BIO 2010 Microbiology - Chapter 6A: Non-Adaptive Immunity Notes

Two Arms of the Immune System

  • Non-Adaptive Immunity

    • Includes intrinsic and innate defenses.

    • Same response for all pathogen types.

  • Adaptive Immunity

    • Specific responses for each microorganism.

Non-Adaptive Immunity: Lines of Defense

  • First Line: External body membranes (skin and mucosae).

  • Second Line: Antimicrobial proteins, phagocytes, and other cells; inflammation is key.

  • Characteristics:

    • General response system functioning the same way, eliminating almost all pathogens.

    • Does not identify individual pathogens.

Adaptive Immunity: Third Line of Defense

  • Attacks particular foreign substances, slower to react.

  • Adaptive system tailors its response to individual pathogens.

  • Innate and adaptive defenses are intertwined.

Surface Barriers

  • Skin, mucous membranes, and secretions act as physical barriers.

  • Keratin resists acids, bases, bacterial enzymes, and toxins.

  • Mucosae provide similar mechanical barriers.

Protective Chemicals

  • Inhibit or destroy microorganisms.

    • Skin acidity.

    • Lysozyme in saliva and lacrimal fluid.

    • Mucus.

Intrinsic Processes

  • Always present in uninfected cells; includes:

    • Apoptosis.

    • Autophagy.

    • RNA silencing.

    • Antiviral proteins.

Apoptosis

  • Programmed cell death; intrinsic (self-initiated) and extrinsic (induced by external signals).

    • Neutrophils undergo apoptosis after about 1 day.

CISPR

  • Mechanism bacteria use to edit their DNA after virus insertion.

Pattern Recognition

  • Pathogen attaches to multiple host receptors, triggering a specific immune response.

  • Non-adaptive immunity uses cell receptors that recognize pathogen-associated molecular patterns (PAMPS).

Cytokines

  • Secreted proteins that kill bacteria or infected host cells after patterned attachment signals.

Innate Immunity

  • Attacks pathogens without specificity, acts quickly.

  • Cells and proteins needed if microorganisms invade deeper tissues.

  • Antimicrobial proteins (interferons and complement proteins).

  • Inflammation/Fever.

Macrophages

  • Ingest and eliminate infectious agents; present antigens.

  • Attracted by chemicals from dying cells.

Dendritic Cells

  • Specialized for antigen presentation and T-cell activation (adaptive immunity).

  • Migrate to lymphoid organs with antigen.

Lymphocytes

  • T-lymphocytes: seek and destroy.

  • B-lymphocytes: produce antibodies.

MHC Protein

  • Specific MHC protein matches the original antigen absorbed by the cell and moves to the cell surface.

  • MHC attachment programs the cytotoxic T-Lymphocyte (CTL).

Natural Killer (NK) Cells

  • Recognize normal vs. low "self" protein (MHC) levels.

  • Release perforins (punch holes) and granzymes (induce apoptosis).

T-Cell Receptors (TCRs) and CD28 Receptors

  • TCR function is recognition, and CD28 is activation.

Neutrophils

  • Become phagocytic upon encountering infectious material.

  • Release toxic chemicals and induce intrinsic apoptosis.

Mast Cells

  • Release substances (e.g., histamine) contributing to inflammation.

  • Important in allergic responses and innate immunity.

  • Antihistamines: competitive inhibitors of histamine receptors.

Antimicrobial Proteins (Cytokines)

  • Interferons (IFNs) and complement proteins.

    • Attack microorganisms or hinder reproduction.

Interferons (IFNs)

  • Signal response to viral and some cancer infections.

  • Induce antiviral proteins in host cells.

  • Guide NK cells to release perforin and stimulate macrophage consumption.

  • Cause flu-like symptoms.

Complement Proteins

  • Proteins circulating in the blood in an inactive state.

  • Play a role in inflammatory responses.

  • Create osmotic imbalance.

  • Antibodies activate complement.

Inflammation

  • Response of vascular tissue to injury or infection.

    • Seeks to destroy injurious agents and confine them.

  • Sequence of events:

    • Histamine release, capillary widening, increased permeability, leukocyte attraction, fever.

Fever

  • Triggered by bacterial endotoxins.

  • Positive Effects: Stimulates phagocytosis, slows bacterial growth.

  • Negative Effects: Extreme heat, enzyme denaturation (above 39°C is dangerous).

  • Moderated by the medulla oblongata.