ABSTRACT
Enterococcus gallinarum and other Enterococcus species commonly inhabit the human gastrointestinal tract. While the pathogenicity of Enterococcus gallinarum remains incompletely understood, its infections are alarmingly severein humans, as evidenced by numerous cases. Formerly, Vancomycin was the preferred drug, but recent findings indicate that clinical isolates of Enterococcus gallinarum are resistant, leading to the emergence of vancomycin-resistant enterococci (VRE) strains. The escalation of drug resistance is often linked to overexpressed virulence factors, some of which are implicated in biofilm formation in Enterococcus infections. Henceforth, this research investigates the potential of phytocompounds to combat E. gallinarum infection, employing both in vitro and in silico methodologies. In vitro techniques were employed to assess the efficacy of various phytocompounds, ultimately identifying 4,5,7-trihydroxyflavanone (THF) as particularly effective in inhibiting microbial growth. THF displayed over 80% antibacterial activity at 200 µg/ml against E. gallinarum. Subsequent qualitative and quantitative hemolysin assays implicated hemolysin as a target of THF. Molecular docking analysis of THF and Hemolysin A revealed a strong binding affinity. Notably, residues Asn18, Asp85, and His199 formed hydrogen bonds, while His22 and His86 were involved in robust π-π stacking and π-cation interactions with THF. Overall, this study highlights THF's potential in combating E. gallinarum infections.Communicated by Ramaswamy H. Sarma.
ABSTRACT
Gene expression is tremendously altered in the brain during memory acquisition, recall, and forgetfulness. However, non-genetic factors, including environmental elements, epigenetic changes, and lifestyle, have grabbed significant attention in recent years regarding the etiology of neurodegenerative diseases (NDD) and age-associated dementia. Epigenetic modifications are essential in regulating gene expression in all living organisms in a DNA sequence-independent manner. The genes implicated in ageing and NDD-related memory disorders are epigenetically regulated by processes such as DNA methylation, histone acetylation as well as messenger RNA editing machinery. The physiological and optimal state of the epigenome, especially within the CNS of humans, plays an intricate role in helping us adjust to the changing environment, and alterations in it cause many brain disorders, but the mechanisms behind it still need to be well understood. When fully understood, these epigenetic landscapes could act as vital targets for pharmacogenetic rescue strategies for treating several diseases, including neurodegeneration- and age-induced dementia. Keeping this objective in mind, this updated review summarises the epigenetic changes associated with age and neurodegeneration-associated dementia.
