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level: Neutrophils and Macrophages

Questions and Answers List

level questions: Neutrophils and Macrophages

Question	Answer
Vasodilation slows blood flow in postcapillary venules and causes cells to marginate from center of flow to the periphery	Margination
Selectins on endothelial cells slow down the marginating cells	Rolling
From Weber-Palade bodies; Mediated by histamine	P-selectin
Induced by TNF and IL-1	E-selectin
Produces P-selectin and von Willebrand factor ("W"=willebrand, "P"=P-selectin)	Weber-Palade bodies
Binding site of selectins on leukocytes	Sialyl Lewis X
Firm adhesion of leukocytes on vessel wall due to interaction between CAMs and integrins	Adhesion
Intercellular/Vascular Cell Adhesion Molecule found on endothelium; upregulated by TNF and IL-1	ICAM, VCAM
Binding site of CAMs on leukocytesl upregulated by C5a and LTB4	Integrins
Autosomal recessive defect of CD 18 subunit of integrins; Manifests as delayed cord separation, increased circulating neutrophils, recurrent bacterial infection with no pus formation	Leukocyte Adhesion Deficiency
Leukocytes cross the endothelium of postcapillary venules and are attracted to chemotactic agents	Transmigration and Chemotaxis
Consumption of pathogens and necrotic tissue; Enhanced by opsonisation (IgG, C3b)	Phagocytosis
Autosomal recessive microtubule defect leading to a protein trafficking defect and impaired phagolysosome formation	Chediak Higashi Syndrome
Increased risk of pyogenic infections, neutropenia, giant granules in leukocytes, defective primary hemostasis, albinism, peripheral neuropathy	Clinical features of Chediak Higashi Syndrome
Most effective mechanism of destroying phagocytosed material	O2 dependent killing
Produces HOCl from H2O2	Myeloperoxidase
Conversion of superoxide from O2 by NADPH oxidase	Oxidative burst
Responsible for destruction of phagocytosed substance in O2 dependent killing	HOCl
Autosomal recessive or X-linked NADPH oxidase defect -> Poor O2 dependent killing	Chronic Granulomatous Disease (CGD)
Catalase positive bacteria associated with recurrent infection in CGD	Staph aureus, Pseudomonas cepacia, Serratia marcescens, Nocardia, Aspergillus
Screening test fo CGD	Nitroblue tetrazolium test
Increased risk for this infection in MPO deficiency; Generally asymptomatic	Candida infection
Enzyme in macrophage utilized in O2-independent killing	Lysozyme
Enzyme in eosinophil utilized in O2-independent killing	Major basic protein
Neutrophils undergo apoptosis within 24 hours	Resolution
Macrophages replace neutrophils and predominate	48-76 hours post-inflammation
Primary mechanism of destruction of phagocytosed materials by macrophages	O2-independent killing
Anti-inflammatory cytokines produced by macrophages for resolution and healing	IL-10, TGF-B
Cytokine produced by macrophages to recruit additional neutrophils -> persistent pus formation	IL-8
Produced by macrophages to stimulate abscess wall formation	FGF
Stimulated by macrophages through antigen presentation to CD4+ helper T cells	Chronic Inflammation