Biol 251 - Exam 3

Hyaluronidase

An exoenzyme that helps bacteria invade its host by degrading hyaluronic acid, keeps cells together.

Bacteria carrying hyaluronidase

Staph, Strep, C.perfringens.

Collagenase

A protease (enzyme that breaks down protein) that degrades collagen between endothelial cells, allowing bacteria to enter the cell.

Bacteria carrying collagenase

Clostridium perfringens and S. Pyogenes.

Collagenase effects

Leads to septicemia (infection of the bloodstream).

Phospholipases

An enzyme that lyses cells, leading to necrosis.

C.perfringens fermentation

Creates gas, leading to gas gangrene or myonecrosis (soft tissue death).

Hyperbaric oxygen therapy

Introduces oxygen to anaerobic bacteria like C.perfringens.

Treatment methods for C.perfringens invasion

Surgery, intravenous antibiotics, hyperbaric oxygen therapy, amputation.

Necrotizing fasciitis

Flesh eating disease that targets the fascia caused by S.pyogenes.

S.pyogenes virulence factor

Exotoxin Spe B, which cleaves junctional proteins, allowing bacteria to travel across the epithelial barrier.

Treatments for necrotizing fasciitis

Debridement (surgical removal of infected tissue), amputation, intravenous antibiotics.

Virus adherence to host cells

Lipoproteins + glycoproteins bind to receptors on host cells.

Bacteria adherence to host cells

Fimbriae, flagella, capsules.

Pili

Allows bacteria to attach to tissue.

Neisseria gonorrhoeae adhesion

Uses pili to stick to mucosal epithelial cells.

Glycocalyx

A layer of sticky coat used to help bacteria stick to surfaces.

Example of bacteria using glycocalyx

S.mutans creates biofilm with glycocalyx that induces tooth decay.

Neisseria gonorrhoeae effects

Causes gonorrhea, urethritis, cervicitis.

S.pyogenes adherence

Adheres to respiratory epithelial cells via protein F.

Endotoxin vs Exotoxin

Endo: toxic substance made by gram - bacteria; Exo: toxic substance made by both gram - & +.

Endotoxins composition

Made of lipopolysaccharides, with Lipid A being the most toxic part that triggers inflammatory response.

Parts of an endotoxin

Lipid A: toxic part, elicits inflammatory response;

Core glycolipid: connects lipid A to O antigen;

O Antigen: aids in immune evasion.

Exotoxins composition

Made of highly toxic proteins + enzymes that damage cells by inhibiting specific metabolic functions.

Classes of exotoxins

Intracellular targeting toxins

membrane disrupting toxins

superantigens.

Intracellular toxin

AB toxin;

B: binds to host receptors, allows endocytosis;

A: poisons/attacks cell.

Examples of bacteria with intracellular targeting toxins

Diphtheria

Cholera

Botulinum

Tetanus.

Botulinum toxin

Neurotoxin that inhibits acetylcholine release from the presynaptic nerve terminal, leading to flaccid paralysis.

Tetanus toxin

Neurotoxin that inhibits release of glycine and GABA from interneuron, leading to permanent muscle contraction/spasms.

E.coli O157:H7

Life threatening strain of E.coli that secretes cytotoxins.

Cytotoxin

Shiga toxin that inhibits protein synthesis, causing hemolytic uremic syndrome (intense inflammatory response)

Cytotoxin Definition

Exoenzyme that has a toxic effect on cell functions

Listeria Monocytogenes virulence factor

Forms biofilm on food processing equipment (Ready-to-eat items)

Listeriosis

Caused by Listeria Monocytogenes; affects immunocompromised individuals and pregnant women

Effects of Listeriosis

Affects CNS and causes meningitis, meningoencephalitis, septicemia

Danger of Listeriosis

It has a high mortality rate

Membrane disrupting toxin

Exotoxin that uses bacterial phospholipases to disrupt eukaryotic cytoplasmic membranes and lyse cells

Phospholipases

Breaks down phospholipid bilayer

Types of membrane disrupting toxins

Hemolysis: toxin that creates pores in cell membranes and leads to lysing of the cell; Phospholipases: enzyme made by bacteria that breaks down phospholipid bilayer in cells

Super antigens

Exotoxin that overstimulates the immune system, forcing it into cytokine storm, causing high fever and inflammation

How super antigens work

1) Superantigen binds to both MHC class 2 and T-cell receptor; 2) T cell interprets this as an antigen recognition; 3) Massive cytokine release

Capsules in bacteria

Help bacteria evade host defenses by preventing phagocyte detection

Phagocytosis

A process where immune cells engulf and digest harmful particles

Strains of S.pyogenes

Strains causing necrotizing fasciitis produce proteases, invasins and Spe B, differing from those causing strep throat

Endotoxin

Produced by gram-negative bacteria and in large quantities can cause septic shock in patients

Antibodies and tetanus toxin

Antibodies bind to the toxin and prevent it from attaching to the host cell receptor

True or false?

Endotoxins have heat stability

True

First line of defense

The line of defense that defends against anything (innate)

Second line of defense

The line of defense that specifically targets specific antigens, develops as the body is exposed to different antigens (Adaptive)

Physical barriers of innate immunity

Skin/mucous barriers, cell-cell junctions in epithelial cells, Blood brain barrier, Mucous membranes

Mechanical barriers of innate immunity

Mucociliary escalator, peristalsis, flushing of urine and tears, shedding of skin cells

Mucociliary escalator

Ciliated epithelial cells push away mucous trapped particles and debris from lungs

Peristalsis

Moves out harmful microbes from the GI tract through wave-like contractions

Chemical defenses of the innate immune system

Cytokines, Antimicrobial substances, Antimicrobial peptides (AMPS)

Antimicrobial substances of innate chemical defense system

Lysozyme: degrades peptidoglycan in cell walls; Lactoferrin & Transferin: binds to iron needed for cell growth; Lactoperoxidase

AMPS

A substance secreted by macrophages and neutrophils in response to microbial invasion, creates pores in microbe membranes

Complement system of innate immunity

Group of non-specific unactivated proteins floating in blood and tissue fluid, that attack all invading microbes (C1-C9)

Different pathways of the complement system

Alternative, Lectin, Classical

Classical pathway

When antibodies bind to the antigen (AB-AG complex), C1 activates, and creates a cascade

Lectin pathway

When a mannose binding lectin binds to a mannose sugar on a microbial surface, alerts and cascades protein system

Spontaneous activation of C3

Protein occurs constantly in the blood.

Opsonization

A secretment from C3b, lectins, and antibodies that binds to bacterial cells, tagging them for phagocytes.

Inflammatory response

Protein C5a & C3a attracts phagocytes to an area by increasing blood vessel permeability.

Chemotaxis

The ability of protein C5a to secrete a chemoattractant, drawing in neutrophils and leukocytes to an area.

Cytolysis

The lysis of foreign cells by the MAC (membrane attack complex) C6-C9.

Regulatory proteins in the complement system

They prevent the host cells from activating the complement system by inactivating C3b, keeping the body from attacking its own cells during an invasion.

Phagocyte Associate Molecular Patterns (PAMPS)

Structures or molecules that are commonly found on microbes and are easily recognized by phagocytes.

Pattern recognition receptors (PRR's & TLR's)

Receptors that sense signs of microbial invasions and trigger cytokine release.

Cytokine

A regulatory molecule that facilitates communication between cells by producing chemical messages in response to antigen detection.

Cytokine response to antigens

Stimulate hematopoiesis (formation of blood cells) and bind to cytokine receptors on other immune cells to activate cytokine production.

Chemokines

Cytokines made during inflammation that recruit white blood cells to the site of infection/inflammation.

Colony stimulating factors (CSF's)

Cytokines that multiply and differentiate leukocytes.

Interferons

Cytokines that control viral infections but are only released by virally infected cells.

Interleukins

Cytokines that are produced by leukocytes and adjust/regulate immune functions.

Tumor necrosis factors (TNFs)

Cytokines that aid in inflammation and apoptosis (cell suicide).

Types of cytokines

Chemokine, CSF, Interferon, Interleukin, TNF.

Types of Interferons

Type 1: interferon A & B, released by virally infected cells; Type 2: interferon y, released after A & B, alerts other immune cells of infection.

8 step methodology of the complement system

1) AB-AG complex is created. 2) AB-AG complex binds to C1, creates active enzyme and initiates cascade. 3) C1 cleaves into C2 and C4. 4) C2 and C4 join back together to create C3, which has two subunits (C3a + C3b). 5) C3b + C2 = C5, which has subunits (C5a + C5b). 6) C3b and C5b are opsonins. 7) C5a is a chemoattractant. 8) C5b alerts MAC C6-C9.

Hematopoiesis

Formation/development of blood cells that originate from stem cells in the bone marrow that have differentiated via CSF.

Cells of the immune system

Erythrocytes, Platelets, leukocytes.

Types of leukocytes

Granulocytes, Mononuclear phagocytes, Lymphocytes.

Lymphocytes

Leukocytes that recognize and respond to specific antigens.

Granulocytes

Leukocytes that contain granules full of chemicals to fight and trigger infection.

Mononuclear phagocytes

Individual phagocytes part of the mononuclear phagocyte system that mature into dendrites or macrophages when they leave the bloodstream.

Macrophage vs Dendrites

Macro: present always, scavenges for invaders to eat. Dendrite: scouts that only work in the body's external environment/mucus membranes.

Phagocytes

Cells that are recruited by chemoattractants secreted by other cells.

Chemoattractants

Substances that attract phagocytes to the site of infection.

Phagocytosis

The process by which phagocytes engulf and digest pathogens.

PAMPs

Pathogen-associated molecular patterns recognized by phagocytes.

Phagosome

A vesicle formed around an ingested particle during phagocytosis.

Exocytosis

The process by which remaining debris in phagocytes is expelled from the cell.

Inflammation

A response triggered by cell stress or damage caused by pathogen invasion or tissue damage.

Bradykinin

An inflammation mediator that binds to capillary receptors, causing vasodilation and increased blood vessel permeability.

Leukotrienes

Inflammation mediators that trigger symptoms to remove pathogens quickly, such as cough, vomiting, and diarrhea.

Histamine

A proinflammatory chemical that induces symptoms of inflammation.

Prostaglandins

Substances that develop at the site of tissue damage, causing and regulating inflammation.

Events of Inflammation

1) Vasoconstriction -> Vasodilation 2) Increased vascular permeability 3) Fluid leakage into the site 4) Five signs of inflammation arise 5) Immune cell recruitment 6) Diapedesis 7) Clotting factors wall off the site 8) Pus formation.

Acute Infection

Involves neutrophils for short-term inflammation, cleaned by macrophages.

Chronic Infection

Occurs when acute inflammation fails, leading to macrophages and granulomas attempting to fix the issue.

Mycobacterium tuberculosis

A bacterium that causes chronic inflammation by forming granulomas in the lungs.