Bacterial Infections and the Immune System – Key Vocabulary

Vocabulary flashcards covering key terms, mechanisms, and bacterial evasion strategies from the lecture on bacterial infections and immune responses.

Infection

Invasion and multiplication of microorganisms in body tissues causing local or systemic injury through metabolism, toxins, intracellular replication, or aberrant host responses.

Extracellular bacteria

Bacteria that replicate outside host cells and are mainly countered by humoral immunity, phagocytosis, and complement-mediated mechanisms.

Intracellular bacteria

Bacteria that survive and replicate inside host cells; defense relies on cell-mediated immunity such as TH1 cytokines, activated macrophages, NK cells, and Tc cells.

Innate immunity

Rapid, non-specific host defenses that include physical barriers, phagocytes, complement, NK cells, and inflammatory mediators.

Adaptive immunity

Antigen-specific defense involving T and B lymphocytes that generates immunological memory and tailored responses.

Humoral immunity

Branch of adaptive immunity mediated by antibodies and complement proteins circulating in body fluids.

Complement system

Cascade of plasma proteins (classical, lectin, alternative pathways) that opsonize microbes, recruit inflammatory cells, and form the membrane attack complex.

Opsonisation

Coating of microbes with antibody or complement fragments (e.g., C3b) to enhance phagocytosis via Fc or complement receptors.

Anaphylatoxins

Complement fragments C3a and C5a that trigger mast-cell degranulation, vascular permeability, and chemotaxis of leukocytes.

Membrane Attack Complex (MAC)

Terminal complement complex (C5b-9) that forms pores and lyses Gram-negative bacteria and enveloped viruses.

Helicobacter pylori

Gram-negative, urease-producing bacterium associated with gastritis, peptic ulcers, and gastric carcinoma; elicits TH1-biased immune responses.

Urease (H. pylori)

Enzyme that converts urea to ammonia and bicarbonate, raising local pH and liquefying gastric mucus to aid bacterial colonization.

CagA

Oncoprotein injected by H. pylori into gastric epithelial cells, disrupting cell functions and provoking strong innate immune signaling via Nod1.

VacA

Vacuolating cytotoxin of H. pylori that damages epithelial cells and can inhibit T-cell IL-2 signaling.

Pattern Recognition Receptor (PRR)

Host sensor (e.g., Toll-like receptor, Nod1) that detects conserved microbial motifs and initiates innate immune responses.

Nod1

Intracellular PRR that recognizes peptidoglycan fragments; detects CagA activity and induces IL-8 and defensin production.

TH1 response

T-helper subset that secretes IFN-γ, TNF-α, and IL-12, activating macrophages and promoting cell-mediated immunity against intracellular microbes.

Type I cytokines

Cytokines (e.g., IFN-γ, TNF-α, IL-12) characteristic of TH1 responses that enhance macrophage microbicidal activity.

IgA

Antibody isotype that is trans-cytosed across mucosal epithelium to neutralize pathogens and toxins in secretions.

NETosis

Neutrophil death pathway releasing DNA-based extracellular traps laden with histones, enzymes, and antimicrobial peptides to ensnare and kill pathogens.

Neutrophil Extracellular Traps (NETs)

Webs of chromatin and granule proteins expelled by neutrophils that immobilize bacteria, fungi, and parasites.

METosis

Formation of extracellular traps by macrophages (and other myeloid cells) analogous to NETs, contributing to innate defense.

Reactive Oxygen Species (ROS)

Highly reactive molecules such as superoxide and hydrogen peroxide produced by enzymes (e.g., myeloperoxidase) to damage pathogens.

Histones (antimicrobial role)

Basic nuclear proteins within NETs that disrupt microbial membranes and contribute to pathogen killing.

Side effects of NETosis

Persistent NET remnants can expose autoantigens and promote chronic inflammation and autoimmunity (e.g., lupus, atherosclerosis).

Myeloperoxidase

Granule enzyme that generates hypochlorous acid within phagosomes and NETs for oxidative microbial killing.

Classical complement pathway

Complement activation route initiated by antibody–antigen complexes leading to C3 convertase formation.

Alternative complement pathway

Antibody-independent pathway initiated by spontaneous C3 hydrolysis on microbial surfaces.

Lectin complement pathway

Pathway triggered by mannose-binding lectin recognizing microbial carbohydrates, activating complement without antibodies.

Extracellular trap

Network of DNA and antimicrobial proteins released by immune cells to immobilize and kill pathogens.

Cytosolic bacteria

Intracellular pathogens that escape phagosomes into the cytoplasm (e.g., Listeria, Shigella) and are exposed to cytosolic immunity.

Intravesicular bacteria

Pathogens that remain within phagosomes and block fusion with lysosomes (e.g., Salmonella, M. tuberculosis).

Cross-presentation

Process by which dendritic cells present extracellular or phagocytosed antigens on MHC I to activate CD8+ T cells.

Tubercule

Granulomatous lesion in tuberculosis containing infected macrophages, lymphocytes, and caseous necrosis at the core.

Ghon complex

Calcified primary tuberculous lesion and associated lymph node visible on chest X-ray.

Mycobacterium tuberculosis

Acid-fast intracellular bacillus that causes tuberculosis, evades killing by inhibiting phagolysosome maturation.

Granuloma

Organized collection of macrophages, epithelioid cells, and lymphocytes formed to contain persistent pathogens like TB.

Delayed-type hypersensitivity (DTH)

TH1-mediated cellular immune reaction characterized by cytokine release and macrophage activation; important against intracellular bacteria.

Bacterial capsule

Outer carbohydrate layer that masks PAMPs, hinders complement deposition, and resists phagocytosis.

Pili (fimbriae)

Hair-like bacterial surface structures that mediate adhesion to host cells and contribute to colonization.

Antigenic variation

Strategy in which pathogens alter surface antigens through gene rearrangements or hypermutation to evade antibody recognition.

IgA protease

Enzyme produced by Neisseria and Haemophilus that cleaves IgA antibodies, facilitating mucosal colonization.

C5a peptidase

Streptococcal and Haemophilus enzyme that degrades complement fragment C5a, reducing leukocyte chemotaxis.

Bacterial Fc receptor

Surface protein that binds the Fc portion of antibodies, blocking opsonization and immune clearance.

Phagolysosome

Intracellular compartment formed by fusion of phagosome and lysosome; site of microbial killing by enzymes and ROS.

Apoptosis suppression by Chlamydia

Chlamydial inhibition of caspases and cytochrome-c release to keep host cells alive and allow intracellular replication.

Apoptosis initiation by Salmonella

Salmonella-induced macrophage death facilitating bacterial dissemination within the host.