title: CX3CR1 signaling on monocytes is dispensable after intracerebral hemorrhage.
abstract: Intracerebral hemorrhage is a subset of stroke for which there is no specific treatment. The Ly6Chi CCR2+ monocytes have been shown to contribute to acute injury after intracerebral hemorrhage. The other murine monocyte subset expresses CX3CR1 and lower Ly6C levels, and contributes to repair in other disease models. We hypothesized that the Ly6Clo CX3CR1+ monocytes would contribute to recovery after intracerebral hemorrhage. Intracerebral hemorrhage was modeled by blood injection in WT and CX3CR1-null bone marrow chimeras. Neurological outcomes and leukocyte recruitment were quantified at various time points. Functional outcomes were equal at 1, 3, 7, and 14 days after intracerebral hemorrhage in both genotypes. No differences were observed in leukocyte recruitment between genotypes on either 3 or 7 days after intracerebral hemorrhage. A few hundred Ly6Clo monocytes were found in the ipsilateral hemisphere in each genotype and they did not change over time. Peripherally derived CX3CR1+ monocytes were observed in the perihematomal brain 7 and 14 days after intracerebral hemorrhage. Our data suggests CX3CR1 signaling on monocytes does not play an influential role in acute injury or functional recovery after intracerebral hemorrhage and therefore CX3CR1 is not a therapeutic target to improve outcome after intracerebral hemorrhage.
authors.affiliation: Department of Immunology, University of Connecticut Health Center, Farmington, Connecticut, United States of America; Department of Neurology, Yale University School of Medicine, New Haven, Connecticut, United States of America.
authors.forename: Roslyn A
authors.initials: RA
authors.lastname: Taylor
authors.affiliation: Department of Neurology, Yale University School of Medicine, New Haven, Connecticut, United States of America; Department of Neuroscience, University of Connecticut Health Center, Farmington, Connecticut, United States of America.
authors.forename: Matthew D
authors.initials: MD
authors.lastname: Hammond
authors.affiliation: Department of Neurology, Yale University School of Medicine, New Haven, Connecticut, United States of America.
authors.forename: Youxi
authors.initials: Y
authors.lastname: Ai
authors.affiliation: Department of Neurology, Yale University School of Medicine, New Haven, Connecticut, United States of America.
authors.forename: Lauren H
authors.initials: LH
authors.lastname: Sansing
mesh_terms: D000818:Animals; D001921:Brain / Q000378:metabolism / Q000473:pathology; D000073883:CX3C Chemokine Receptor 1; D002543:Cerebral Hemorrhage / Q000378:metabolism* / Q000473:pathology; D008297:Male; D057507:Mice, 129 Strain; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic; D009000:Monocytes / Q000378:metabolism*; D019707:Receptors, Chemokine / Q000502:physiology*; D015398:Signal Transduction
chemical_list: D000073883:CX3C Chemokine Receptor 1; C471885:Cx3cr1 protein, mouse; D019707:Receptors, Chemokine