Kyle B Walsh1, Begoña Campos2, Kimberly Hart3, Charuhas Thakar4, Opeolu Adeoye5. 1. Department of Emergency Medicine, University of Cincinnati (UC), Cincinnati, Ohio; UC Neuroscience Institute, Cincinnati, Ohio. Electronic address: walshk4@ucmail.uc.edu. 2. Department of Internal Medicine, Division of Nephrology, UC, Cincinnati, Ohio; UC Kidney C.A.R.E. (Clinical Advancement, Research & Education) Program, Cincinnati, Ohio. 3. Department of Emergency Medicine, University of Cincinnati (UC), Cincinnati, Ohio. 4. Department of Internal Medicine, Division of Nephrology, UC, Cincinnati, Ohio; UC Kidney C.A.R.E. (Clinical Advancement, Research & Education) Program, Cincinnati, Ohio; Cincinnati VA Medical Center, Cincinnati, Ohio. 5. Department of Emergency Medicine, University of Cincinnati (UC), Cincinnati, Ohio; UC Neuroscience Institute, Cincinnati, Ohio.
Abstract
BACKGROUND: Intracerebral hemorrhage (ICH) is a severe neurologic condition with no proven treatment. Recent evidence suggests that monocytes, a heterogenous group of cells with M1 and M2 phenotypes, contribute to secondary damage following ICH. Microparticles are vesicles .1-1 µm in size that are released from cells. We hypothesized that M1 and M2 monocyte microparticles (mMP) would be differentially expressed in ICH cases and controls. METHODS: In a single-center, prospective, observational study, consecutive ICH cases were enrolled within 12 hours of symptom onset. Age (±5 years)-, race-, and sex-matched controls were recruited. M1 and M2 mMP numbers were determined in plasma samples using flow cytometry and protein biomarkers using standardized assays. The Mann-Whitney U test compared M1 and M2 mMP counts between cases and controls. Standardized regression coefficients compared M1 and M2 mMP with C-reactive protein (CRP) and serum amyloid A (SAA). RESULTS: Nineteen ICH case-control pairs were enrolled. The median number of M1 mMP was not significantly different between ICH cases (8.63 × 107/milliliter (mL)) compared with controls (8.64 × 107/mL), (P = .525). The median number of M2 mMP was significantly higher in ICH cases (1.61 × 106/mL) compared with controls (4.46 × 105/mL) (P = .027). There were no significant associations for M1 or M2 mMP with CRP or SAA. CONCLUSION: Higher numbers of M2 mMP in ICH cases compared with controls is hypothesis generating. It may represent differences in the chronic inflammatory status in patients susceptible to ICH, such as cellular activation or apoptosis. Further research is needed, including serial plasma samples, to elucidate the pathophysiology of monocytes and mMP following ICH.
BACKGROUND:Intracerebral hemorrhage (ICH) is a severe neurologic condition with no proven treatment. Recent evidence suggests that monocytes, a heterogenous group of cells with M1 and M2 phenotypes, contribute to secondary damage following ICH. Microparticles are vesicles .1-1 µm in size that are released from cells. We hypothesized that M1 and M2 monocyte microparticles (mMP) would be differentially expressed in ICH cases and controls. METHODS: In a single-center, prospective, observational study, consecutive ICH cases were enrolled within 12 hours of symptom onset. Age (±5 years)-, race-, and sex-matched controls were recruited. M1 and M2 mMP numbers were determined in plasma samples using flow cytometry and protein biomarkers using standardized assays. The Mann-Whitney U test compared M1 and M2 mMP counts between cases and controls. Standardized regression coefficients compared M1 and M2 mMP with C-reactive protein (CRP) and serum amyloid A (SAA). RESULTS: Nineteen ICH case-control pairs were enrolled. The median number of M1 mMP was not significantly different between ICH cases (8.63 × 107/milliliter (mL)) compared with controls (8.64 × 107/mL), (P = .525). The median number of M2 mMP was significantly higher in ICH cases (1.61 × 106/mL) compared with controls (4.46 × 105/mL) (P = .027). There were no significant associations for M1 or M2 mMP with CRP or SAA. CONCLUSION: Higher numbers of M2 mMP in ICH cases compared with controls is hypothesis generating. It may represent differences in the chronic inflammatory status in patients susceptible to ICH, such as cellular activation or apoptosis. Further research is needed, including serial plasma samples, to elucidate the pathophysiology of monocytes and mMP following ICH.
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