2.5 Chemotaxis Flashcards
(62 cards)
Chemotaxis
movement of a cell up a concentration gradient of a signal. When receptors bind their ligand they lock and aggregate so binding on on side leads the cells in that direction
mediators of chemotaxis
bacterial wall product - n-formyl-methionine terminal amino acid which is specifically in bacteria, endogenous inflammatory mediators - C5a, leukotrienes (LTB4), chemokines (IL8)
leukocyte receptors
7TM Gprotein coupled receptors, TLRs (10)
7 transmembrane g - protein coupled receptors bind
n-formylmethinyl residues, and a number of cytokines and other inflammatory mediators such as C5a and LTB4. (chemotaxis)
TLRs are linked to CD14 bind
bacterial products like: LPS, unmethylated CpG sequences and double stranded RNAs (leukocyte activation and function changes)
cytokine receptor binds
cytokines
phagocitic receptor binds
probably opsonins
7tm receptor initiates
cytoskeletal changes
7tm downstream signal transduction
increased integrin avidity –> adhesion to endothelium, chemotaxis –>migration into tissues
TLRs and cytokine receptsr lead to
production of mediators like arachidonic acid metabolites and cytokines, production of ROS and lysosomal enzymes
TLR–>mediators like AA metabolites and cytokines lead to
amplification of the inflammatory reaction
TLR–>production of ROS and lysosomal enzymes leads to
leukocyte activation –> killing of microbes
phagocytic receptor binding leads to
production of ROS and lysosomal enzymes, phagocytosis of mocrobe into phagosome
phagocytic receptor –> ROS production and phagocytosis of micorbe leads to –>
leukocyte activation –> killing of microbes
mechanisms of chemoattractants
receptor-ligand interaction, cytoskeletal modulation, intra-cellular ca2+ concentration - a major factor in actin and myosin assemble and disassembly
ex of gprotein signal
binding to rec –> PLC –> PIP2 –> DAG + IP3 –> inc intracellular Ca++
in alveolar space bacteria cause
acute inflammation and recruitment of neutrophils. The bacteria can survive in the spaces themselves so you’ll see a flood of neutorphils
in alveolar space viruses cause
chronic inflammation and recrutiment of lymphocytes. Viruses need host cells so you see lypmphocyte accumulation in interstitium, not in acutaly spaces
next step after chemotaxis
leukocyte activation and phagocytosis
leukocyte activation
aquiring additional functions induced by chemical mediators such as: production of arachidonic acid products, degranulation and secretion of enzymes, activation of oxidative burst, secretion of cytokines, modulation of adhesion molecules, mediated mostly by TLRs and cytokine receptors
how can you die due to leukocyte activation
if enough LPS leaks out all the macs will get activated releasing inflammatory mediators sending you into septic shock
phagocytosis
recognition/attachment, engulfment - energy dependant, degredation/killing
recognition of what to eat by
complement and Ig opsonins
leukocytes + bacteria
nothing happens
