BACKGROUND/AIMS: Chemokines play a critical role in inflammation and neurodegenerative disease in the central nervous system. In this study, endotoxin-induced uveitis (EIU) was induced to test the expression of fractalkine, a special neuronal chemokine, and its receptor CX3CR1 in acute inflammation of the retina. METHODS: EIU was induced by footpad injections of lipopolysaccharide (LPS). Eight rats were sacrificed at each time point (0, 8, 16, 24, 48, and 72 h) after LPS injection. Sections were made for histopathological tests. Immunohistochemistry was performed using antibodies specific to fractalkine and CX3CR1. Retinas were collected, and total protein and mRNA from both the induced and control rats were extracted. mRNA and protein expression of fractalkine and CX3CR1 in the retina were determined by reverse transcription-polymerase chain reaction (RT-PCR) and Western blots, respectively. RESULTS: The EIU model was successfully induced. In control rats, both fractalkine and its receptor CX3CR1 were detected in the retina. LPS injection induced a transient upregulation of both proteins at 24 h as determined by the increased number of positively stained cells as well as increased levels of mRNA and protein (p < 0.05). CONCLUSION: A transitory increased expression of fractalkine and its receptor CX3CR1 occurred at the crest time of EIU, and this change in expression may play a role in the turnover of LPS-induced acute retina inflammation.
BACKGROUND/AIMS: Chemokines play a critical role in inflammation and neurodegenerative disease in the central nervous system. In this study, endotoxin-induced uveitis (EIU) was induced to test the expression of fractalkine, a special neuronal chemokine, and its receptor CX3CR1 in acute inflammation of the retina. METHODS: EIU was induced by footpad injections of lipopolysaccharide (LPS). Eight rats were sacrificed at each time point (0, 8, 16, 24, 48, and 72 h) after LPS injection. Sections were made for histopathological tests. Immunohistochemistry was performed using antibodies specific to fractalkine and CX3CR1. Retinas were collected, and total protein and mRNA from both the induced and control rats were extracted. mRNA and protein expression of fractalkine and CX3CR1 in the retina were determined by reverse transcription-polymerase chain reaction (RT-PCR) and Western blots, respectively. RESULTS: The EIU model was successfully induced. In control rats, both fractalkine and its receptor CX3CR1 were detected in the retina. LPS injection induced a transient upregulation of both proteins at 24 h as determined by the increased number of positively stained cells as well as increased levels of mRNA and protein (p < 0.05). CONCLUSION: A transitory increased expression of fractalkine and its receptor CX3CR1 occurred at the crest time of EIU, and this change in expression may play a role in the turnover of LPS-induced acute retina inflammation.