BIO 246 Microbiology - Exam 4 Flashcards: Innate and Adaptive Immunity

Comprehensive set of 113 vocabulary flashcards covering Innate Immunity (Chapter 16) and Adaptive Immunity (Chapter 17) for BIO 246 Microbiology Exam 4.

Susceptibility

Lack of resistance; being vulnerable to a disease.

Resistance

The ability to withstand or defend against disease.

Innate vs. Adaptive Immunity

Innate immunity is rapid, nonspecific, and lacks memory; adaptive immunity is antigen-specific, slower initially, and possesses memory.

Lines of Defense in Innate Immunity

The first and second lines of defense.

First Line of Defense

External barriers that block, trap, or remove microbes before they enter tissues.

Second Line of Defense

Nonspecific cells and substances that act after microbes pass the first-line barriers.

Third Line of Defense

Specific adaptive defenses involving B cells, T cells, antibodies, and memory cells.

First-Line Physical Defenses

Physical barriers and processes that remove microbes, including skin, mucous membranes, cilia, tears, saliva, urine flow, and mechanical removal.

Skin (Innate Defense)

Tightly packed, keratinized epidermal cells that form a physical barrier, complemented by dryness and shedding that discourage microbial growth.

Mucous Membranes

Epithelial surfaces that secrete mucus to trap microbes and make microbial attachment and entry more difficult.

Ciliary Escalator

Ciliated mucosal cells that move mucus and trapped microbes upward toward the throat to keep them out of the lungs.

Tears (Innate Defense)

Secretions that wash the eye surface, spread via blinking, and contain lysozyme to destroy bacterial cell walls.

Saliva (Innate Defense)

Oral secretion that dilutes and washes away microorganisms and contains substances that inhibit microbial growth.

Gastrointestinal Flushing Mechanisms

Peristalsis, defecation, vomiting, and diarrhea that help flush microbes and toxins out of the gastrointestinal tract.

Urine Flow and Vaginal Secretions

Physical fluid flows that remove microorganisms, with vaginal acidity adding chemical protection.

Nasal Hairs and Ear Defenses

Nasal hairs that trap inhaled particles, along with ear hairs and cerumen that keep foreign material out of the ear canal.

Chemical Defenses

Substances that inhibit or destroy microbes, such as acids, enzymes, fatty acids, and antimicrobial proteins.

Sebum and Skin pH

Sebum fatty acids and lactic acid that maintain an acidic skin pH around $3\text{--}5$, discouraging microbial growth.

Perspiration (Innate Defense)

Sweat that physically washes microbes away and contains salt that can inhibit microbial growth.

Lysozyme

An enzyme that breaks down bacterial peptidoglycan; found in tears, saliva, sweat, nasal secretions, tissue fluids, and urine.

Gastric Juice

Stomach acid and enzymes operating at a very low pH to destroy many ingested bacteria and toxins.

Mucus (Chemical Role)

A secretion that traps microbes and contains enzymes and other substances with antibacterial and antiviral effects.

Normal Microbiota Protection

Resident microbes that protect the host by competing for nutrients and space, altering local conditions, and producing bacteriocins that inhibit pathogens.

Microbial Antagonism (Competitive Exclusion)

The mechanism by which normal microbiota limit pathogen colonization by competing for space and nutrients and inhibiting growth.

PAMPs

Pathogen-associated molecular patterns; molecular structures shared by groups of microorganisms that are recognized by the immune system.

PRRs

Pattern-recognition receptors; host cell receptors that recognize PAMPs and activate defense signaling.

Toll-Like Receptors (TLRs)

A specific class of pattern-recognition receptors (PRRs) that bind PAMPs to trigger cytokine release and regulate immune responses.

Cytokines

Chemical signaling molecules that trigger, enhance, and coordinate immune defense mechanisms.

Major Cytokine Classes (Interleukins, Chemokines, Interferons, TNF)

Interleukins signal between leukocytes; chemokines attract leukocytes; interferons interfere with viral infections; TNF participates in inflammation.

Neutrophils

Motile, phagocytic granulocytes that act as the primary first responders to an infection and enter damaged tissues early.

Basophils and Mast Cells

Non-phagocytic cells that release histamine to promote inflammation and participate in allergic responses.

Eosinophils

Slightly phagocytic leukocytes that fight multicellular parasites such as helminths by releasing toxic substances.

Monocyte Maturation

The process by which circulating blood monocytes exit the bloodstream and differentiate into macrophages within tissues.

Macrophages

Phagocytic cells that engulf microbes, dead cells, and debris, support tissue repair, and present antigens to T cells.

Resident Macrophages

Tissue-fixed macrophages that remain in specific organs, including Kupffer cells (liver), microglia (CNS), and alveolar macrophages (lungs).

Dendritic Cells

Antigen-presenting cells that phagocytose microbes and present antigens to T cells, helping initiate adaptive immunity.

Natural Killer (NK) Cell Cytotoxicity

Direct attack and killing of infected or cancerous cells using perforin and granzymes without utilizing phagocytosis.

Phagocytosis

The cellular ingestion of microbes or particles, followed by their internal digestion and destruction.

Phagocytic Cells of the Immune System

Neutrophils, macrophages, eosinophils, and dendritic cells.

Stages of Phagocytosis

Chemotaxis → recognition/attachment → engulfment → phagosome–lysosome fusion → digestion → residual body → exocytosis.

Chemotaxis (in Phagocytosis)

The directed movement of a phagocyte toward chemical attractants released at an infection or site of tissue damage.

Opsonins

Molecules, such as antibodies or complement proteins, that coat microbes to enhance their attachment to phagocytes.

Opsonization vs. Phagocytosis

Opsonization is the process of coating a pathogen to facilitate recognition; phagocytosis is the physical engulfment and digestion process.

Bacterial Evasion of Phagocyte Attachment

Mechanisms such as capsules or M protein (found in Streptococcus pneumoniae and Streptococcus pyogenes) that hinder phagocytic adherence.

Staphylococcus aureus Phagocytosis Evasion

The production of leukocidins that kill phagocytic leukocytes directly.

Shigella and Mycobacterium Phagocytosis Evasion

Evasion tactics where Shigella escapes from the phagosome into the cytoplasm, and Mycobacterium resists enzymatic digestion inside the phagolysosome.

Inflammation

A local response to tissue injury or infection that acts to destroy/remove threats, limit spread, and support tissue repair.

Classic Signs of Inflammation

Redness, heat, swelling (edema), and pain.

Cause of Redness and Heat in Inflammation

Vasodilation resulting in increased local blood flow to the damaged tissue.

Cause of Swelling and Pain in Inflammation

Increased vascular permeability allowing fluid to accumulate in tissue (swelling), paired with nerve stimulation or physical pressure (pain).

Histamine

An inflammatory chemical released by mast cells that induces vasodilation and increased vascular permeability.

Kinins, TNF-α, Prostaglandins, and Leukotrienes

Inflammatory mediators: kinins attract neutrophils; TNF-α amplifies inflammation; prostaglandins intensify histamine effects; leukotrienes increase permeability and aid phagocyte attachment.

Stages of Inflammation

Vasodilation/permeability increase → phagocyte migration and phagocytosis → tissue repair and regeneration.

Margination and Diapedesis

Margination is the sticking of phagocytes to blood vessel walls; diapedesis is their migration between endothelial cells into surrounding tissue.

Fever

An abnormally elevated body temperature that acts as a systemic defense response.

Pyrogen

A substance that triggers fever when released into or circulating within the bloodstream.

Exogenous vs. Endogenous Pyrogens

Exogenous pyrogens originate outside the host body (such as endotoxin); endogenous pyrogens are cytokines produced by host cells (such as IL-1 and TNF-α).

Fever Induction Pathway

Detection of microbial products stimulates phagocytes to release IL-1 and TNF-α, which signal the hypothalamus to alter body temperature.

Hypothalamic Temperature Resetting

Cytokines trigger hypothalamic prostaglandin synthesis to elevate the thermal set point, causing vasoconstriction and shivering to raise temperature.

Fever Resolution (Crisis)

The phase occurring when the hypothalamic set point drops back to normal, prompting vasodilation and sweating to release heat.

Beneficial Effects of Moderate Fever

Accelerates immune defenses and tissue repair, inhibits pathogen multiplication, enhances antimicrobial enzymes, and increases transferrin and IL-1 activity.

Major Outcomes of Complement Activation

Inflammation, opsonization (enhanced phagocytosis), and cytolysis via the membrane attack complex (MAC).

Complement Cytolysis

Formation of a membrane attack complex (MAC) pore in the microbial membrane, allowing extracellular fluid to rush in and burst the cell.

Bacterial Evasion of Complement

Capsules preventing activation, Gram-negative surface alterations inhibiting MAC insertion, and Gram-positive enzymatic destruction of C5a.

IFN-α and IFN-β

Type I interferons that signal uninfected neighboring cells to produce antiviral proteins (AVPs) that block viral replication and protein synthesis.

IFN-γ

Type II interferon that activates neutrophils and macrophages to enhance their bactericidal killing capacity.

Interferons in Cancer Defense

Host defense proteins shown to inhibit the expression of cancer genes.

Iron-Binding Proteins

Host proteins that sequester free iron to deny pathogens an essential nutrient necessary for growth and survival.

Four Human Iron-Binding Proteins

Transferrin (blood, lymph, interstitial fluid), lactoferrin (mucus, saliva, breast milk), ferritin (liver, spleen, red bone marrow), and hemoglobin (red blood cells).

Siderophores

Bacterial iron-chelating compounds that bind and strip iron away from host iron-binding proteins.

Antimicrobial Peptides (AMPs)

Short peptides produced by the host that inhibit cell-wall synthesis, form membrane pores, or destroy microbial DNA and RNA.

Inflammation vs. Fever Scope

Inflammation is a localized defensive response at the site of damage; fever is a systemic response involving hypothalamic set point elevation.

Adaptive Immunity

Specific, acquired defense system that develops after exposure to foreign antigens and generates immunological memory.

Hallmarks of Adaptive Immunity

Antigen specificity and immunological memory.

Humoral vs. Cell-Mediated Immunity

Humoral immunity is antibody-mediated and governed by B cells; cell-mediated immunity is cellular and directed primarily by T cells.

Antigen

A substance capable of inducing a specific immune response mediated by B cells, T cells, or both.

Epitope

The specific antigenic determinant site recognized by an antibody or T-cell receptor.

Antibody (Immunoglobulin)

A specific antigen-binding glycoprotein synthesized and secreted by differentiated plasma cells.

Structural Chains of an Antibody

Four polypeptide chains comprising two identical heavy chains and two identical light chains.

Variable (V) Regions

Terminal regions on antibody chains that fold to form the antigen-binding site and confer unique antigen specificity.

Constant (C) Regions

Conserved regions of antibody chains that determine the structural class of the antibody and its effector functions.

Classes of Immunoglobulins

The five classes of antibodies: IgG, IgA, IgM, IgD, and IgE.

IgG

The most abundant antibody in serum (accounting for approximately $80\%$), capable of crossing the placenta to confer passive immunity to the fetus.

IgA

Dimeric mucosal antibody found in secretions such as saliva, tears, breast milk, and mucus that protects mucosal surfaces.

IgM

The first antibody class synthesized upon primary antigen exposure; secreted predominantly as a pentamer.

IgD and IgE

IgD functions primarily as an antigen receptor on B-cell surfaces; IgE binds to mast cells and basophils, mediating allergic reactions and protection against parasitic worms.

Consequences of Antigen-Antibody Binding

Agglutination, opsonization, complement activation, antibody-dependent cell-mediated cytotoxicity (ADCC), and neutralization.

Agglutination

The cross-linking of particulate antigens by antibodies, causing cells or particles to aggregate into clumps.

Opsonization (Antibody-Mediated)

The coating of foreign antigens with antibodies to enhance recognition and engulfment by phagocytic cells.

Neutralization

Antibody binding to toxins, viruses, or bacterial adhesins to block their attachment and prevent harm to host cells.

Antibody-Dependent Cell-Mediated Cytotoxicity (ADCC)

A mechanism in which effector immune cells destroy antibody-coated target pathogens that are too large to be ingested by phagocytosis.

Clonal Selection vs. Clonal Expansion

Clonal selection is the activation of an individual lymphocyte matching an epitope; clonal expansion is the subsequent proliferation of that cell into identical clones.

B-Cell Origin and Maturation

B lymphocytes originate from hematopoietic stem cells in the bone marrow and complete their maturation within the bone marrow.

T-Cell Origin and Maturation

T lymphocytes originate from hematopoietic stem cells in the bone marrow and migrate to mature within the thymus.

Antigen Recognition: B Cells vs. T Cells

B cells can directly bind free, intact antigens; T cells can only recognize processed peptide antigens presented on MHC molecules.

Steps of B-Cell Activation

Antigen binds BCR → endocytosis and MHC II presentation → helper T-cell costimulation → clonal expansion → differentiation into plasma and memory B cells.

Plasma Cells

Effector B cells specialized in secreting high concentrations of soluble antibodies into fluids.

Memory B Cells

Long-lived lymphocytes that persist in the body to mount a swift and potent immune response upon secondary antigen exposure.

Helper T Cells (CD4+)

T lymphocytes that recognize antigen fragments presented on MHC II and secrete cytokines to activate B cells, cytotoxic T cells, and macrophages.

Cytotoxic T Cells (CD8+)

Effector T lymphocytes that recognize foreign or abnormal antigens displayed on MHC class I and kill infected or malignant host cells.