Lecture 1: Acute & Chronic Infections Flashcards
What role do N-formylated peptides have in Neutrophil Signalling?
They play a major role as potent chemoattractants
What are N-formylated peptides recognised by?
Recognised by the macrophage
Where do N-formylated peptides originate from?
Degraded bacterial proteins
What changes occur in macrophages to allow for engulfing?
Changes in actin filaments
How do antigen presenting cells act?
Presenting antigenic determinants to T cells via MHC II proteins
(communication between T-helper and macrophage)
How do antigen presenting cells become effective ‘killers’?
They become up-regulated
What is involved in the acute response to infection?
Hypothalamus - fever, re-setting body temperature
Brain - somnulence
Vascular permeability changes - hypotension & shock
(tight junctions between blood capillaries opening up)
Mobilisation of WBC - neutrophilia
(from the bone marrow)
Enhancement of neutrophil killing mechanism
Release of acute phase proteins from liver
What are the characteristics of the chronic response to infection?
Muscle and fat mobilisation - weight loss
(chronic bacterial infections are a catabolic process)
Fibroblasts stimulated - healing and repair
(continued release of acute phase proteins)
What are the components of acute phase proteins and what is the role of each?
C-reactive protein, mannose binding lectin and fibrinogen
Mannose binding lectin: binds non-specifically to the surface of bacteria - aids phagocytic process
C-reactive protein: marker of the response to infection
Fibrinogen: increases erythrocyte sedimentation rate
What is the cause of the increased erythrocyte sedimentation rate in the acute response to infection?
Fibrinogen binds to red blood cells and causes them to sediment faster
What are the differences between the 3 complement activation pathways?
Classical pathway: antigen-antibody complexes (pathogen surfaces)
MB-lectin pathway: mannose-binding lectin binds mannose on pathogen surfaces
Alternative pathway: pathogen surfaces
What marker drives a pathogen for phagocytosis?
C3b
What do C3a and C5a do in the complement activation pathway?
Peptide mediators of inflammation
Phagocyte recruitment
What does C3b do in the complement activation pathway?
Binds to complement receptors on phagocytes
Opsonization of pathogens
Removal of immune complexes
What do the terminal complement components do?
Membrane-attack complex
Lysis of certain pathogen and cells