Discover and read the best of Twitter Threads about #Inflammasome
Most recents (6)
9) Many risk factors modulate the propensity of LDL-C to traverse the endothelium and enter the arterial intima. See 🔓academic.oup.com/eurheartj/arti…. 
10) It now appears that the passage of #LDL into the #intima is not a merely passive process whereby the concentration in blood & the permeability of the endothelium determine LDL accumulation.
11) It’s #Transcytosis (an active process), through a vesicular pathway involving #caveolae, scavenger receptors (#SRB1) and activin like receptor kinase 1 (#ALK1). Hence for a given blood level of LDL-C the amount of atherosclerosis is variable.
#BHB inhibits #inflammasome activation to attenuate #Alzheimer’s disease #pathology | Journal of #Neuroinflammation |
“Here, we find BHB levels are lower in red blood cells and brain parenchyma of AD patients when compared with non-AD controls... jneuroinflammation.biomedcentral.com/articles/10.11…
“Here, we find BHB levels are lower in red blood cells and brain parenchyma of AD patients when compared with non-AD controls... jneuroinflammation.biomedcentral.com/articles/10.11…
...Furthermore, exogenous BHB administration reduced plaque formation, microgliosis, apoptosis-associated speck-like protein containing a caspase recruitment domain (Asc) speck formation, and caspase-1 activation in the 5XFAD mouse model of AD.”
“Taken together, our findings demonstrate that BHB reduces AD pathology by inhibiting NLRP3 inflammasome activation. Additionally, our data suggest dietary or pharmacological approaches to increase BHB levels as promising therapeutic strategies”
Very excited to share this work by the heroic team - @carolilucas Pat Wong @sneakyvirus @tiago21bio et al on “Longitudinal analyses reveal immunological misfiring in severe COVID-19”. A thread on our findings. #COVID19 #Pathogenesis (1/n)
nature.com/articles/s4158…
nature.com/articles/s4158…
In this study, we enrolled COVID+ patients and analyzed their immune responses and viral load over the course of their hospital stay. We also compared samples from COVID- healthy health care workers (HCWs) as comparison. (2/n)
As reported by others, we found that COVID patients with severe disease have low T cell numbers and increased monocytes and neutrophils. We also found eosinophils come up in patients. This is bizarre 🧐 (3/n)
As the elderly are more susceptible to #COVID19 w/ signs of lung #inflammation, here's a thread about our @virusesimmunity 2016 flu paper on #antiviral resistance, excessive lung #inflammation, & a strategy to boost disease tolerance! science.sciencemag.org/content/352/62…
First we demonstrated that monos & macs from older adults have impaired type I IFN (antiviral) & #ISG responses but intact cytokine responses after #flu infection. To probe the possible in vivo consequences of weak #IFN responses in the face of robust inflammation...
... we made a mouse model that mimicked this immune response in the elderly (Mx1+/+ mice w/ genetic deletion of tlr7, mavs). Failure to induce type I IFN led to high viral titer, 2º bacterial infection, severe lung inflammation, and death.
Platelets are sufficient to drive inflammasome up regulation and activation in myeloid cells, and are *necessary* for full IL-1 production biorxiv.org/content/10.110…. Another great platelet immunology preprint! @bernardo647 #Immunology #Platelets #Inflammasome
Looking at malaria patients with thrombocytopenia shows decreased circulating IL-1 inversely correlating with platelet, but not total leukocyte, numbers, and depletion during PBMC prep almost eliminated IL-1 (and TNF) production in response to LPS!
This preprint also has very thorough evidence that platelets *do not* express inflammasomes or meaningfully contribute IL-1/18, and an exhaustive list of all the ways that platelets *don’t* stimulate myeloid inflammasome activation. Super solid work!
Extracellular acidity in atherosclerosis is one of my favorite topics, so I'm really, really excited about this study (2/15)
The authors show that some individuals have carotid atherosclerotic lesions that have an acidic pH. They show this is due to activation of Na+-H+ exchanger in macrophages, which leads to extrusion of H+ and extracellular acidification (3/15)
rdcu.be/bRXph
rdcu.be/bRXph
