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Ageing block > Inflammation and ageing > Flashcards

Inflammation and ageing Flashcards

1
Q

List the pro-ageing factors

A

IL-6
CRP
HSP90
TNF alpha

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2
Q

Which factors determine the extent of immune senescence in ageing?

A
  • Microbiome
  • Epigenetics
  • Genetics
  • Environmental exposure
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3
Q

List the anti-ageing factors

A
  • TGF beta
  • IL-10
  • Cortisol
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4
Q

Outline how ageing affects infection

A 
-Infections occur more frequently 
PRESENTATIONS CHANGE:
-atypical manifestations
-Lack of fever
-Non-specific symptoms (confusion,malaise,fatigue,myalgia)
-Mortality increased
-eg TB reactivation could occur 
-Chronic viral stimulation
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5
Q

Why does infection change with ageing?

A
  • Ab titre declines with age
  • Vaccine responses diminish
  • Comorbidity contributes
  • Malnutrition
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6
Q

Which diseases may reactivate due to ageing

A
  • Shingles

- TB

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7
Q

What is shingles

A
  • Caused by varicella zoster virus
  • virus that causes chicken pox lives dormant in DRG
  • can reactivate at any point in life
  • When it reactivates it causes a rash in a dermatomal distribution and causes a blistering rash
  • Virus controlled by T cells
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8
Q

What is post herpetic neuralgia

A
  • Complication of shingles
  • pain syndrome you can get in the distribution the rash had been present in
  • As time goes on and people get older, the incidence of this increases
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9
Q

Outline the thymic changes with age

A
  • Newborn; thymus=v large

- 70years barely any left; adipose tissue fills perivascular space

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10
Q

Outline the changes in T cells that occurs in the elderly

A
  • Absolute T cell counts fall
  • Naive T cell numbers drop(thymic decline)
  • CD4:CD8 ratio changes (inverses)- normally people have more CD4 cells than CD8 but as people age that changes
  • But peripheral regulatory T cell pool increases
  • NKc numbers remain stable (not in everyone)
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11
Q

outline the presence of herpes virus in ageing

A

CMV (HHV-5):

  • Persistent herpes virus present in 60-90% of adults
  • Asymptomatic in immunocompetent hosts
  • Viral reactivation well described in sepsis
  • CMV positivity associated with premature immunosenescence (suppress T cell repertoire i.e ability to make different types of T cell receptors)
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12
Q

Outline the changes in autoimmunity seen in ageing

A
  • autoimmunity increases with age
  • ageing associates with more autoantibodies but a lower incidence of autoimmune disease
  • Increase in prevalence of: RF, antinuclear antibodies,anti-cardiolipin abs
  • autoimmune diseases are rare: thymic decline in elderly may explain the rarity of T cell mediated autoimmune diseases
  • Peripheral T reg cell pool increases with age
  • The T cell is essential for most autoimmune diseases
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13
Q

Which diseases are exceptions to the decline in appearance of autoimmune diseases in ageing

A
  • Giant cell arteritis
  • Polymyalgia rheumatica
  • You have to be over 50 to be diagnosed with these & these diseases are linked
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14
Q

What are the 2 major systems of tumor suppression

A
  • Production of IFN-gamma and the perforin pathway used by cytotoxic T cells
  • Natural killer cells
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15
Q

Why are autoimmune diseases rare in the elderly?

A
  • Diminished naive T cells (Thymic decline) could be the reason why there is rarity of T cell mediated autoimmune diseases
  • HLA associated eg’s
  • Peripheral Treg cell pool increases with age
  • The T cell is essential for most autoimmune diseases
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16
Q

Why is cortisol known as the ‘death hormone’

A
  • It is the one hormone that increases as we get older
  • Our neurons are extremely sensitive to the effects of cortisol, so when cortisol circulates at a high level, it can cause brain cells to die
17
Q

Outline the role of IL-10 in ageing

A
  • Aging-associated inflammation and increased cytokine responses may be caused by a declining level of IL-10 during aging
  • function of IL-10 =an essential cytokine, mainly produced by macrophages, and is responsible for suppressing proinflammatory response in various tissues, including skeletal muscle
18
Q

Outine the pleiotropic effects of IL-6

A
  • Keratinocyte proliferation
  • B/T cell activation
  • Hepatocyte activate
  • Haematopoetic stem cell (HPC) drive
  • Mesangial cell proliferation
  • Angiogenesis

(Seems to be a cardinal cytokine in the development of giant cell arteritis)

Note-increases in ageing

19
Q

Explain the increased cancer risk seen in ageing

A
  • Environmental exposures( toxins,sunlight,diet)
  • Genetic alterations (especially epigenetic-DNA methylation)
  • Declining immune surveillance
20
Q

What is a challenge to the immune senescence theory regarding cancer

A

-Risk of breast cancer declines in women>80

21
Q

What trends in T cells are likely to impact response to tumourigenesis?

A
  • Reduced naive T cell numbers
  • Altered T cell sub-populations
  • Diminished TCR repertoire

Ageing block (16 decks)

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