Plant growth-promoting endophytic microbes have drawn the attention of researchers owing to their ability to confer fitness benefits in many plant species. Here, we report agriculturally beneficial traits of rice-leaf-adapted endophytic Microbacterium testaceum. Our polyphasic taxonomic investigations revealed its identity as M. testaceum. The bacterium displayed typical endophytism in rice leaves, indicated by the green fluorescence of GFP-tagged M. testaceum in confocal laser scanning microscopy. Furthermore, the bacterium showed mineral solubilization and production of IAA, ammonia, and hydrolytic enzymes. Tobacco leaf infiltration assay confirmed its non-pathogenic nature on plants. The bacterium showed antifungal activity on Magnaporthe oryzae, as exemplified by secreted and volatile organic metabolome-mediated mycelial growth inhibition. GC-MS analysis of the volatilome of M. testaceum indicated the abundance of antimicrobial compounds. Bacterization of rice seedlings showed phenotypic traits of MAMP-triggered immunity (MTI), over-expression of OsNPR1 and OsCERK, and the consequent blast suppressive activity. Strikingly, M. testaceum induced the transcriptional tradeoff between physiological growth and host defense pathways as indicated by up- and downregulated DEGs. Coupled with its plant probiotic features and the defense elicitation activity, the present study paves the way for developing Microbacterium testaceum-mediated bioformulation for sustainably managing rice blast disease.

Chronic alcohol intake substantially changes host immunity via complex neuro-hepatic-immune interactions, considerably increasing vulnerability to bacterial, viral, and opportunistic diseases. Alcohol causes systemic immunological dysregulation via metabolic, oxidative stress, damage to the intestinal barrier, and hepatic inflammation, all of which weaken the innate and adaptive immunity. In the liver, ethanol is metabolized and generates acetaldehyde and reactive oxygen species (ROS) by alcohol dehydrogenase, CYP2E1, and catalase pathways, resulting in mitochondrial dysfunction, lipid peroxidation, and NAD⁺/NADH imbalance. These metabolic disturbances activate Kupffer cells (KC), cause hepatocyte damage, and impair pathogen clearance, thereby driving the production of pro-inflammatory cytokines (TNF-α, IL-1β, and IL-6). By disrupting the gut microbial ecosystem, alcohol weakens epithelial barrier function, facilitating endotoxemia and subsequent systemic inflammatory responses. Through persistent exposure, alcohol reprograms neuroimmune signaling toward a pro-inflammatory microglial M1 profile via NF-κB and HMGB1–TLR4 activation, compromising synaptic integrity and central immune balance, with systemic inflammation amplified by autonomic nervous system dysfunction and HPA axis dysregulation. The Dysfunction of neutrophils, NK cells, B and T lymphocytes, and complement proteins reduces the host defense while promoting chronic inflammation. Collectively, these processes converge on the gut-liver-brain axis, generating a maladaptive immune landscape marked by paradoxical hyperinflammation and immunodeficiency. In this review, we summarize the molecular and cellular basis of alcohol-induced neuro-hepatic immune dysfunction, which is important for designing specific therapies to decrease infection susceptibility and organ damage.