Bacterial infection and the immune response
About this set
Created by:
katsowa on September 11, 2010
Subjects:
immunology, bacteriology, animals
Description:
General immune system an the immune respose to a bacterial infection
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19 terms
Terms | Definitions |
|---|---|
 Routes of infection | Mucosal surfaces: airway (inhaled droplet, spores), GI tract (contaminated water/food), reproductive tract (physical contact) External surfaces: external surface (physical contact), wounds/abrasions(minor skin abrasions, puncture wound, handling infected animals), insect bites (mosquito - 2 species, deer tick) |
| Barriers to infection | Mechanical (epithelial cells joined by tight junctions - skin, GI, lungs, eye, nose; longitudinal flow air/fluid - skin, GI; movement mucus by cilia - lungs) Chemical (fatty acids - skin; low pH/pepsin - GI; lysozyme - eye, nose; antibacterial peptides - skin, GI, lungs) Microbiological (normal flora - skin, GI) |
| Where are commensal bacteria and what do they do | They colonize microenvironmental niches contributing to healthy epithelial interface - disturbance leads to an opportunity for pathogenic bacteria Produce antibacterial proteins (colicins) Compete for nutrients Necessary for proper development of the host mucosal immune system Possibly secrete products that inhibit the virulence gene of some pathogenic bacteria |
| Probiotics | Products with live organisms of commensal bacteria |
| Prebiotic | Indigestible oligosaccharides which promote the activity of commensal bacteria |
| Synbiotic | A product with a combination of pro- and prebiotics |
| Extracellular bacteria | Outside host cells (on epithelial surfaces/interstitial space) Damages host by inducing inflammation and producing toxins |
| Intracellular bacteria | Within host cells (phagosome/endosome, phagolysosome, cytoplasm) Damage host by affecting functional activity of the cell and inducing the host immune system |
| Effective control of bacterial infections requires... | Both the innate and adaptive immune system Innate system: cellular components (phagocytic cells, NK cells, γδ T cells), humoral components (complement, antibacterial molecules, cytokines) Adaptive system: cellular components (B and T cells), humoral components (antibodies, cytokines) |
| Stages of response to infection | Bacterial adherence to epithelium (normal flora, local chemical factors, phagocytes) -> local infection/penetration of epithelium (wound healing, antibacterial proteins/peptides, phagocytes, γδ T cells) -> local infection (alternative complement pathway, phagocytes, cytokines, NK cells, macrophage activation) -> lymphatic spread (phagocytes, antigen trapping, NK cells) -> adaptive immunity (antibodies, T-cell activation macrophages, cytotoxic T cells) |
| Bactericidal agents within phagocytes after ingestion of microorganism | low pH (acidification), toxic oxygen-derived products (superoxide, H2O2, singlet oxygen, etc), toxic nitrogen oxides (NO), antimicrobial peptides (defensins, cationic proteins), enzymes (lysosome - dissolves cell wall gram neg; acid hydrolase - further digestion), competitors (lactoferrins - binds Fe, and vitamin B12-binding protein) |
| Macrophage cytokines | IL1, IL6, TNFα Acute phase protein production by liver -> activate complement/opsonization Neutrophil mobilization from bone marrow endothelium -> phagocytosis Increased body temp (hypothalamus), and protein/energy mobilization to allow for fever from fat/muscle -> decreased replication, increased antigen processing, increased specific immune response TNFα stimulates migration of dendritic cells to lymph nodes and maturation -> adaptive immune response |
| Acute phase proteins | SP-A, SP-D, mannose-binding lectin, fibrinogen, C-reactive protein, serum amyloid protein* * - are all pentamers and can activate compliment (like IgM) |
| Effector functions of antibodies | Neutralize toxins Block colonization Bind Fc receptors - opsonization, antibody-dependent cell-mediated cytotoxicity, mast cell/basophil degranulation Complement activation |
| Effector functions of TH1 cells | Cell binds to macrophage and activates it leading to killing of intravesicular bacteria Production of INFγ that activates macrophages and B cells to produces IgG leading to compliment fixation |
| Granulomatous inflammation | Partial activation of macrophages leads to granuloma formation (macrophages - multinucleated giant cells, bacteria, and T-cells) |
| Bacterial evasion of the immune system | Complement resistance (enzymes cleaving C3a/C5a) Block phagocytosis (M protein, type III secretion products) Kill phagocytes (alpha toxins) Binding of IgG (protein A binds Fc region) IgA degradation (proteases cleaving IgA) Intracellular life style Modulation of surface antigens Generalized subversion of immune response (superantigen) |
| Superantigens | No antigen processing required Activates CD4 T cells which causes disease and suppresses adaptive immune response |
| Cell mediated immunity and fungal infections | Natural resistance from macrophages and neutrophils NK cells kill fungi by release of granules with cytolysin NK cells secrete IFNγ activating macrophages |
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