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Understanding how leading bacterial pathogens subvert innate immunity to reveal novel therapeutic targets
Reviews and feature articles
Continuing Medical Education examination
Understanding how leading bacterial pathogens subvert innate immunity to reveal novel therapeutic targets Instructions for category 1 Continuing Medical Education credit The American Academy of Allergy, Asthma & Immunology is accredited as a provider of Continuing Medical Education (CME) by the Accreditation Council for Continuing Medical Education. Test ID no.: mai00120 Contact hours: 1.5 Expiration date: June 30, 2009 Category 1 credit can be earned by reading the text material and taking this CME examination online. For complete instructions, visit the Journal’s Web site at www.jacionline.org.
The Editors thank the University of Pennsylvania Allergy/Immunology training program for developing this CME examination. The individuals who contributed to its preparation were Pierre Yong, MD, Sumita Roy-Ghanta, MD, and Arnold I. Levinson, MD.
Learning objectives: ‘‘Understanding how leading bacterial pathogens subvert innate immunity to reveal novel therapeutic targets’’ 1. To learn general concepts, as well as specific information, about the methods used by Staphylococcus aureus (SA) and Group A Streptococcus (GAS) to evade the immune system. 2. To discern the advantages of targeting the host innate immune system in the therapeutic treatment of SA- or GAS-induced disease.
CME items Question 1. How do polysaccharide capsules on SA and GAS surfaces help these bacteria evade the immune system? A. They promote deposition of complement factors on the bacterial surface. B. They serve as a superficial ‘‘cloak,’’ limiting phagocyte access to opsonins on bacteria’s surface. C. They bind the Fc portion of immunoglobulin, thereby presenting the immunoglobulin in a ‘‘backwards,’’ nonopsonic manner. D. They allow bacteria to escape from neutrophil phagosomes into the cytoplasm. Question 2. Which protein has been associated with severe cases of community-acquired methicillin-resistant Staphylococcus aureus? A. bacteriophage encoded Panton-Valentine leukocidin (PVL) B. g-hemolysin C. streptolysin O D. M protein
J ALLERGY CLIN IMMUNOL
Question 3. What is the advantage of targeting host molecules that enhance phagocytic recruitment or activation as part of a novel therapeutic approach? A. increased efficacy of antimicrobials B. limited inflammatory damage to host tissues C. decreased risk of bacterial resistance D. targeting a specific pathogen Question 4. Which of the following is not a virulence factor used by SA and/or GAS to evade the host innate immune system? A. electrostatic repulsion of host cationic antimicrobial peptides B. production of proteases that can cleave chemokines, such as IL-8 C. prevention of antibody-directed cellular cytotoxicity by binding the Fc portion of IgG D. binding of vitronectin, which decreases the accumulation of surface C3 convertase
July 2007
23
24 Nizet
Reviews and feature articles
Question 5. Which of the following are not methods used by SA and/or GAS to interfere with antibody-mediated opsonization or phagocytosis? A. expression of proteases that can cleave immunoglobulins B. blockage of CD16 (FcgRIII) on neutrophils inhibiting phagocytosis C. acquiring resistance to pathogen specific IgG through mutation of M proteins D. hydrolysis of IgG, preventing recognition of the immunoglobulin by phagocyte Fc receptors Question 6. How does the golden pigment of a carotenoid molecule promote bacterial survival? A. by providing antioxidant properties B. by acting as a cofactor in bacterial superoxide dismutase C. by decreasing the stability of surface C3 convertases D. by enhancing bacterial degradation of neutrophil extracellular traps Question 7. Which of the following families of molecules has been incriminated in bacterial superinfection in atopic dermatitis? A. antimicrobial peptides B. antibodies C. complement proteins D. collectins
J ALLERGY CLIN IMMUNOL JULY 2007
Question 8. Which of the following is the strongest and most specific host-derived stimulus for neutrophil chemotaxis? A. extracellular adherance protein B. IL-8 C. intercellular adhesion molecule 1 D. surface dehydrogenase Question 9. How does Fba promote the survival of GAS? A. It mediates binding to complement regulatory proteins. B. It interferes with IL-8 activity. C. It inhibits phagosome maturation. D. It inhibits antibody-dependent cellular cytoxicity. Question 10. Which therapy has been shown to increase cathelicidin expression in the skin? A. innate defense regulator peptide-1 B. salicylic acid C. synthetic thiolactone D. vitamin D
Continuing Medical Education examination
Understanding how leading bacterial pathogens subvert innate immunity to reveal novel therapeutic targets Instructions for category 1 Continuing Medical Education credit The American Academy of Allergy, Asthma & Immunology is accredited as a provider of Continuing Medical Education (CME) by the Accreditation Council for Continuing Medical Education. Test ID no.: mai00120 Contact hours: 1.5 Expiration date: June 30, 2009 Category 1 credit can be earned by reading the text material and taking this CME examination online. For complete instructions, visit the Journal’s Web site at www.jacionline.org.
The Editors thank the University of Pennsylvania Allergy/Immunology training program for developing this CME examination. The individuals who contributed to its preparation were Pierre Yong, MD, Sumita Roy-Ghanta, MD, and Arnold I. Levinson, MD.
Learning objectives: ‘‘Understanding how leading bacterial pathogens subvert innate immunity to reveal novel therapeutic targets’’ 1. To learn general concepts, as well as specific information, about the methods used by Staphylococcus aureus (SA) and Group A Streptococcus (GAS) to evade the immune system. 2. To discern the advantages of targeting the host innate immune system in the therapeutic treatment of SA- or GAS-induced disease.
CME items Question 1. How do polysaccharide capsules on SA and GAS surfaces help these bacteria evade the immune system? A. They promote deposition of complement factors on the bacterial surface. B. They serve as a superficial ‘‘cloak,’’ limiting phagocyte access to opsonins on bacteria’s surface. C. They bind the Fc portion of immunoglobulin, thereby presenting the immunoglobulin in a ‘‘backwards,’’ nonopsonic manner. D. They allow bacteria to escape from neutrophil phagosomes into the cytoplasm. Question 2. Which protein has been associated with severe cases of community-acquired methicillin-resistant Staphylococcus aureus? A. bacteriophage encoded Panton-Valentine leukocidin (PVL) B. g-hemolysin C. streptolysin O D. M protein
J ALLERGY CLIN IMMUNOL
Question 3. What is the advantage of targeting host molecules that enhance phagocytic recruitment or activation as part of a novel therapeutic approach? A. increased efficacy of antimicrobials B. limited inflammatory damage to host tissues C. decreased risk of bacterial resistance D. targeting a specific pathogen Question 4. Which of the following is not a virulence factor used by SA and/or GAS to evade the host innate immune system? A. electrostatic repulsion of host cationic antimicrobial peptides B. production of proteases that can cleave chemokines, such as IL-8 C. prevention of antibody-directed cellular cytotoxicity by binding the Fc portion of IgG D. binding of vitronectin, which decreases the accumulation of surface C3 convertase
July 2007
23
24 Nizet
Reviews and feature articles
Question 5. Which of the following are not methods used by SA and/or GAS to interfere with antibody-mediated opsonization or phagocytosis? A. expression of proteases that can cleave immunoglobulins B. blockage of CD16 (FcgRIII) on neutrophils inhibiting phagocytosis C. acquiring resistance to pathogen specific IgG through mutation of M proteins D. hydrolysis of IgG, preventing recognition of the immunoglobulin by phagocyte Fc receptors Question 6. How does the golden pigment of a carotenoid molecule promote bacterial survival? A. by providing antioxidant properties B. by acting as a cofactor in bacterial superoxide dismutase C. by decreasing the stability of surface C3 convertases D. by enhancing bacterial degradation of neutrophil extracellular traps Question 7. Which of the following families of molecules has been incriminated in bacterial superinfection in atopic dermatitis? A. antimicrobial peptides B. antibodies C. complement proteins D. collectins
J ALLERGY CLIN IMMUNOL JULY 2007
Question 8. Which of the following is the strongest and most specific host-derived stimulus for neutrophil chemotaxis? A. extracellular adherance protein B. IL-8 C. intercellular adhesion molecule 1 D. surface dehydrogenase Question 9. How does Fba promote the survival of GAS? A. It mediates binding to complement regulatory proteins. B. It interferes with IL-8 activity. C. It inhibits phagosome maturation. D. It inhibits antibody-dependent cellular cytoxicity. Question 10. Which therapy has been shown to increase cathelicidin expression in the skin? A. innate defense regulator peptide-1 B. salicylic acid C. synthetic thiolactone D. vitamin D