attaching the neutrophil to the endothelial cell. The neutrophil then extends a pseudopod to an intercellular junction. Histamine and heparin released at the injury site by perivascular mast cells open the intercellular junction, allowing the neutrophil to  migrate into the connective tissue. With the TEM, the cytoplasmic contents of a neutrophil pseudopod appear as an expanse of finely granular cytoplasmic matrix with no membranous organelles (see Fig. 10.5). The finely granular appearance is attributable to the presence of actin filaments, some
FIGURE 10.5 • Electron micrograph of a human mature neutrophil. The nucleus shows the typical multilobed configuration with the heterochromatin at the periphery and the euchromatin more centrally located. A small Golgi apparatus (G) is present; other organelles are sparse. The punctate appearance of the cytoplasm adjacent to the convex aspect of the nuclear profile is caused by glycogen particles. Adjacent to the concave aspect of the nuclear profile are numerous granules. Specific granules appear less dense and more rounded than azurophilic granules. The latter are fewer in number and are extremely electron dense. 22,000. (Courtesy of Dr. Dorothea Zucker-Franklin.) For comparison, the inset shows a neutrophil from a blood smear observed in the light microscope. 1,800.
FIGURE 10.6 • Diagram of events in the migration of a neutrophil from a postcapillary venule into the connective tissue. a.
Circulating neutrophils are slowed down by the interaction of their surface adhesion molecules, selectins (CD62L), with the endothelium of the venule (b). c. As the result of this interaction, the cell rolls on the surface of the endothelium. The neutrophil then adheres to the endothelium and responds to chemokines secreted by the endothelial cells. d. Their secretion induces the expression of other adhesion molecules on the surface of the neutrophil such as integrins (VLA-5) and the immunoglobulin superfamily of adhesion molecules (e.g., intercellular adhesion molecule-1 [ICAM-1], vascular cell adhesion molecule-1 [VCAM-1]). e. These adhesion molecules allow the neutrophil to bind to adhesion molecule receptors on the endothelial cells. f. The neutrophil then extends a pseudopod to an intercellular junction previously opened by histamine and heparin released from the mast cells in the connective tissue, allowing the neutrophil to migrate through the vessel wall (g).
microtubules, and glycogen, which are involved in the extension of the cytoplasm to form the pseudopod and the subsequent contraction that pulls the cell forward. Once the neutrophil enters the connective tissue, further migration to the injury site is directed by a process known as chemotaxis, the binding of chemoattractant molecules and extracellular matrix proteins to specific receptors on the surface of the  neutrophil.
Neutrophils are active phagocytes that utilize a variety of surface receptors to recognize bacteria and other infectious agents at the site of inflammation.