Using intravital microscopy to study the role of chemokines during infection and inflammation in the central nervous system

• Published in: Journal of neuroimmunology Vol. 224; no. 1; pp. 62 - 65
• Main Authors: Teixeira, Mauro M, Vilela, Marcia C, Soriani, Frederico M, Rodrigues, David H, Teixeira, Antonio L
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 27.07.2010
• Subjects: Allergy and Immunology; Animals; Brain; Central Nervous System Diseases - immunology; Central Nervous System Diseases - metabolism; Central Nervous System Diseases - pathology; Chemokines; Chemokines - analysis; Chemokines - physiology; Encephalitis, Herpes Simplex - immunology; Encephalitis, Herpes Simplex - metabolism; Encephalitis, Herpes Simplex - pathology; Encephalomyelitis, Autoimmune, Experimental - immunology; Encephalomyelitis, Autoimmune, Experimental - metabolism; Encephalomyelitis, Autoimmune, Experimental - pathology; Experimental autoimmune encephalomyelitis; Herpes simplex virus 1; HSV-1; Humans; Inflammation Mediators - analysis; Inflammation Mediators - physiology; Intravital microscopy; Microscopy, Fluorescence - methods; Neuroinflamamation; Neurology; Intravital microscopy; Neuroinflamamation; Experimental autoimmune encephalomyelitis; HSV-1; Chemokines
• ISSN: 0165-5728; 1872-8421
• DOI: 10.1016/j.jneuroim.2010.05.018

Abstract The interaction between a microorganism and a potential host may modify each other in multiple ways. Because of their central role in controlling leukocyte trafficking and activation, chemokines may be essential in defining these interactions. Here, we describe potential uses of intravital microscopy to define the role of chemokines and their receptors in the context of HSV-1 infection and EAE. We show that CCL5 plays a major role in driving neuropathology by mediating leukocyte adhesion and consequent migration in HSV-1 encephalitis. In contrast, CCR5 is important to attract cell types that modulate negatively CNS damage at the cost of allowing greater viral replication in the brain. Finally, intravital microscopy studies were crucial to determine that induction of leukocyte adhesion and subsequent emigration into the CNS is a major mechanism of action of CCL2 in EAE.