Dr. Lalitha Biswas joined as Assistant Professor at Amrita Institute of Medical Sciences in Jan 2010. She is a successful Ph D degree achiever with various fellowships in hand. A couple of research projects on which she is currently working on is concentrated on molecular biology and Infection biology which is funded by DST and ICMR.

She adds to her achievements the author and co - author of nearly 8 publications in various reputed journals like journal of immunology, journal of Bacteriology etc. She qualified CSIR - NET in the year 2000. Apart from these she owned the DFG fellowship from 2002 - 2006 and also received the fellowship from German Sonder Forshungs Bereich for the year 2007 - 2009.



Publication Type: Journal Article
Year of Publication Publication Type Title
2015 Journal Article Na Nair, Vinod, Va, Suresh, M. Ka, Vijayrajratnam, Sa, Biswas, La, Peethambaran, Rb, Vasudevan, A. Kc, and R.a Biswas, “Amidase, a cell wall hydrolase, elicits protective immunity against Staphylococcus aureus and S. epidermidis”, International Journal of Biological Macromolecules, vol. 77, pp. 314-321, 2015.[Abstract]

The morbidity and the mortality associated with Staphylococcus aureus and S. epidermidis infections have greatly increased due to the rapid emergence of highly virulent and antibiotic resistant strains. Development of a vaccine-based therapy is greatly desired. However, no staphylococcal vaccine is available till date. In this study, we have identified Major amidase (Atl-AM) as a prime candidate for future vaccine design against these pathogens. Atl-AM is a multi-functional non-covalently cell wall associated protein which is involved in staphylococcal cell separation after cell division, host extracellular matrix adhesion and biofilm formation. Atl-AM is present on the surface of diverse S. aureus and S. epidermidis strains. When used in combination with Freund's adjuvant, Atl-AM generated a mixed Th1 and Th2 mediated immune response which is skewed more toward Th1; and showed increased production of opsonophagocytic IgG2a and IgG2b antibodies. Significant protective immune response was observed when vaccinated mice were challenged with S. aureus or S. epidermidis. Vaccination prevented the systemic dissemination of both organisms. Our results demonstrate the remarkable efficacy of Atl-AM as a vaccine candidate against both of these pathogens. © 2015 Elsevier B.V.

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2013 Journal Article Va Sukhithasri, Nisha, Na, Biswas, La, Kumar, VbAnil, and R.a Biswas, “Innate immune recognition of microbial cell wall components and microbial strategies to evade such recognitions”, Microbiological Research, vol. 168, pp. 396-406, 2013.[Abstract]

The innate immune system constitutes the first line of defence against invading microbes. The basis of this defence resides in the recognition of defined structural motifs of the microbes called "Microbial associated molecular patterns" that are absent in the host. Cell wall, the outer layer of both bacterial and fungal cells, a unique structure that is absent in the host and is recognized by the germ line encoded host receptors. Nucleotide oligomerization domain proteins, peptidoglycan recognition proteins and C-type lectins are host receptors that are involved in the recognition of bacterial cell wall (usually called peptidoglycan), whereas fungal cell wall components (N- and O-linked mannans, β-glucans etc.) are recognized by host receptors like C-type lectins (Dectin-1, Dectin-2, mannose receptor, DC-SIGN), Toll like receptors-2 and -4 (TLR-2 and TLR-4). These recognitions lead to activation of a variety of host signaling cascades and ultimate production of anti-microbial compounds including phospholipase A2, antimicrobial peptides, lysozyme, reactive oxygen and nitrogen species. These molecules act in cohort against the invading microbes to eradicate infections. Additionally pathogen recognition leads to the production of cytokines, which further activate the adaptive immune system. Both pathogenic and commensal bacteria and fungus use numerous strategies to subvert the host defence. These strategies include bacterial peptidoglycan glycan backbone modifications by O-acetylation, N-deacetylation, N-glycolylation and stem peptide modifications by amidation of meso-Diaminopimelic acid; fungal cell wall modifications by shielding the β-glucan layer with mannoproteins and α-1,3 glucan. This review focuses on the recent advances in understanding the role of bacterial and fungal cell wall in their innate immune recognition and evasion strategies. © 2013 Elsevier GmbH.

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