The importance of different arsenic forms in public health is well recognized owing to its distinct physical characteristics and toxicity. Chronic arsenic exposure has left a trail of disastrous health consequences around the world. However, the mechanisms behind the toxicity and the consequential diseases occurring after acute or chronic exposure to arsenic are not well understood. The toxicity of trivalent arsenic primarily occurs due to its interaction with cysteine residues in proteins. Arsenic binding to protein may alter its conformation and interaction with other functional proteins leading to tissue damage. Therefore, there has been much emphasis on studies of arsenic-bound proteins, for the purpose of understanding the origins of toxicity and to explore therapeutics. This book chapter illustrates the molecular mechanisms of arsenic toxicity with a special emphasis on arsenic binding to proteins and its consequences in alteration of tissue homeostasis.
Part of the book: Arsenic
Meningoencephalomyelitis emanates under the umbrella relating inflammatory changes of the Central Nervous System (CNS). Meningitis denotes inflammation in the meningeal layers, encephalitis is an acute diffuse inflammation of the brain, and inflammation in the spinal cord is denoted as myelitis. These can be interrelated or independent of each other depending on the etiology. The entire mechanism of meningoencephalomyelitis is governed by an acute innate inflammatory branch followed by a chronic progressive, adaptive branch of immunity with clinical signs like hyperthermia, weight loss, hypoxia, leukocytosis. This book chapter will focus on viral-induced meningitis, encephalitis, and myelitis. Thirty years of experience working with a murine-β-coronavirus (m-CoV); Mouse hepatitis virus (MHV)-A59 induced experimental model system provided us a thorough understanding of neuroglial cell-mediated acute neuroinflammation, denoted by the accumulation of leukocyte-common-antigen (LCA) positive or CD45+ leukocytes in perivascular infiltrates referred to as perivascular cuff formation and microglial nodules in the brain parenchyma, which mimics specific pathology of human neurological disease multiple sclerosis (MS). Additionally, in this chapter, we summarized the role of CNS resident microglial activation and its interaction with peripheral migratory T cells in mounting neuropathogenesis and host immunity in different families of neurotrophic encephalomyelitis viruses that cause CNS inflammation.
Part of the book: RNA Viruses Infection
Murine models are widely used in scientific research because they share many genetic similarities with humans, making them a valuable tool for studying various diseases. C57BL/6 is an experimental mouse model to study the demyelination and inflammation aetiology of multiple sclerosis (MS). Intracranial inoculation of neurotropic murine β-coronavirus strain of mouse hepatitis virus in C57BL/6 mice induces demyelination with or without axonal loss, providing many insights regarding the mechanism of MS as well as SARS-CoV-2-mediated pulmonary and neuropathology in humans. By selectively using knockout mice in the wild-type C57BL/6 background, researchers can gain insights into the immunomodulatory nexus and can identify pathways involved in immune regulation which further can be efficiently studied with CD4−/−, CD40−/−, and CD40L−/− mice. In addition, C57BL/6 mice can also be used to generate syngeneic mouse models to investigate the aetiology and mechanism of various cancers, including ovarian cancer. Similarly, along with C57BL/6 mice, different immunocompromised mice models, such as nude mice, SCID mice, and NOD/SCID mice, can be used to study the aetiology, host-tumour interaction, function of the microenvironment, and tumour heterogeneity in tumour metastasis.
Part of the book: Rodents and Their Role in Ecology, Medicine and Agriculture