Biol 2420 Lecture 33

Mast Cells - differentiate in the tissue - not in circulation

non-phagocytotic

release Histamine - inflammation

release Chemotaxins - recruit other cells

Neutrophils

respond to chemotaxins

major phagocytic immune cell

innate response

go fight and die

Eosinophils

related to Neutrophils

attack big things - not phagocytes but phagocytic

form pocket on large parasites, dump in perforin and other stuff

Phagocytosis - ingesting a foreign particle

wrap membrane around the particle - becomes a phagosome

lysosome fuses with phagosome (phagolysosome) digests phagosome

bacterial killing by - O2 independent mechanisms or O2 dependent mechanisms

degraded material is reused or discarded

O2 independent killing

enzymatic breakdown

lysozyme - breaks down peptidoglycan aka cell wall of bacteria

hydrolytic enzymes

Defensins & TNF x- don't degrade but cause lysis

O2 dependent killing
 reactive oxygen/nitrogen species ROS/RNS

damage aything they touch (antioxidants attack these things)

respiratory burst

rapid increase in O2 comsumption but its not respiration its because O2 becomes ROS

Oxidase turns O2 into O2-

O2- does not want this electron, it wants to give it away like asap.

O2- -> OH -> H2O2 -> HOCl

O2 + NO -> ONOO-

these are only made when needed

remember when inflammatory response

Death by NK Cell

the innate lymphocyte

it kills altered self-cells (virus infected, cancerous etc)

interacts with all the cells, if normal doesn't do anything, if not, KILLS

Healthy cells show 2 signals - +(kill me) and -(don't kill me)

NK is prevented by the don't kill me

Unhealthy cells bc or IFNa don't have a - signal

activates NK

kills cells by apoptosis with perforoin and GranzymeB

Inflammatory Barrier - a complex cascade

invading organisms or tissue damage

The Inflammatory Process

 Recognition of Bacteria by Macrophages and Mast Cells

they have "Toll like receptors" that react to stuff only bacteria have

e.g. Peptidoglycan, lipopolysaccharide, flagella etc.

these activate the cells

Inflammation

1. chemical signals (TLR stuff)

2. Mast Cells (they have the TLRs)

release histamine - vasodilation - red colour, more blood flow for more neutrophils

make endothelial selectins appear on blood vessel (like handles for the neutrophils)

chemotaxins - create a concentration gradient that makes it go into the blood and
around everywhere. Neutrophils follow the gradient towards the site of release

3. Neutrophils jump out of the blood stream (Extravasation)

a. Margination - move to edge

b. Rolling - to slow momentum (and integrins react with selectin)

c. Arrest - stop

d. Diapedesis - squeeze between cells to leave the blood stream