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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: Animals, Brain Stem, Chemokine CXCL10, Chemokine CXCL9, Chemokines, CXC, Cornea, Disease Susceptibility, Encephalitis, Herpes Simplex, Flow Cytometry, Herpesvirus 1, Human, Immunity, Innate, Keratitis, Herpetic, Mice, Mice, Inbred BALB C, Mice, Inbred C57BL, Receptors, CXCR3, Receptors, Chemokine, Reverse Transcriptase Polymerase Chain Reaction, Signal Transduction, Skin Diseases, Viral, Trigeminal Ganglion, Up-Regulation.
user
Are effects of CXCR3 signaling on development of fatal encephalitis and corneal and periocular skin disease in HSV-infected mice mouse-strain dependent? Context: The host inflammatory response to ocular infection with herpes simplex virus (HSV) can be either protective, with disease-free survival, or it can promote diseases such as HSV corneal disease (or herpes stromal keratitis [HSK] in humans) and encephalitis (HSE), depending on mouse strain. The role of CXCR3 chemokine signaling in HSV-induced central nervous system (CNS) inflammation and corneal disease was evaluated, and responses in genetically susceptible and resistant strains of mice were contrasted. Resistant C57BL/6J (B6) and susceptible 129S6 (129) mice were given monoclonal antibodies (mAbs) to neutralize the CXCR3 ligands monokine induced by interferon-gamma (MIG, CXCL9) and interferon inducible protein-10 (IP-10, CXCL10) during HSV infection. In addition, the development of HSV disease was monitored in CXCR3-null mutant mice derived from resistant (B6) and susceptible (BALB/c) strains. Inflammatory cells infiltrating the cornea and brain stem were isolated and stained for flow cytometric analysis. MIG and IP-10 were induced in nervous system tissue after HSV inoculation by the corneal route. HSV-infected 129 mice treated with MIG- or IP-10-neutralizing mAbs showed significantly enhanced survival compared with mice treated with control isotype antibody, whereas survival of the B6 mice was unaltered. Similarly, greater survival was observed for BALB.CXCR3(-/-) mice compared with control BALB/c mice. Reduced CNS inflammation was documented that extended to the cornea, such that HSV corneal disease severity was reduced in susceptible BALB.CXCR3(-/-). In contrast, although survival of B6 and B6.CXCR3(-/-) mice was indistinguishable, B6.CXCR3(-/-) mice developed more severe corneal and periocular skin disease.
assistant
The effects of CXCR3 signaling in HSV infection are strongly dependent on mouse strain. Final Decision: yes