Basic Tissues
Figure 8-6.
A representation of neutrophil phagocytosis of bacteria.
play a central role in cellular defense against bacterial and fungal infections. They are highly motile cells and respond
quickly to infl
ammation in cases of microbial invasion. Acute infl
ammation, one of the body’s defense mechanisms, occurs in the
very early stage of tissue response to injuring agents, such as bacteria and fungi. During acute infl
ammation, microvessels dilate,
and their permeability increases as a result of histamine and other infl
ammatory chemicals, which are released into the connective
tissue by mast cells (see Chapter 4, “Connective Tissue”). Neutrophils quickly enter tissues from the blood circulation by adhering to
activated endothelial cells of capillaries and venules at the site of the infl
ammation. Bacteria are neutralized by several mechanisms,
which include the complement system and antibodies. Neutrophil phagocytosis of bacteria occurs in several steps:
(1) Recognition
The process begins with recognition of the bacterium by
and complement C3b fragments) that coat the bacterium and
render it more susceptible to phagocytes.
(2) Receptor binding
Fc receptors
of neutrophils recognize and bind IgG that has bound to
the bacterium, or complement C3b receptors bind C3b fragments on the surface of the bacterium.
(3) Pseudopod extension
are slender cytoplasmic processes of neutrophils, which engulf (or “phagocytose”) the bacterium that has been recognized and
bound by receptors.
(4) Formation of phagosome
: The engulfment of the bacterium sequesters it in a membrane-bound vesicle, the
(food vacuole).
(5) Killing and digestion of bacterium
: Immediately after or even during formation of the phagosome,
proton pumps
in the membrane of the phagosome generate an acidic pH; both primary and secondary neutrophil granules fuse
with the phagosome and release their components into the phagosome to kill the bacterium and break down the constituents (pro-
teins, carbohydrates, nucleic acids) of the bacterium. Lysosomal enzymes and other products may leak into the extracellular space,
causing damage to endothelial cells and nearby tissues.
(6) Formation of the residual body
: Most of the remaining digested materials
residual bodies
(vesicles containing leftover products of indigestible materials after fusion with the contents of a lysosome)
inside the cells.
(7) Cell death
: Soon after neutrophils have F nished their job of killing and digesting bacteria, they die. The dead
neutrophils may be phagocytosed by macrophages, or they may accumulate locally with tissue debris and fl
uid to form pus.
Neutrophils use
nonoxidative mechanisms
in killing bacteria and destroying other microbes. The
oxidative mecha-
, also known as
, involves generation of hydrogen peroxide by the NADPH
(nicotinamide adenine dinucleotide phosphate) oxidase system and generation of hypochlorous acid by myeloperoxidase (components
of primary granules). The
nonoxidative mechanism
is involved in
in the following manner: Primary and secondary gran-
ules fuse with the phagosome, and their granule components are released directly onto the microbe (see above steps 4 and 5). These
components include
neutral serine protease
, and
from the primary granules as well as
from the secondary granules. They perform their antimicrobial function by disrupting the phagosomal membrane, degrading bacterial
membranes, breaking down the protein and carbohydrate of the bacterium, and binding iron (which is needed for bacterial growth) to
prevent bacterial growth. Both oxidative and nonoxidative mechanisms work in concert to facilitate killing of the microbes.
D. Cui
D. Cui
3. Pseudopod extension
2. Receptor binding
1. Recognition
4. Formation of phagosome
5. Killing and digestion
of bacterium
6. Formation of
residual body
7. Cell death
Fc receptor
of IgG
Residual body
A pathologic condition known as
myeloperoxidase de±
is caused by a defect in the NADPH oxidase complex. This
condition results in the inability to produce “superoxides” in neutrophils and other phagocytic cells. Affected individuals are
unable to kill invading microbes that are normally engulfed by these phagocytic cells. People with this defect can have frequent
and prolonged bacterial and fungal infections.
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