Innate Immune System II: Primary Protective Barriers, Recognition & Phagocytosis

Vocabulary flashcards covering key terms related to primary barriers, pathogen recognition and phagocytic mechanisms of the innate immune system.

Innate Immune System

The body’s first-line, non-specific defence that prevents, recognises and eliminates pathogens without prior exposure.

Primary Protective Barriers

Anatomical, chemical and biological defences (e.g., skin, mucosa, low pH, microbiota) that stop pathogens reaching internal tissues.

Anatomical (Physical) Barrier

A structural feature such as tightly joined epithelial layers that blocks microbial entry.

Skin

Multilayered barrier with low pH, antimicrobial peptides and sebaceous fatty acids that inhibits microbial invasion.

Epidermis

Outer skin layer of dead, keratin-filled cells providing waterproof, pathogen-resistant protection.

Dermis

Inner vascular skin layer containing connective tissue, hair follicles, glands, and resident immune cells.

Psoriasin

Skin-derived antimicrobial peptide particularly effective against Escherichia coli.

Mucosal Epithelium

Epithelial lining of gastrointestinal, respiratory and urogenital tracts that secretes mucus and antimicrobial factors.

Lysozyme

Enzyme in tears, saliva and mucus that hydrolyses bacterial peptidoglycan, exposing membranes to further attack.

Defensins

Cationic antimicrobial peptides (α- or β-types) that insert into and disrupt microbial membranes.

Cathelicidins

Positively charged antimicrobial peptides that damage pathogen membranes and neutralise endotoxin.

Histatins

Salivary antimicrobial peptides effective particularly against fungi.

Immunoglobulin A (IgA)

Secretory antibody that opsonises microbes on mucosal surfaces, blocking attachment and facilitating clearance.

Mucus

Gel formed by mucins that traps microbes and prevents adhesion to epithelial cells.

Cilia

Motile surface projections on respiratory epithelium that sweep mucus-entrapped microbes out of airways.

Opsonisation

Coating of a microbe by opsonins to enhance recognition and ingestion by phagocytes.

Opsonin

Soluble molecule (e.g., antibody, complement fragment, MBL) that binds pathogen surfaces to promote phagocytosis.

Peptidoglycan

Cell-wall polymer targeted by lysozyme; thick in Gram-positive, thin in Gram-negative bacteria.

Chemical Defence: Low pH

Acidic environments (e.g., stomach pH≈2, vaginal pH≈4.5, skin pH≈5.5) hostile to many microbes.

Bile Acids

Detergent-like molecules (e.g., deoxycholic acid) in bile that disrupt bacterial membranes, inhibiting Helicobacter pylori.

Pulmonary Surfactant

Mixture of lipids and proteins lining alveoli that lowers surface tension and contains collectins with antimicrobial activity.

Collectins

Surfactant proteins that bind pathogen carbohydrates, act as opsonins and facilitate macrophage phagocytosis.

Commensal Microflora

Normal microbial inhabitants that compete with pathogens, aid nutrient absorption and modulate immunity.

Colonisation Resistance

Protection provided by commensals through competition for nutrients and attachment sites with invading microbes.

Antimicrobial Peptides (AMPs)

Small, cationic peptides (< 60 aa) that disrupt microbial membranes or inhibit nucleic-acid/protein synthesis.

Pathogen-Associated Molecular Patterns (PAMPs)

Microbial structures (e.g., LPS, flagellin, unmethylated CpG DNA) absent from host cells but common to pathogens.

Pattern Recognition Receptors (PRRs)

Host receptors that detect PAMPs or opsonins, initiating phagocytosis or inflammatory signalling.

Mannose-Binding Lectin (MBL)

Soluble PRR that recognises mannose/fucose on microbes and triggers the lectin complement pathway.

Scavenger Receptors

Phagocytic PRRs that bind anionic polymers and lipoproteins on pathogens for uptake.

Complement Receptors (CRs)

Phagocyte surface molecules that bind complement fragments (e.g., C3b) opsonising microbes.

Fc Receptors

Phagocytic receptors that bind the constant region of opsonising antibodies attached to pathogens.

Phagocytosis

Active engulfment of particles by neutrophils, macrophages or dendritic cells leading to intracellular killing.

Oxidative Attack

Phagocytic killing mechanism that generates reactive oxygen and nitrogen species to damage pathogens.

Reactive Oxygen Species (ROS)

Highly reactive molecules (e.g., O₂⁻, H₂O₂, •OH) produced by NADPH oxidase during phagocytosis.

Respiratory Burst

Rapid increase in oxygen consumption and ROS production by activated phagocytes.

Inducible Nitric Oxide Synthase (iNOS)

Enzyme activated in phagocytes to produce microbicidal nitric oxide (NO).

Reactive Nitrogen Species (RNS)

Nitric oxide and derivatives that damage microbial DNA, proteins and membranes.

Non-Oxidative Attack

Phagocytic killing using lysosomal enzymes, antimicrobial peptides and acidification without ROS/RNS.

Phagolysosome

Intracellular vesicle formed by fusion of a phagosome with lysosomes where pathogens are destroyed.

Toll-Like Receptors (TLRs)

Membrane or endosomal signalling PRRs that detect distinct PAMPs and induce type I interferons.

Nod-Like Receptors (NLRs)

Cytosolic PRRs that sense intracellular PAMPs/DAMPs and activate inflammatory gene expression.

C-Type Lectin Receptors (CLRs)

Surface or soluble PRRs that bind carbohydrate motifs on pathogens for signalling or phagocytosis.

Antigen-Presenting Cells (APCs)

Cells such as dendritic cells and macrophages that process antigens and activate adaptive immunity.

Cytokines

Small signalling proteins released by immune cells to regulate inflammation and immunity.

Chemokines

Cytokines that direct leukocyte migration towards infection sites.

NADPH Oxidase

Multisubunit enzyme complex that transfers electrons to oxygen, generating superoxide during the oxidative burst.