Laboratory medicine · 2022
Potential Role of Neutrophil-Platelet Interaction in Increased Susceptibility to Infection of Patients with Down Syndrome.
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Abd El-Ghany Hoda M, Abdel Meguid Iman Ehsan, El Hawary Rabab, Meshaal Safa, Shimila Iman Taha Lafy, Radwan Eman Roshdy
Аннотация
OBJECTIVE: Recurrent infection in Down syndrome (DS) has been previously documented; the potential role of platelets and neutrophil-platelet interaction has not been addressed in previous studies.
PATIENTS AND METHODS: Using flow cytometry, we evaluated CD40 and CD18 expression as activation markers for neutrophils and CD62p as an activation marker for platelets, before and after lipopolysaccharide (LPS) stimulation, in 34 patients with DS and 39 control patients.
RESULTS: Markers were evaluated as percentage of positivity, mean fluorescent intensity (MFI), and activation index (MFI after stimulation/MFI before stimulation). Patients showed a significantly lower CD40 MFI (P = .019) after LPS stimulation, a lower CD62p percentage before and after LPS stimulation (P = .013 and P = .029), and a higher CD62p MFI (P = .011) after LPS stimulation. Patients showed a lower activation index for CD40 and CD18 (P ≤ .001) but not for CD62p (P = .338). Dysfunctional efficiency in neutrophils and in the neutrophil-platelet interaction could not be correlated to infection.
CONCLUSION: A consensus on a scoring system for infection is needed for an objective evaluation of correlation to infection.
PATIENTS AND METHODS: Using flow cytometry, we evaluated CD40 and CD18 expression as activation markers for neutrophils and CD62p as an activation marker for platelets, before and after lipopolysaccharide (LPS) stimulation, in 34 patients with DS and 39 control patients.
RESULTS: Markers were evaluated as percentage of positivity, mean fluorescent intensity (MFI), and activation index (MFI after stimulation/MFI before stimulation). Patients showed a significantly lower CD40 MFI (P = .019) after LPS stimulation, a lower CD62p percentage before and after LPS stimulation (P = .013 and P = .029), and a higher CD62p MFI (P = .011) after LPS stimulation. Patients showed a lower activation index for CD40 and CD18 (P ≤ .001) but not for CD62p (P = .338). Dysfunctional efficiency in neutrophils and in the neutrophil-platelet interaction could not be correlated to infection.
CONCLUSION: A consensus on a scoring system for infection is needed for an objective evaluation of correlation to infection.