Intro to Inflammation and Infection Part 2 Flashcards
describe the specific inflammatory defense mechanisms/mediators of neutrophils
- phagocytosis: fuse with lysosome to create phagolysosome; reactive oxygen species generated
- degranulation
- neutrophil extracellular traps: microbicidal, released in response to cytokines (IL-8) and stimuli (LPS); contain enzymes to break down microbes
describe the specific inflammatory defense mechansims/mediators of eosinophils
eosinophils have hella products in their granules, but main one is major basic protein, which is cytotoxic to helminths!
describe the specific inflammatory defense mechansims/mediators of NK cells
these are innate lymphoid cells with 2 types of receptors:
1. activation receptor: recognized viral proteins, altered surface glycoproteins, and antibody-coated cells
2. inhibitory receptor: recognizes self via MHC I expressed on all nucleated cells (stop signal)
if inhibitory signal is absent, NK cells release lytic granules perforin and granzyme; perforin inserts into membrane and granzyme enters that pore and triggers apoptosis; NK cells also secrete IFN-gamma, which activates macrophages
recognize products of cell membrane damage and how they contribute to inflammation, identifying opportunities for pharmaceutical intervention
phospholipases break down cell membrane phospholipids and lead to downstream vasodilation: steroids inhibit these
phospholipases trigger arachidonic acid, which can trigger cyclooxygenase to release inflammatory prostaglandins, which can lead to inflammation, but COX-1 and COX-2 inhibitors, aspirin, and indomethacin inhibit cyclooxygenase
briefly describe neutrophil clearance mechanisms that lead to resolution of inflammation
neutrophil apoptosis is programmed cell death, a quiet cleanup by macrophages, and release of anti-inflammatory mediators to assist with resolution of inflammation
recognize that components of innate immune response can influence adaptive responses, and vice versa
- helper T cells influence and drive responses and also play a role in cytokine release
- cytotoxic T cells kill infected cells
- B cells produce antibodies that have many functions, but bridge divide between innate and immune via opsonizing targets for innate cells to kill too
describe clinical signs of inflammation, SIRS, and sepsis
inflammation: redness, heat, pain, swelling, loss of function
SIRS: two or more of: fever, increased heart rate, increased respiratory rate, increased WBC count
sepsis: SIRS plus a documented or highly suspected infection, can escalate to organ dysfunction, hypoperfusion, or hypotension, (severe sepsis) and then can escalate to multi organ dysfunction and unresponsive low BP (septic shock)