Lipopolysaccharide structures of Gram-negative populations in the gut microbiota and effects on host interactions

Monocyte reconstitution and gut microbiota composition after hematopoietic stem cell transplantation

“…The myeloablation associated with HCT provides a unique platform for exploring the nascent, re-development of immune reconstitution. Prior studies have supported the symbiotic relationship between the gut microbiota and the systemic immune system [59, 60], but most prior work has focused on the role the microbiota has on shaping different populations of T cells [30-32]; little is known about the impact intestinal commensalism has on monocyte maturation. We followed a systematic strategy to identify three subsets of monocytes (classical, intermediate, and non-classical monocytes) [10] during immune reconstitution post-HCT to assess whether constituents of the microbiota affect monocyte recovery.…”

“…Monocyte migration out of the bone marrow and into the blood circulation is driven by low level lipopolysacharide (LPS)-mediated signaling [30]. Further, basal circulating LPS levels derived from the intestinal microbiota have been detected in immunocompromised hosts [31, 32]. Therefore, we hypothesized that microbial communities of gram-negative bacteria through the production of LPS [33, 34] and commensal obligate anaerobes [35] influence monocyte maturation post-HCT.…”

Microbiota changes and intestinal microbiota transplantation in liver diseases and cirrhosis

“…These are most often components of Enterobacteriaceae, which are the major causative organisms in the pathogenesis of SBP and express a potently immunostimulatory endotoxin. 44,45 Taxa of oral origin, especially those belonging to Streptococcaceae and Porphyromonadaceae, increase in relative abundance with advancing cirrhosis and can be modulated by oral health and the use of proton pump inhibitors (PPIs). [46][47][48] Bacterial taxa that are usually lacking in cirrhosis belong to Firmicutes, specifically Lachnospiraceae and Ruminococcaceae families.…”

Gastrointestinal (GI) Tract Microbiome-Derived Neurotoxins—Potent Neuro-Inflammatory Signals From the GI Tract via the Systemic Circulation Into the Brain

“…Because of aging, traumatic brain injury (TBI), cerebrovascular deficits (some of which may be genetic), neurovascular pathology or neuroinflammatory brain degeneration, neurotoxic molecules can "leak" into the systemic circulation, prompting some investigators to propose that progressive neurodegenerative diseases such as AD supplied via the reflect a malfunction of key biophysical barriers including those of the GI-tract and BBB, and that AD is in fact a "defective barrier" disease (Bhattacharjee and Lukiw, 2013;Montagne et al, 2017;Sweeney et al, 2018Sweeney et al, , 2019Erdo and Krajcsi, 2019). The abundance of blood-borne bacterial components including LPS, for example, represents a variable component of the human blood serum that can elicit variable systemic pro-inflammatory and innate-immunemodulatory responses in the host, resulting in systemic-immune activation by pathogen-associated molecular patterns (PAMPs), a process sometimes referred to as "microbial translocation" (Zhao et al, 2017a,b;Tulkens et al, 2018;Di Lorenzo et al, 2019;Logsdon et al, 2018;Patrick et al, 2019). Multiple recent reports further suggest that GI-tract dysbiosis and "leaky gut syndrome" constitute a vastly under-appreciated, under-studied and critical pathophysiological passageway for transport of GI-tract microbiome-derived neurotoxins across GI-tract and blood-brain biological barriers resulting in an age-related progression from systemic inflammation to neurovascular disease to CNS inflammation and degeneration that progressively contribute to critical aspects of neuropathology associated with age-related neurodegenerative disorders.…”

“…Multiple recent reports further suggest that GI-tract dysbiosis and "leaky gut syndrome" constitute a vastly under-appreciated, under-studied and critical pathophysiological passageway for transport of GI-tract microbiome-derived neurotoxins across GI-tract and blood-brain biological barriers resulting in an age-related progression from systemic inflammation to neurovascular disease to CNS inflammation and degeneration that progressively contribute to critical aspects of neuropathology associated with age-related neurodegenerative disorders. These include neuropathological disorders such as AD, anxiety, autism spectrum disorder (ASD), depression, epilepsy, multiple sclerosis, Parkinson's disease (PD), prion disease, systemic inflammatory response syndrome, and other incapacitating and/or ultimately lethal neurological diseases of the human CNS (Hill et al, 2014a,b;Köhler et al, 2016;Li and Yu, 2017;Varatharaj and Galea, 2017;Zhao et al, 2017aZhao et al, ,b, 2019Griffiths and Mazmanian, 2018;Di Lorenzo et al, 2019;Fox et al, 2019;Patrick et al, 2019;Sarkar and Banerjee, 2019).…”