Year: 2022

THREAT ASSESSMENT. "Multicellular organisms have evolved highly sophisticated mechanisms to detect the presence of pathogens (or injurious agents) and activate the proper defense processes. Not all foreign microorganisms that multicellular organisms come in contact with are necessarily harmful; thus a complex mechanism of recognition of microbes as well as of their “dangerousness” had to be developed during evolution." https://lnkd.in/eNNPn5D View in LinkedIn

DANGER SENTINEL. "Traditionally, innate immunity has been viewed as the first line of defense discriminating “self” (e.g., host proteins) from “nonself” (e.g., microorganisms). However, emerging literature suggests that innate immunity actually serves as a sophisticated system for sensing signals of “danger,” such as pathogenic microbes or host-derived signals of cellular stress, while remaining unresponsive to nondangerous motifs, such as normal host molecules, dietary antigens, or commensal gut flora." https://lnkd.in/e4CzrPZ View in LinkedIn

"THE INNATE IMMUNE SYSTEM engages an array of germline-encoded pattern-recognition receptors (PRRs) to detect invariant microbial motifs. PRRs are expressed by cells at the front line of defense against infection, including macrophages, monocytes, dendritic cells, neutrophils, and epithelial cells, as well as cells of the adaptive immune system. PRRs include the membrane-bound Toll-like receptors (TLRs) and C-type lectins (CTLs), which scan the extracellular milieu and endosomal compartments for pathogen-associated molecular patterns (PAMPs)." http://www.sciencedirect.com/science/article/pii/S0092867410000759 View in LinkedIn

VIRAL CONTRIBUTION. "The bottom line is that many major diseases that have been associated with inflammation—including cardiovascular disease, neurodegeneration, allergic diseases, cancer, and autoimmunity—occur in persons that are chronically infected by viruses." http://www.sciencedirect.com/science/article/pii/S0092867409007831 View in LinkedIn

SLEEPERS. "These new data suggest that we should consider that many or all humans are genetically “immunocompromised” to a greater or lesser extent for specific infections, including infection by viruses that constitute our virome. Thus, a virus present in all of us may cause disease only in those unfortunate enough to have a specific constellation of genes." http://www.sciencedirect.com/science/article/pii/S0092867409007831 View in LinkedIn

DANGEROUS REMEDY. "Inflammation is the most important host response to any agent that threatens internal homeostasis. The weaponry that can be mobilized is ample and potentially very dangerous for the host itself, therefore the ignition phase of inflammation must be accurately controlled." https://lnkd.in/eNNPn5D View in LinkedIn

FIRST LINE. "Inflammation is the key pathophysiological response triggered by noxious agents in multicellular organisms. Virtually no perturbation in body homeostasis can occur without generating a local or systemic inflammatory response. Inflammation is intimately intertwined with innate and adaptive immunity and therefore deeply involved in the pathogenesis of immune-mediated diseases." https://lnkd.in/eNNPn5D View in LinkedIn

NUMEROUS TRIGGERS. "It is well known that inflammation can be started by a multiplicity of causes: microorganisms and viruses, trauma, cancer, foreign particles, ischemia, exposure to radiations, metabolic disorders, and many more. The common feature of all causes of inflammation is cell or tissue damage." https://lnkd.in/eNNPn5D View in LinkedIn

"INFLAMMATION is based on the efficient cooperation between signals, sensors, and effector systems." https://lnkd.in/eNNPn5D View in LinkedIn

"THE INFLAMMASOME resides within the cytoplasm, therefore we can reasonably assume that it is perfectly equipped to sense intracellular pathogens with cytoplasmic location, but it is also clear that it needs a system of communication (extracellular sensor, intracellular messengers) that convey alarm signals delivered by extracellular PAMPs/MAMPs or DAMPs." https://lnkd.in/eNNPn5D View in LinkedIn