Dr Anuradha VAJJALA
Research Fellow

Name: Dr Anuradha Vajjala

Qualification: PhD

Thesis title: Development of in vitro and in vivo models to characterize biofilm formation by a necrotizing strain of group A Streptococcus

Current Position: Research Fellow

Supervisor: Asst Prof. Kimberly Kline

Co-supervisor: Dr Emanuel Hanski

Social media links:


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Personal blog:


Research profile:

Anuradha’s key area of research is to delineate mechanisms by which Group A Streptococci (GAS) propagate biofilm formation in the host during soft-tissue infections. GAS is the causative agent of a number of fulminant diseases including necrotising fasciitis (NF) or the “flesh eating disease” in which GAS rapidly infects fascia and muscle tissue that turn necrotic resulting in extreme morbidity. Although there are several reports about GAS “tissue communities/biofilms”, a distinct relation between GAS pathogenesis and biofilm formation has not been explored due to dearth of physiologically relevant models.

Towards that goal, she established and characterized in vitro (using mammalian cells) and in vivo (mice) models and demonstrated that GAS forms dense aggregates on mammalian cells that display hallmark biofilm characteristics including a 3-dimensional architecture, a matrix rich in proteins and enhanced tolerance to antibiotics. Her results also demonstrate a novel role of GAS streptolysin-mediated endoplasmic reticulum (ER) stress in the development and spread of GAS biofilms. She has also shown that host-associated biofilm formation depends on the release of a host-associated factor that promotes microcolony formation and GAS spread in vivo.

She is currently working in a project towards screening a GAS transposon mutant library to determine genes that are important in biofilm formation and dispersal in the host. By delineating these factors, she hopes to provide an insight into the pathogenesis of this virulent, necrotising strain of GAS and pave the way to identify new drug targets in anti-biofilm therapies against group A streptococcal infections.


Previous publications:

Ge X., McFarlane C., Vajjala A., Lokireddy S., Ng Z.H., Tan C.K., Tan N.S., Wahli W., Sharma M., Kambadur R. Smad3 signaling is required for satellite cell function and myogenic differentiation of myoblasts. Cell Res. 2011 Nov; 21(11):1591-604.

Ge X., Vajjala A., McFarlane C., Wahli W., Sharma M., Kambadur R. Lack of Smad3 signaling leads to impaired skeletal muscle regeneration. Am J Physiol Endocrinol Metab. 2012 Jul 1; 303(1)

McFarlane C., Vajjala A., Arigela H., Lokireddy S., Ge X., Bonala S., Manickam R., Kambadur R., Sharma M. Negative auto-regulation of myostatin expression is mediated by Smad3 and microRNA-27. PLoS One. 2014 Jan 31;9(1)

Streptolysin-induced endoplasmic reticulum stress drives group A streptococcal in vivo biofilm formation. (in communication)


Conferences attended:

60th Nobel Conference on Biofilm formation, its clinical impact and potential treatment (Karolinska Institutet, Stockholm, Sweden; Aug 2013)

Research Innovation in Infectious and Inflammatory Diseases, CREATE Joint Symposium (HUJ, Israel, NUS, Singapore, Singapore-MIT Alliance for Research and Technology, SMART; July 2013)

7th APOCB (Asia Pacific Organization of Cell Biology) Congress and ASCB workshop (Biopolis, A*STAR, Singapore; Feb 2014)

Gordon Research Seminar/Conference on Bacterial Toxins and Pathogenicity (Waterville Valley, New Hampshire; USA, Jul 9th-15th, 2016)