Microbio 310 1st Edition Lecture 25Outline of Last Lecture I. 28.1 Cells and Organs of the Immune SystemII. 28.2 Innate ImmunityIII. 28.3 Adaptive ImmunityIV. 28.4 AntibodiesOutline of Current Lecture I. 28.5 InflammationII. 28.6 Natural ImmunityIII. 28.7 Artificial Immunity and ImmunizationIV. 28.9 Allergy, Hypersensitivity, and AutoimmunityV. 28.10 Superantigens: Overactivation of T cellsCurrent Lecture28.5 Inflammation• Inflammation is a nonspecific reaction to noxious stimuli– Redness, swelling, pain, and heat localized at site of infection• Molecular mediators of inflammation are proteins called cytokines and chemokines(signaling molecules)– Effective inflammatory response isolates and limits tissue damage, destroying damaged cells and pathogensThese notes represent a detailed interpretation of the professor’s lecture. GradeBuddy is best used as a supplement to your own notes, not as a substitute.– Inflammation can result in considerable damage to healthy tissue (overproduction of free radicals)• Neutrophils are the first to arrive at infection– Attracted to site by interleukins• Activated neutrophils release chemokines to recruit macrophages by guiding them along a chemokine gradient (move in direction of higher concentrations)• Usual outcome of inflammation is a rapid localization and destruction of pathogen• In some cases inflammation fails to localize pathogen and the reaction becomes widespread– Can lead to septic shock, a life-threatening condition where blood pressure drops and organs fail• Systemic inflammatory reactions may have serious consequences– Uncontrollable fever (proteins denature because temp is too high)– Death in up to 30% of individuals• Septic shock can be more dangerous than the initial infection• (localized heat VS whole body --heart failure)28.6 Natural Immunity• Animals normally develop– Natural active immunity• By acquiring an infection that initiates an adaptive immune response – Natural passive immunity(passive=going to wear off)• Through antibody transfer across the placenta or in breast milk• Immune Deficiencies (ways that the immune system goes wrong)– Agammaglobulinemia - patients cannot produce antibodies because of genetic defects in theirB cells– DiGeorge’s syndrome - a developmental defect that prevents maturation of the thymusand inhibits production of mature T cells– The lack of an adaptive immune response is observed in individuals with acquired immunodeficiency syndrome (AIDS)28.7 Artificial Immunity and Immunization• Artificial induction of immunity to individual infectious diseases is a major weapon in the treatment and prevention of diseases– Artificial active immunity (vaccination)• Exposure to a controlled dose of a harmless antigen to induce formation of antibodies – Artificial passive immunity• Injection of an antiserum (serum containing antibodies) derived from an immune individual (rabies-treated with hyper immune serum, Ebola)• Immunization– The process of generating an artificial active immune response by exposure to an antigen or antigen mixture (vaccine)• Immunization with live cells or virus is usually more effective than that with dead or inactivated material (more antigen around, more likely to activate the immune system)• Most agents used for immunization are either attenuated (weakened) or inactivated pathogens or inactivated forms of microbial products such as toxins (Toxoid)• The importance of immunizations in controlling infectious diseases is well established- Immunizations usually involve a series of secondary or “booster” immunizations to produce a secondary response and a higher antibody titer- Whooping Cough-now a subunit (acellular vaccine/only a portion) vaccine; we should have gotten a booster in high school because the subunit vaccine doesn’t work as well28.9 Allergy, Hypersensitivity, and Autoimmunity• Hypersensitivity– Inappropriate immune response that results in host damage• Hypersensitivity diseases are categorized according to antigens and effector mechanisms that produce disease• Allergy: antibody-mediated immediate hypersensitivity (type I hypersensitivity)– Caused by release of vasoactive products from IgE antibody-coated mast cells– Reactions occur within minutes after exposure to antigen– Can be mild to life-threatening (e.g., anaphylaxis—swelling, throat closing)– ~20% of population suffers from allergies to a wide variety of agents• ImmediateHypersensitivityAllergens – Pollen and fungal spores– Insect venom (bee sting)– Certain foods– Animal dander – Dust mites• Delayed-type hypersensitivity• (DTH; type IV hypersensitivity)– Cell-mediated hypersensitivity characterized by tissue damage due to inflammatory responses produced by TH1 inflammatory cells– Symptoms appear several hours following secondary exposure to eliciting antigens– Typical antigens include microbes, self antigens, and chemicals that covalently bind to skin, creating new antigens (i.e., contact dermatitis)- Type IV Hypersensitivity– Multiple Sclerosis– Rheumatoid arthritis– Type I Diabetes-immunological insulin; disregulation of the immune response where your body attacks the pancreatic beta cells that are producing insulin– Crohn’s disease– Poison ivy (Urushiol-active/allergic component)– Celiac-inflammation of the bowel associated with specific MHC class types; 1% of population have this• Autoimmune diseases– Occur when T and B cells are activated to produce immune reactions against self-proteins– Result in host tissue damage– Some diseases caused by autoantibodies, antibodies that interact with self antigens– Cytotoxic hypersensitivity – Type II• Juvenile diabetes• Antibodies (IgG) against cell surface antigen– Immune complex hypersensitivity - Type III• Systemic lupus erythematosus (SLE)• Antibodies (IgG) against soluble or circulating antigen28.10 Superantigens: Overactivation of T Cells• GAS group A streptococci • Toxic Shock syndrome (TSS)-caused by a strain of Staphylococcus aureus• Superantigens– Proteins capable of eliciting a strong response because they activate more T cells than a normal immune response– Produced by many viruses and bacteria that interact with TCRs– Superantigen-activated T cells may produce systemic diseases characterized by systemic inflammatory