Neutrophils and Macrophages: Defenders of the Body

Posted on Feb 20, 2025 in Biology

Defensive Properties of Neutrophils and Macrophages

  • Mainly responsible for the destruction of bacteria, viruses, and pests.
  • Neutrophils: Mature cells that destroy bacteria, even in the circulating blood.
  • Macrophages: Initially monocytes in the blood that migrate to the tissues and develop into macrophages (growth and lysosomes).

Diapedesis and Movement of Neutrophils and Macrophages

  1. Neutrophils and macrophages enter the tissue spaces by diapedesis.
  2. They move through the tissues.
  3. Amoeboid movement: Tissues possess chemicals that attract neutrophils and macrophages.

Phagocytosis

  • Ingestion: Cell phagocytosis of the attacking agent.
  • Three processes for phagocytosis to occur: “Opsonization”
  1. Surface roughness increases phagocytosis probability.
  2. Dead tissue and foreign particles lack a protective protein coat.
  3. Antibodies bind to bacteria, making them susceptible to phagocytosis.

Neutrophil Phagocytosis

  • Binds to the particle.
  • Issues pseudopodia.
  • Forms a closed chamber.
  • Invaginates inwards.
  • Appears from the outer cell membrane.
  • Forms a phagocytic vesicle.

Macrophage Phagocytosis

  • More powerful than neutrophils.
  • Can phagocytose up to 100 bacteria (20-30 is typical).
  • Phagocytose larger particles than bacteria.
  • Longer shelf life.
  • They have abundant lysosomes filled with proteolytic enzymes.

Types of Macrophages

  1. Tissue Macrophages (Histiocytes): Found in the skin and subcutaneous tissues; more macrophages are produced upon injury.
  2. Lymph Node Macrophages
  3. Alveolar Macrophages (Pulmonary)
  4. Sinusoidal Liver Macrophages (Kupffer cells)
  5. Bone Marrow and Spleen Macrophages

Inflammation and Function of Neutrophils and Macrophages

A. Inflammation
  1. Local vessel dilation (increased local blood flow).
  2. Increased capillary permeability (increased fluid into the interstitial spaces).
  3. Interstitial coagulation due to excessive amounts of fibrinogen.
  4. Migration of granulocytes and monocytes to the tissue.
  5. Swelling of the tissue cells. Response of macrophages and neutrophils to swelling.
Tissue Macrophages: (1st line of defense)
  • Increased size of these fixed cells. Macrophages become mobile for the first time.
Invasion of Neutrophils into the Inflamed Area (2nd line of defense)
  • Altered internal surface of the capillary endothelium: “Marginalization” increasing openings between endothelial cells (capillary-venular).
  • Chemotaxis of neutrophils to injured tissues. Increased blood tissues: 4-5 thousand to 15-25 thousand… “Neutrophils”.
Second Invasion of Macrophages (3rd line)
  • Monocytes in inflamed tissue. Increased tissue size; macrophages reach full capacity in tissue after 8 or more hours.
Increased Granulocyte Production by Bone Marrow and Macrophages (4th line of defense)
  • Takes 3 to 4 days to reach the stage where they leave the bone marrow.

Mechanism of Platelet Plug

  1. Platelets adhere to the damaged vascular wall.
  2. Emit pseudopodia.
  3. Contractile proteins become active.
  4. Granules contract powerfully.
  5. Release factors that adhere to collagen and a tissue factor protein called von Willebrand factor.
  6. Secrete large amounts of enzymes, ADP, and Thromboxane A2.
  7. ADP + Thromboxane A2 attract and activate neighboring platelets.
  8. Fibrin strands form.

Glomerular Capillary Membrane

  1. Capillary endothelium (fenestrations)
  2. Basement Membrane
  3. Layer of epithelial cells (podocytes)

These three layers are called the filtration barrier.

Substances that Control Renal Circulation

  1. Epinephrine, Norepinephrine, and Endothelin: Constriction of afferent and efferent arterioles. Decrease in GFR and RBF.
  2. Angiotensin II: Potent vasoconstrictor; constricts the efferent arterioles. Increases hydrostatic pressure and decreases glomerular RBF.
  3. Nitric Oxide: Decreases endothelial renal vascular resistance and increases GFR.
  4. Prostaglandins and Bradykinin: Tend to increase GFR. Sodium chloride in the macula densa causes dilation of afferent arterioles and increased renin release (Juxtaglomerular cells).