In this study, we have shown that microRNAs (miRNAs) released from the activated microglia upon Japanese Encephalitis virus (JEV) infection may exacerbate CNS damage. We have provided evidence that let-7a and let-7b (let-7a/b secrete through the vesicles from microglial cells in response to JEV infection and induces caspase activation in the primary cortical neurons that are a major target for JEV infection and pathogenesis in vivo. Our results suggest a new dimension of extracellular vesicle-mediated events that may cause neuronal damage and link to JEV pathogenesis.
A collaborative effort involving interdisciplinary domains from Dr. C. V. Srikanth and Dr. Vengadesan Krishnan addresses a fascinating mechanism involved in host-pathogen interactions. Several particularly problematic bacterial pathogens require a sophisticated type III secretion system, and a number of type III secreted effectors, to colonize their hosts and subsequently cause disease. Secreted effectors are key components of the bacterial arsenal, as they function in an orchestrated manner to highjack host vesicular transport system (VTS) and thus gain a suitable intracellular niche.
Freeman-Sheldon Syndrome (FSS) is a genetic disease where patients exhibit musculoskeletal abnormalities such as joint deformities, bent fingers, club feet, curved spine and facial anomalies. FSS patients have compromised movement, respiratory, speech and feeding problems and delayed growth and development. Mutations in the MYH3 gene, a gene belonging to the myosin family which helps in muscle contraction, has been reported to be the primary cause of FSS. Interestingly, how mutations in the MYH3 gene leads to musculoskeletal abnormalities seen in FSS patients is unclear.
Bacteria assemblevariety of hair-like surface organelles called pili or fimbriae on their surface for multiple purposes including adhesion, biofilm formation, immunomodulation, motility conjugation, and conducting electricity. Subtle differences in the pilus assembly and structure distinguish the bacterial strains and dictate tissue tropism and host specificity. Targeting pili and pili-mediated interaction appear to be a promising approach in combating infection and improving health. However, thesenanofibresare so small in size (~0.7nm diameter i.e.
Inflammatory bowel disease (IBD) is characterised by chronic inflammation of the gastrointestinal (GI) tract and includes Chron’s disease and ulcerative colitis. Currently the treatment to this disease mainly involves immune-suppressants that often results in severe side effects. To overcome poor success rates and challenges associated with current therapeutic strategies, Drs. Bajaj and Srikanth’s group tested gene therapy as an alternative treatment option. However, oral delivery of nucleic acids (NAs) to an inflamed colon is challenged by multiple barriers presented by the GI tract.
Bacteria are versatile organisms that instantly respond to changing environmental signals. Motility in bacteria is mediated by multi-protein complex thread like structure called flagella that allows bacteria to move towards favourable conditions. However, bacteria can also form sessile sedentary surface attached communities embedded in think polysaccharide matrix called biofilms.
The presence of ribonucleotides in DNA can lead to genomic instability and cellular lethality. To prevent adventitious rNTP incorporation, the majority of the DNA polymerases (dPols) possess a steric filter in the form of a bulky residue that stacks against the ribose sugar and clashes with 2’ -OH of incoming ribonucleotide. MsDpo4 from Mycobacterium smegmatis, naturally lack this steric filter and hence is capable of rNTP addition.
