RT Book, Section
A1 Warren, Jeffrey S.
A1 Ward, Peter A.
A2 Kaushansky, Kenneth
A2 Lichtman, Marshall A.
A2 Prchal, Josef T.
A2 Levi, Marcel M.
A2 Press, Oliver W.
A2 Burns, Linda J.
A2 Caligiuri, Michael
SR Print(0)
ID 1121089968
T1 The Inflammatory Response
T2 Williams Hematology, 9e
YR 2015
FD 2015
PB McGraw-Hill Education
PP New York, NY
SN 9780071833004
LK accessmedicine.mhmedical.com/content.aspx?aid=1121089968
RD 2024/04/24
AB SUMMARYThe  acute  inflammatory  response  is  characterized  by  a  rapid  but  relatively  short-lived  localized  increase  in  blood  flow,  an  increase  in  microvascular  permeability  and  the  sequential  recruitment  of  different  types  of  leukocytes.  Acute  inflammation  may  be  followed  by  “chronic”  inflammation  and  a  superimposed  series  of  reparative  processes  (e.g.,  angiogenesis,  production  of  extracellular  matrix,  parenchymal  regeneration  and  scar  formation).  The  early  hemodynamic  changes  at  a  site  of  inflammation  establish  low  shear  conditions  that  enable  marginated  leukocytes  to  engage  in  low-affinity  selectin-mediated  rolling  interactions  with  activated  endothelial  cells.  In  response  to  locally  produced  soluble  and  cell  surface  mediators,  endothelial  cells  and  rolling  leukocytes  sequentially  express  several  sets  of  complementary  adhesion  molecules  that  include  selectins,  integrins,  and  members  of  the  immunoglobulin  superfamily.  Leukocyte  and  endothelial  cell  adhesion  molecules  mediate  the  high-affinity  adhesive  interactions  necessary  for  leukocyte  emigration  from  the  vascular  space  along  chemotactic  gradients.  Analogous,  temporally  regulated,  soluble  mediators  and  cellular  adhesion  molecules  also  orchestrate  succeeding  monocyte-  and  lymphocyte-rich  chronic  inflammatory  responses.  This  paradigm  is  modulated  by  a  vast  network  of  surface-active  and  soluble  inflammatory  mediators.  Recruited  leukocytes  and  cells  indigenous  to  the  anatomic  site  of  inflammation  both  play  critical  roles  in  host  defense,  resolution  of  inflammation  and  tissue  repair.