Page 75 - Veterinary Immunology, 10th Edition

VetBooks.ir LEARNING OBJECTIVES

After reading this chapter, you should be able to:

• Understand how stimulation of toll-like receptors (TLRs) and other pattern-
recognition receptors (PRRs) activates sentinel cells and triggers secretion of
cytokines.

• Recognize that sentinel cells and damaged cells produce many other molecules
that trigger and maintain inflammation.
• Be aware that some inflammatory mediators are produced by nerves.

• Explain how these molecules trigger local increases in blood flow to cause the
redness and swelling associated with inflammation.
• Discuss how these molecules also attract defensive cells such as neutrophils

that can kill invading microorganisms.
• Identify the differences between acute and chronic inflammation.
• List the basic steps of the process of acute inflammation.

• Describe the basic properties and sources of interleukin-1, tumor necrosis factor
α, and type I interferons.

• Explain the antimicrobial properties of defensins.
• Define cytokine, chemokine, defensin, prostanoids, prostaglandin, and kinins.
• List two important vasoactive amines.
• List the major antimicrobial peptides.

Acute inflammation develops within minutes after tissues are
damaged. The damaged tissue generates three types of signal. First,
broken cells release molecules (or damage-associated molecular
patterns [DAMPs]) that trigger the release of cytokines,

chemokines, and enzymes from sentinel cells. Second, invading
microbes provide molecules (pathogen-associated molecular
patterns [PAMPs]) that trigger additional sentinel cell responses.
Third, pain due to tissue damage causes sensory nerves to release

bioactive peptides. This complex mixture of molecules collectively
attracts defensive white blood cells (leukocytes) and at the same
time acts on blood vessels, resulting in increased local blood flow
and leading to redness and swelling.

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