Prealighting and Postalighting Volatile Organic Compounds Emitted by Rice Influence the Behavior of .

Yellow stem borer (YSB), , is a major rice pest causing significant yield losses worldwide. We investigated how volatile organic compounds (VOCs) released by the rice variety TN1, both before and after infestation, as well as by its companion weeds, and , influence the behavior of YSB in host selection, recognition, and establishment. Olfactometry bioassays showed that uninfested TN1 plant VOCs attracted YSB more than those from YSB-infested rice plants and weeds.

Regulation of neuroinflammation in Alzheimer's disease via nanoparticle-loaded phytocompounds with anti-inflammatory and autophagy-inducing properties.

Background: Alzheimer's disease (AD) is characterized by neuroinflammation linked to amyloid β (Aβ) aggregation and phosphorylated tau (τ) protein in neurofibrillary tangles (NFTs). Key elements in Aβ production and NFT assembly, like γ-secretase and p38 mitogen-activated protein kinase (p38MAPK), contribute to neuroinflammation. In addition, impaired proteosomal and autophagic pathways increase Aβ and τ aggregation, leading to neuronal damage.

An Immunoinformatics-Based Study of Mycobacterium tuberculosis Region of Difference-2 Uncharacterized Protein (Rv1987) as a Potential Subunit Vaccine Candidate for Preliminary Ex Vivo Analysis.

Mycobacterium tuberculosis (Mtb) is the pathogen that causes tuberculosis and develops resistance to many of the existing drugs. The sole licensed TB vaccine, BCG, is unable to provide a comprehensive defense. So, it is crucial to maintain the immunological response to eliminate tuberculosis.

Epigenetic orchestration of host immune defences by Mycobacterium tuberculosis.

Being among the top 10 causes of adult deaths, tuberculosis (TB) disease is considered a major global public health concern to address. The human tuberculosis pathogen, Mycobacterium tuberculosis (Mtb), is an extremely competent and well-versed pathogen that promotes pathogenesis by evading the host immune systems through numerous tactics. Investigations revealed that Mtb could evade the host defense mechanisms by reconfiguring the host gene transcription and causing epigenetic changes.

Host-mycobacteria conflict: Immune responses of the host vs. the mycobacteria TLR2 and TLR4 ligands and concomitant host-directed therapy.

Tuberculosis (TB), caused by Mycobacterium tuberculosis (Mtb), is one of the most grievous infectious diseases with long-term morbidity and unpredicted mortality rates globally. Thus, understanding the host-pathogen interactions to develop potential drugs is the most focused area of research. Mtb has many antigens communicating with host cells via various pattern recognition receptors (PRRs).

Acetyltransferase Suppresses Oxidative Stress by Inducing Peroxisome Formation in Macrophages.

() inhibits host oxidative stress responses facilitating its survival in macrophages; however, the underlying molecular mechanisms are poorly understood. Here, we identified a acetyltransferase (Rv3034c) as a novel counter actor of macrophage oxidative stress responses by inducing peroxisome formation. An inducible deletion mutant of failed to induce peroxisome biogenesis, expression of the peroxisomal β-oxidation pathway intermediates (ACOX1, ACAA1, MFP2) in macrophages, resulting in reduced intracellular survival compared to the parental strain.

Computational discovery and ex-vivo validation study of novel antigenic vaccine candidates against tuberculosis.

Tuberculosis (TB) is a complex infectious bacterial disease, which has evolved with highly successful mechanisms to interfere with host defenses and existing classes of antibiotics to resist eradication. The single obtainable TB vaccine, Bacille Calmette-Guerin (BCG) has failed to provide regular defense for respiratory TB in adults. In this study, a bioinformatics and immunoinformatics approach was applied on Mycobacterium tuberculosis (Mtb) H37Rv proteomes to discover the potential subunit vaccine candidates that elicit both tuberculosis-specific T-cells and B-cell immune response.

Identification and evaluation of immunogenic MHC-I and MHC-II binding peptides from Mycobacterium tuberculosis.

Due to several limitations of the only available BCG vaccine, to generate adequate protective immune responses, it is important to develop potent and cost-effective vaccines against tuberculosis (TB). In this study, we have used an immune-informatics approach to identify potential peptide based vaccine targets against TB. The proteome of Mycobacterium tuberculosis (Mtb), the causative agent of TB, was analyzed for secretory or surface localized antigenic proteins as potential vaccine candidates.

Mycobacterium tuberculosis EsxL induces TNF-α secretion through activation of TLR2 dependent MAPK and NF-κB pathways.

Mycobacterium tuberculosis (Mtb) employs distinct strategies to circumvent host immune responses during the infection process. Various Mtb cell-wall associated and secretory proteins are known to play a critical role in the orchestration of host innate immune responses through modulation of signaling pathways. Mtb genome encodes for 23 (EsxA-EsxW) proteins belonging to the ESAT-6 like family; however, most of them are functionally unknown.

Mycobacterium tuberculosis Rv3034c regulates mTORC1 and PPAR-γ dependant pexophagy mechanism to control redox levels in macrophages.

Mycobacterium tuberculosis survives inside the macrophages by employing several host immune evasion strategies. Here, we reported a novel mechanism in which M. tuberculosis acetyltransferase, encoded by Rv3034c, induces peroxisome homeostasis to regulate host oxidative stress levels to facilitate intracellular mycobacterial infection.