Profile

Dr. Karthika Rajeeve is an infection biologist specializing in human pathogens such as Simkania negevensis, Chlamydia sp. and Mycobacterium tuberculosis. She completed her Ph.D. under the supervision of Prof. Thomas Rudel at the University of Wuerzburg, Germany, investigating on cell death evasion mechanism of the emerging human pathogen Simkania negevensis. Following her Ph.D., Dr. Rajeeve received a junior scientist fellowship from the Bavarian state government to pursue postdoctoral research. During this period, she conducted extensive research on various aspects of immune cell evasion of intracellular bacteria, with a particular focus on Chlamydia trachomatis. Subsequently, she attained a group leader position at the University of Wuerzburg, where she further advanced her investigations into metabolomics. Dr. Rajeeve excels in utilizing human ex-vivo models such as organoids and 3D tissue models for studying host-pathogen interactions. After six years of postdoctoral experience, she transitioned to Aarhus University as an Assistant Professor (tenure track), where she delved into cutting-edge technology, single-cell sequencing. Later, she took on the position of Scientist E at RGCB, India. Here, her group remains dedicated to unraveling the immune evasion mechanisms of Mycobacterium tuberculosis, a bacterium of immense significance due to its substantial impact on public health.

Current Focus Areas

  • Our laboratory specializes in studying host-pathogen interactions and the mechanisms of immune evasion. We use cutting edge technologies like human organoids and single cell sequencing to address disease mechanisms and the development of new therapies.

  • We investigate the mechanism underlying Mycobacterial reactivation in order to create biomarkers that can detect infections in their early stages. This approach aims to minimize the need for prolonged antibiotic treatment regimens.

  • Our team is also dedicated to understanding the general mechanism of immune evasion employed by Chlamydia trachomatis to maintain an asymptomatic mode of infection.

Selected Publications

  • Vollmuth N, Schlicker L, Guo Y, Hovhannisyan P, Janaki-Raman S, Kurmasheva N, Schmitz W, Schulze A, Stelzner K, Rajeeve K*, Rudel T*. (2022). c-Myc plays a key role in IFN-γ-induced persistence of Chlamydia trachomatis. ELife. doi.org/10.7554/elife.76721. (*equal contribution)

  • Rajeeve K*, Vollmuth N, JanakiRaman S, Wulff T, Schmalhofer M, Schmitz W, Baluapuri A, Huber C, Fink J, Dejure F, Wolf E, Eisenreich W, Schulze A, Seibel J, Rudel T*. (2020). Reprogramming of host glutamine metabolism during Chlamydia trachomatis infection and its key role in peptidoglycan synthesis. Nature Microbiology. 5, 1390-1402. 2020. (* Corresponding author)

  • Rajeeve K, Das S, Prusty BK and Rudel T. (2018). Chlamydia trachomatis paralyzes neutrophils to evade the host innate immune response. Nature Microbiology. 3, 824-835. doi: 10.1038/s41564-018-0182-y.

  • Chowdhury S, Reimer A, Sharan M, Kozjak‐Pavlovic V, Eulalio A, Prusty B, Fraunholz M, Karunakaran K and Rudel T. (2017) Chlamydia preserves the mitochondrial network necessary for replication via microRNA‐dependent inhibition of fission. Journal of Cell Biology. doi: 10.1083/jcb.201608063.

  • Karunakaran K, Subbarayal P, Vollmuth N and Rudel T. (2015). Molecular Microbiology. Chlamydia infected cells shed Gp96 to prevent Chlamydial re‐infection. doi: 10.1111/mmi.13151.

Skills & Proficiency

Chlamydia trachomatis Mycobacterium tuberculosis Single cell sequencing Organoids antimicrobial peptide 3D tissue model metabolomics Viral bacterial co-infection latency/dormancy reactivation.