Biology subjects

Niranjan, R.

Publications and source records attributed to Niranjan, R..

3 recordsLinked to original sources

bioRxiv2023

Assessment of genetic diversity patterns of different serotypes of dengue virus, prevalent in patients from Kerala, India: a strain specific mutation study and its relevance to pathogenesis

The mutations are the key mechanisms responsible for virus survival and its fitness in the host. This process of mutation is implicated in the development of pathogenesis of the dengue viral disease. We report that, all the four serotypes were found to be circulating in Kerala sate of India. Serotypes 1 and 3 were the predominant type (33.3 %) compared to others. The prevalence of co-infection of serotype 1 and 4 was the highest percentage (11.1 %) compared to serotype 2 and serotype 3 (5.5 %). We further highlighted the immunopathological mechanisms of antibody neutralization, CD4+ T cell response and antibody dependent enhancements (ADE) for the possible cause of disease severity in coinfections. Serotype-1 does not show much variations from the previously reported strains from various regions of India. However, serotype-2 showed variations in the sequences from the other strains of serotype-2 previously reported from various regions of India and formed a distinct clade in the genotype-4. Serotype-3 and serotype-4 showed similarity with previously reported strains from India. Moreover, serotype-1 was grouping in genotype-5. Importantly, the serotype-2 grouped with genoptype-4 but exist separately. Serotype-3 was found to be grouped with the genotype-3. The serotype-4 show the very much similarities from the genotype-1 and shows little difference from the previously reported strains from India. Further, mutation in DENV-3 sequences, at position 235 (C to T) and 322 (G to T) shows an important phenomenon which might be adopted by the virus to survive. As severe dengue is linked with the serotype-2, the genetic variations in this serotype points towards the much specific strategy to be adopted in near future to manage the severe dengue disease. In conclusion, we can say that, genetic diversity in the CprM region is present in the different serotypes circulating in the patients from Kerala India and this information may help in the management of dengue viral disease.

immunology↗

bioRxiv2021

Eosinophils restrict diesel exhaust particles induced cell proliferation of lung epithelial A549 cells, vial interleukin-13 mediated mechanisms: implications for tissue remodelling and fibrosis

Diesel exhaust particulates (DEPs) affect lung physiology and cause serious damage to the lungs. A number of studies have demonstrated that eosinophils play a very important role in the development of lung tissue remodelling and fibrosis. However, the exact mechanism of its pathogenesis is not known. We for the first time demonstrate that, Interleukin-13 plays a very important role in the development of tissue remodelling and fibrosis. We demonstrate that, Diesel exhaust particle significantly induce eosinophils cell proliferation and interleukin-13 release in invitro culture conditions. Supernatant collected from DEP induced eosinophils cells significantly restrict cell proliferation of epithelial cells due to exposure of diesel exhast particles. Furthermore, purified interleukin-13 decreases the proliferation of A549 cells. Notably, Etoricoxib (selective COX-2 inhibitor) did not inhibit DEP-triggered release of interleukin-13, suggesting another cell signalling pathway. In, vivo exposer of DEP to the mice lung, resulted in the high level of eosinophils degranulation as depicted by the EPX-1 immunostaining and altered level of mRNA expressions of inflammatory genes. We also found that, a-SMA, fibroblast specific protein (FSP-1) has been changed in response to DEP in the mice lungs along with the mediators of inflammation. Altogether, we elucidated the mechanistic role of eosinophils in the DEP triggered proliferation of lungs cells thus providing an inside in the pathophysiology of tissue remodelling and fibrosis of lungs.

cell biology↗

bioRxiv2020

Proliferation of lung epithelial cells is regulated by the mechanisms of autophagy upon exposure of soots

Soots are known to cause many diseases in humans but their underlying mechanisms of toxicity are still not known. Here, we report that, soots induce cell proliferation of lung epithelial cells via modulating autophagic pathways. Fullerene soot and diesel exhaust particles (DEP) induced cell proliferation of lung epithelial, A549 cells, via distinct autophagic mechanisms and did not cause cell death. Exposure of fullerene soot protected cell death of A549 cells, caused by hydrogen peroxide and inhibited LPS-induced autophagy. Fullerene soot co-localize with the autophagic proteins and inhibited starvation-induced autophagy (downregulated ATG-5, beclin-1, p62 and LC3 expressions) independent of its antioxidant properties. Similarly, it decreased expression profile of autophagic genes and upregulated proliferation responsive gene, Ki-67, in mice. We observed that, expressions of fullerene soot responsive genes (Beclin-1, ATG-5 and p62) were reverted by Akt Inhibitor X, indicating an important role of Akt pathway. On the other hand, DEP up-regulated expressions of autophagy genes. Akt Inhibitor X and Etoricoxib, did not attenuate DEP-induced cell proliferation and autophagic response. However, autophagic inhibiter 3-MA and chloroquine has significantly inhibited DEP-induced cell roliferation. In conclusion, distinct autophagic mechanisms are operational in cell proliferation of lung epithelial cells in response to soots and may have implication in diseases. The proliferation inducing potential of fullerene soot may be utilized as a regenerative agent in autophagy-associated disorders.

cell biology↗