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Jain, Neha
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Preferred name
Jain, Neha
Alternative Name
Jain, N.
Main Affiliation
Scopus Author ID
36548235800
Researcher ID
JAU-0383-2023
Now showing 1 - 3 of 3
- PublicationA Strategy to Combat Bacterial Biofilms Mediated by Plant-Derived Carbon Dots: A Green Shield for Clean Water(2024)
;Sarmistha Mazumder ;Harshita Agarwal; Biofilms in water distribution systems are complex and tenacious populations of microbes surrounded by a protective matrix that may lead to significant water-borne diseases due to contamination and compromised quality of water. To tackle this issue, several small-molecule-based antimicrobials and engineered nanomaterials were developed that show much promise in combating biofilms. Herein, organic carbon dots (LC-CDs) were successfully synthesized from Lantana camara leaf extract, which is an invasive plant, using a one-pot hydrothermal method, requiring no chemical modifications. These LC-CDs were found to be less toxic and exhibited antibacterial and antibiofilm properties, indicating their potential use to combat biofilms. While natural carbon dots have been extensively studied for bioimaging, their antibiofilm activity has not been widely explored. Our study explores the antibacterial activity of naturally derived carbon dots through the generation of reactive oxygen species, thereby expanding the industrial prospects of this system as an antibacterial and antibiofilm agent. The LC-CDs may serve as antibacterial and antibiofilm agents to facilitate clean water production. - PublicationThe molecular interplay between human and bacterial amyloids: Implications in neurodegenerative diseases(2024-07-01)Neurodegenerative disorders such as Parkinson's (PD) and Alzheimer's diseases (AD) are linked with the assembly and accumulation of proteins into structured scaffold called amyloids. These diseases pose significant challenges due to their complex and multifaceted nature. While the primary focus has been on endogenous amyloids, recent evidence suggests that bacterial amyloids may contribute to the development and exacerbation of such disorders. The gut-brain axis is emerging as a communication pathway between bacterial and human amyloids. This review delves into the novel role and potential mechanism of bacterial amyloids in modulating human amyloid formation and the progression of AD and PD.
- PublicationThe menace within: bacterial amyloids as a trigger for autoimmune and neurodegenerative diseases(2024)
;Molly Elkins; Çagla TükelBacteria are known to produce amyloids, proteins characterized by a conserved cross-beta sheet structure, which exhibit structural and functional similarities to human amyloids. The deposition of human amyloids into fibrillar plaques within organs is closely linked to several debilitating human diseases, including Alzheimer's and Parkinson's disease. Recently, bacterial amyloids have garnered significant attention as potential initiators of human amyloid-associated diseases as well as autoimmune diseases. This review aims to explore how bacterial amyloid, particularly curli found in gut biofilms, can act as a trigger for neurodegenerative and autoimmune diseases. We will elucidate three primary mechanisms through which bacterial amyloids exert their influence: 1. Direct interaction with human amyloids: Bacterial amyloids can directly interact with human amyloids, potentially accelerating the aggregation and deposition of amyloid fibrils associated with diseases such as Alzheimer's and Parkinson's disease. This direct interaction may contribute to the pathological progression of these conditions. 2. Induction of inflammation: Bacterial amyloids have the capacity to induce inflammatory responses within the host organism. Chronic inflammation is increasingly recognized as a contributor to neurodegenerative and autoimmune diseases. We will explore how the activation of inflammatory pathways and neuroinflammation by bacterial amyloids can exacerbate disease pathogenesis. 3. Acting as a DNA carrier: Bacterial amyloids may also serve as carriers of DNA, facilitating the activation of host DNA sensors. This mechanism can potentially lead to alterations in the host's immune response and also contribute to the development of autoantibodies. By delving into these three distinct modes of action, this review will provide valuable insights into the intricate relationship between bacterial amyloids and the onset or progression of neurodegenerative and autoimmune diseases. A comprehensive understanding of these mechanisms may open new avenues for therapeutic interventions and preventive strategies targeting amyloid-associated diseases.