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Lecture 12- acute and chronic inflammation

Lecture notes on mechanisms of acute and chronic inflammation
Module

Pathophysiology 

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Academic year: 2023/2024
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Bournemouth University

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Lecture 12: Acute and Chronic

Inflammation

Inflammation

Reaction of tissue to cell injury or death.

 Can be external or internal  Often named as organ/tissue ‘itis’= pancreatitis  5 signs: o calor (heat) o dolor (pain) o rubor (redness) o tumor (swelling) o loss of function

Positives Negatives

Helps clear infection Causes long term pain and loss of function Prevents spread of infection Scarring Helps activate immune memory May predispose to autoimmunity

Inflammation can be a sign of an effective vaccination Can lead to cancer

Promotes wound healing Dysregulates immunity

Inflammation Can Be Acute & Chronic

Strong acute or chronic infection can lead to pathophysiological conditions.

Feature Acute Chronic

Onset Fast: minutes to hours. Innate immune system

Slow: days. Adaptive immune system. Duration Hours to days Weeks, months, years

Cellular infiltrate Mainly neutrophils then macrophages Macrophages, plasma cells, lymphocytes

Vascular changes Prominent (vasodilation- increased permeability) Not prominent; angiogenesis

Tissue injury Self-limited Progressive

Fibrosis Mild Severe Local and systemic signs Prominent Less

Mechanisms of Acute Inflammation

Vascular response= vasculature alters to enable cells to access sites of inflammation.

Cellular response= key white blood cells are mobilised to the site

<aside> 🐀 In acute inflammation the neutrophils act first then macrophages/monocytes, both are involved with phagocytosis.

</aside>

Key cell types in inflammation:

Vascular Stage

Vessels vasodilate...

 heat (calor) and redness (rubor)  Due to chemicals like histamine which dilate arterioles and capillaries

Vessels become permeable...

 Endothelial cells contract [due to histamine and leukotrienes effects]  In some cases, direct damage can increase permeability  Proteins leak into the tissue (exudate) which can contribute to excess fluid in the tissues (oedema)  Cause swelling (tumour) and pain

Cellular Stage

Extravasation/diapedesis= movement of white blood cells in tissue (look in image 2)

Phagocytes= cells capable of absorbing bacteria, apoptotic bodies, etc.

Leucocyte Diapedesis

  1. Rolling
  2. Adhesion

 Vasodilation (smooth muscle contraction)  Increased vascular permeability  Endothelial activation

Mast Cells

Mast cells produce histamine.

 Abundant at potential entry site for pathogens  Activate in allergic individuals within seconds of exposure  Responsible for many allergies and anaphylaxis

Other Mediators of Inflammation

  1. The eicosanoids

A group of membrane derived products called the eicosanoids are produced by leucocytes in inflammation

<aside> 🐀 Eicosanoids are derived from the cell membrane and are the target for drugs like steroids, COX-1, COX-2 and aspirin.

</aside>

Look at diagram:

  1. The cytokines

Cytokine Source Main functions

TNF-a Macrophages, mast cells

Fever, weight loss (cachexia), inflammation, necrosis of some tumours, expression of adhesion molecules, activates neutrophils

IL-

Macrophages, endothelial cells

Fever, induce acute phase proteins, expression of adhesion molecules, activate macrophages, haematopoiesis (new cells)

IL- Macrophages, some tumour cells

Fever, induce acute phase proteins, haematopoiesis, matures B cells

These are all pyrogens...

Pyrogens and Pyrexia

Pyrexia= fever, rise in body temp of

 oral >37 degrees  rectal >37 degrees

Pyrexia is caused by pyrogens.

Bacterial pyrogens include:

 Lipopolysaccharide (LPS)- endotoxin  Enzymes (exfoliative A and B by staphylococcus Aureus)  Neurotoxins (clostridium tetani)  Superantigens (S aureus causing toxic shock syndrome)

IL-1 and IL-6 are pyrogenic cytokines.

Maintenance of Body Temp

Normal body temp is called the thermostatic set point

It's controlled by the hypothalamus

Fever

Resetting the thermostatic set point at a higher level.

<aside> 🐀 Hyperthermia is different: the body temp exceeds the new set point; it leads to confusion in the elderly and convulsions in the young.

</aside>

Setting a new thermostatic set point:

Other Effects of Inflammation

Local- in immediate area

Systemic- whole body

The local immune response to infection is accompanied by multiple systemic effects:

  1. fever (incorporates sweating, chills, sickness behaviour)
  2. tachycardia (increased heart rate)

Immunoglobulins

Antibodies are also known as immunoglobulin or Ig.

They either bind pathogens and inactive them or flag them for immune destruction.

<aside> 🐀 Antigen- anything that activates the immune system

</aside>

<aside> 🐀 Epitope- small region of a pathogen recognised by B or T cell

</aside>

<aside> 🐀 B cell receptor (BCR)- a membrane-bound form of antibody found on inactivated B cells. Once activated the B cells secretes the BCR its known as an antibody

</aside>

<aside> 🐀 Naive cell- a B or T cell that has never bound a pathogen/epitope

</aside>

<aside> 🐀 Plasma cells- previously activated B cell that secretes a lot of an antibody

</aside>

T Cells

T and B cells (lymphocytes) have similarities...

 born in the bone marrow  adaptive immune system  each express a defining receptor  both bind to epitopes on pathogens

but the difference is:

 mature in the thymus  naive B cells express a BCR whereas naive T cells express a TCR which is never secreted  response to infection is different

2 types of T cell:

 CD4+ o most help other cells like B cells and CD8+ cells

o some CD4+ regulate immunity to switch it off  CD8+ o tends to kill virally infected cells

<aside> 🐀 Levels of IL-6 have found to be correlated with disease severity as shown in COVID cases. Tocilizumab is an antibody that blocks IL-6.

</aside>

Cytokine storm

Also called hypercytokinemia, is where the innate immune system causes uncontrolled and excessive release of pro-inflammatory signalling molecules called cytokines. This leads to multisystem organ failure and death.

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Lecture 12- acute and chronic inflammation

Module: Pathophysiology 

30 Documents
Students shared 30 documents in this course

University: Bournemouth University

Was this document helpful?
Lecture 12: Acute and Chronic
Inflammation
Inflammation
Reaction of tissue to cell injury or death.
Can be external or internal
Often named as organ/tissue ‘itis’= pancreatitis
5 signs:
ocalor (heat)
odolor (pain)
orubor (redness)
otumor (swelling)
oloss of function
Positives Negatives
Helps clear infection Causes long term pain and loss of
function
Prevents spread of infection Scarring
Helps activate immune memory May predispose to autoimmunity
Inflammation can be a sign of an effective
vaccination Can lead to cancer
Promotes wound healing Dysregulates immunity
Inflammation Can Be Acute & Chronic
Strong acute or chronic infection can lead to pathophysiological conditions.
Feature Acute Chronic
Onset Fast: minutes to hours. Innate immune
system
Slow: days. Adaptive immune
system.
Duration Hours to days Weeks, months, years
Cellular infiltrate Mainly neutrophils then macrophages Macrophages, plasma cells,
lymphocytes
Vascular changes Prominent (vasodilation- increased
permeability) Not prominent; angiogenesis
Tissue injury Self-limited Progressive
Fibrosis Mild Severe
Local and systemic
signs Prominent Less
Mechanisms of Acute Inflammation

Students also viewed

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