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Flashcards

Inflammation and aging

Andrea B Science 1 English 67 cards

Cards in this deck (67)

  1. 1a biological process in response to any insult/injury, destroys and removes microbial pathogens, dead cells, & damaged tissue (tissue remodeling and repair)Inflammation
  2. 2short duration (minutes to a few daysAcute
  3. 3-longer duration (wks-months-yrs) -persistence of causative stimulus -adaptive immune response -presence of lymphocytes & macrophagesChronic
  4. 4multiple cell types cytokine release in response to general antigensinnate response
  5. 5T cell and B cells bearing specific TCRs and BCRs to specific antigensadaptive response
  6. 6key points of inflammation-everyone experience
    -need to survive
    -healing & in self repair is the first step
  7. 7chronic inflammation is-sign something gone seriously wrong
    -breaks down protective mechanisms(make older and frail)
    -results in disease and illness
  8. 8natural, but not uniform, phenomenon involved in decline in performance, productivity and health (culminating in death with passage of time)Aging
  9. 9biological timeline -mitochondrial aging -oxidative damage -telomeres -genetic alterations with aging (genes switching on and off)Programmed cell death theories
  10. 10changes in hormones that control agingEndocrine theory
  11. 11The immune system declines resulting in increase susceptibility to diseasesimmunological theory
  12. 12trophic factors (decreased)DNA,protein, and membrane damage
  13. 13mitochondrial impairmentless energy-cells do not have the energy they need to do what they need to do
  14. 14aging is accompanied by the development of low-grade systemic inflammation, researchers coined the phraseInflammaging
  15. 15Inflammaging is characterized by?Increase in:
    Serum C-reactive protein (CRP)
    IL-6 (can be pro and anti inflammatory)
    TNF-alpha
  16. 1610 year follow up of study -increase pro-inflammatory factors -decrease in anti-inflammatory factorsInflammatory markers in population studies of aging
  17. 17the immune system is in a more activated state in older ___ compared to older___older women compared to older men
  18. 181-damaged macromolecules and cells (self-debris) 2-host-pathogen balance 3-cellular senescence 4-increasing activation of the coagulation system w/ age 5-defective or inappro. regulation of complement pathwy. 6.dietary habitSources of inflammaging
  19. 19increased production and/or inadequate elimination -can mimic bacterial products -function as endogenous "damage"-associated molecular patterns (activate innate imm.)damaged macromolecules and cells (self-debris)
  20. 20-produce harmful products -bacterial flora itself might change with agehost-pathogen balance
  21. 21senescence is a protective response to damage & stress (cell cycle is arrested) -persistent senescent cells are also thought to drive aging and age associated pathologies though their secretory phenotype (SASP)Cellular senescence
  22. 22higher incidence of arterial and venous thrombosisIncreasing activation of the coagulation system with age
  23. 23age related macular degenerationdefective or inappropriate regulation of the complement pathway
  24. 24diet dependent obesity (greater inflammation and cell infiltration) more detrimental than age dependent obesity? (fatty meats promotes inflammatory response)Dietary Habit
  25. 25source of inflammaginginflammaging is not driven by cytomegalovirus infection (CMV)
  26. 26cells stop cycling to prevent proliferation of DNA damage e.g. due to telomere shorting or other damagesenescence
  27. 27ATM &ATR CDK p21 & p16 RbDNA damage checkpoint
  28. 28ataxia telangiectasia mutatedATM &ATR (ATM and Rad3 related)
  29. 29CDKcyclin dependent kinase
  30. 30p21 & p16CDK inhibitors
  31. 31Rbretinoblastoma protein
  32. 32chromatin remodelingnuclear lamina protein lamin B1>SASP inflammatory cytokines, growth factors
  33. 33autophagya lysomal degradation pathway for remodeling aberrant and dysfunctional molecules that declines with age
    -has been implicated in SASP production via target of rapamycin (TOR) autophagy
    -inhibition of autophagy promotes senescence
  34. 34inhibition of autophagy by transcription factor GATA4 (increase SASPs)required for senescence
  35. 35Inhibit autophagy allinhibit senescence all together
  36. 36GATA4DDR (DNA damage response) activated p21/p16 independent key switch of senescene that promotes SASP (p21,16 don't promote it while NFkB and p38 do)
  37. 37mitochondriapowerhouses of cells-they have their own DNA and their repair is not as effective as DNA repair in the nucleus and can cause problems over time (phosphorylation of DDR and mTOR causing ROS and production of DDR)
  38. 38SAMR1decrease in mitochondrial DNA repair enzyme-decrease in APE1 promote senescence
  39. 39activates PGC-1b and therefore potentiates mitochondrial biogenesis, but does not promote senescence but instead inhibits it by inhibiting p53Silent information regulator -1 (SIRT1)
  40. 40SIRT1 expression_____ with aging (so does SAMP8)decreases
  41. 41SIRTs-regulate autophagy
    -can be potentiated by resveratrol or CR (explains the benefits & extend life span- restore mitochond. function,delay senescence, inhibit apoptosis & inflammation)
  42. 42Senescence: good-prevents replication of DNA Damage
    -involved in development
    -involved in remodeling/repair adult tissue
    -programmed process?
    -removal of cells
  43. 43senescence: Bad-reduces pool of replicating cells
    -long term production of destructive SASP
    -unprogrammed process? ((not due to DDR-unprogrammed when it causes problems)
    -slow build up of senescent cells
  44. 44chronic inflammation (age related diseases)-neurodegenerative diseases (neuroinflam. pathological feature of ALS)
    -metabolic diseases
    -cardiovascular diseases
    -cancer
    -musculoskeletal
  45. 45-decrease size of thymus -deregulation of native T cell homeostasis -decrease FGF21 expression (its expression delays thymus decrease) -drop in CD8T cellsImmunosenescence
  46. 46Immunoregulation in aging-reduced adaptive immune function
    -reduction in T &B cells
    -impaired antigen presentation
    -increase cells that suppress immune system
  47. 47reduction in the number of lymphocytes (T&Bcells) naiive T cells-lower production of antibody
    -impaired ability to clear viral and bac. infection
    -lower proliferation following stimulation with the T cell mitogen ConA
  48. 48-most notably affecting sex steroid hormone production -decrease levels of hormones & increase inflammation -GH (enhance proliferation) ,DHEA(reduce inflam. cytokine) , DHEAS decrease -endocrinosenescence
  49. 49Hormones that decrease with aging-testosterone
    -estrogen
    -aldosterone
    -growth hormone
  50. 50hormones that may increase with ageFSH & LH
  51. 51hormones that remain unchanged or only slightly decreased-cortisol
    -epinephrine
    -insulin
    -thyroid hormones T3 & 4
  52. 52with age enhanced presence of innate immune cells and cytokinesautoimmune phenomena-acceleration of atherosclerosis
  53. 53Proinflammatory factors (destruction)increase with age:
    -IL-2, IFN-y,TNF-B
  54. 54Anti-inflammatory factors (protection)decrease with age:
    -IL-4,IL-6(pro-chronic/anti-acute), IL-10
  55. 55age related changes in glial cellsdon't increase in number but increase in reactive glia
  56. 56HMGB1priming of microglia (sometime be good) but increase with age
  57. 57d-enlargement of the cell
    -loss of fine branches
    -formation of cytoplasmic spheroids
    -fragmentation of the cytoplasm
    -mutation of mitochondria
    -accummulation of lipofuscin
  58. 58microglia with age1-shifts towards more activated
    2-hyper-responsive to LPS activation
    3-increase in expression of inflammatory markers
    4-functional impairment
  59. 59reduction of that enhance microglia-CX3CR1 (fractakline) with age (deactivate microglia)
    -expression of CD200R (on microglia surface-MHC2 expression)
  60. 60Age related changes in astrocytes-increase levels of GFAP & vimentin
    -expression of several cytokines
    -changes in nuclei & lipofuscin accumulation
    (may increase permeability of the BBB)
  61. 61people that live over 100 have good function of their ______ which could be a factor in agingneutrophils
  62. 62NK cells and dendritic cells-no consistent change less cytotoxicity
    -decrease stimulation of T cells
  63. 63changes in glucocorticoid receptor expression on astrocytes in hippocampus of older ratsAnti-inflammatory feedback is impaired in aged brain
  64. 64factors of old systemic environmentdecrease neurogenesis and impaired learning & memory
  65. 65TNF reducedin study total neurotic length, axonal length, number of branch points
  66. 66Neuroinflammationinhibits neurogenesis and inflammatory blockade-restores neurogen.
  67. 67neutrophil & macrophagesnumbers don't decrease with age
    -neutrophils become less active and macrophages become more active

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1 Science Flashcards on Inflammation and aging, created by Andrea B on 20/09/2016.
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Andrea B
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