1).

Figure 1. Increased oocysts in antibiotic treated mosquitoes.

Bacteria elicit mosquito immune factors that overlap with the anti-Plasmodium defense. Stefanie Trop, a rotation student in the Dimopoulos group, used a microarray to assess gene expression in septic and aseptic mosquitoes infected with P. falciparum. The results indicate differential gene regulation between septic and aseptic mosquitoes (Figure 2).


Figure 2. Differential generegulation between Plasmodium infected septic and aseptic mosquitoes.

Although it is known that midgut microbiota are directly responsible for the anti-plasmodium response (Dong et al. 2009, Meister et al. 2009), we suspect there are“Plasmodium-specific” immune factors expressed in the absence of midgut microbiota. I am investigating Stefanie Trop’s microarray data set for known immune genes and genes of unknown function that are differentially regulated in aseptic mosquitoes. I have selected a panel of genes for further phenotypic characterization in aseptic mosquitoes. RNAi knockdown of selected genes, followed by Plasmodium infection and subsequent oocyst counts will determine if these genes are indeed “Plasmodium-specific” factors (Figure 3). We believe identification of these factors will aid in dissecting the complexities of the Anopheles gambiae anti-Plasmodium response.


Figure 3. Characterizing "Plasmodium-specific" genes of interest.

 

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