Page 64 - Veterinary Immunology, 10th Edition

VetBooks.ir Damage-Associated Molecular

Patterns

Inflammation can be triggered not only by microbial infection but
also by physical trauma and tissue damage. Thus the TLRs
recognize not only PAMPs from invading microorganisms but also
molecules escaping from dead, dying, and damaged tissues. These

molecules, collectively called DAMPs or “alarmins,” may be
released when cells die (intracellular) or generated when connective
tissue is damaged (extracellular) (see Fig. 2.7). Other DAMPs may
be produced by stimulated sentinel cells. Some of these DAMPs

have potent antimicrobial properties. Others recruit and activate
cells of the innate immune system and promote adaptive immune
responses (Box 2.5).

Box 2.5

How Cells Die

Cellular death is a feature of many innate and adaptive immune
responses. The body has to get rid of 200 billion cells daily. Cells

can die in several different ways. Irreparable damage to an
essential pathway will kill a cell in an uncontrolled manner.
However, there are ways in which a cell can participate in its own
death. These forms of programmed cell death can benefit the body
by stopping microbial infections, sparing uninfected nearby cells,

and generating alarmins and inflammatory mediators, and are
essentially “suicide.”

Apoptosis

This is the “normal” way unwanted healthy cells are eliminated. It
occurs through two pathways. An extrinsic pathway where the cell
receives signals from extracellular molecules that bind to cell

surface receptors. This generates a cascade of activated caspases
that cause mitochondrial permeability. The intrinsic pathway is
activated by internal cellular events such as DNA damage or
microbial infection and also leads to mitochondrial

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