Page 164 - Veterinary Immunology, 10th Edition
P. 164

neutrophil emigration from blood vessels. The release of HMGB1
  VetBooks.ir  and other damage-associated molecular patterns (DAMPs) from

               damaged tissues stimulates macrophages to produce TNF-α and IL-
               6 as well as neutrophil chemotactic chemokines and reactive

               oxygen species (ROS).
                  Exosomes are small cytoplasmic vesicles, about 50 to 100 nm in
               diameter, that can transmit signals between cells. They are released
               by stimulated macrophages, dendritic cells, and B cells. These

               exosomes carry with them a mixture of immunostimulatory and
               proinflammatory molecules. They can spread through the
               extracellular fluid and interact with nearby cells. Thus exosomes
               from macrophages containing ingested bacteria can express

               bacterial cell wall components such as glycopeptidolipids and other
               pathogen-associated molecular patterns (PAMPs) on their surfaces.
               These exosomes can bind to PRRs on nearby neutrophils and
               macrophages, triggering the release of TNF-α and iNOS, and

               promoting more inflammation.



               Phagocytosis

               When microbial invasion occurs and inflammation develops, blood
               monocytes respond to PAMPs and DAMPs by binding to vascular

               endothelial cells in a manner similar to their partners, the
               neutrophils. Thus adherence and rolling are triggered by selectin
               binding, and the cells are brought to a gradual halt by integrins

               binding to ligands on vascular endothelial cells. The monocytes
               bind to endothelial cell intracellular adhesion molecule-1 (ICAM-1)
               by using their β -integrins and then emigrate into the tissues (and
                                    2
               change their name to macrophages). Several hours after neutrophils
               have entered an inflammatory site, the macrophages arrive.
               Neutrophils can reach targets in damaged tissues within 3 to 4
               hours. Macrophages require at least 12 hours. These macrophages

               are attracted not only by bacterial products and complement
               components such as C5a but also by DAMPs from damaged cells
               and tissues. Once neutrophils have emigrated into tissues, they too
               attract macrophages. Thus neutrophil granules contain macrophage
               chemoattractants such as azurocidin and cathelicidins. Activated

               neutrophils and endothelial cells also produce monocyte





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