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The immunoregulatory abilities of polymorphonuclear neutrophils in the course of multiple sclerosis
Abstract:
The polymorphonuclear neutrophils (PMN) possess sufficient potential to affect both immune response and inflammation, however it has not been yet described in the course of multiple sclerosis (MS). We have studied binding of fluorescein isothiocyanate (FITC)- stained TNF-alpha by PMN, the expression of CD11a, CD11b, and CD18 molecules of beta2-integrines and the expression of CD10 (neutral endopeptidase-NEP) and of CD13 (aminopeptidase N; APN) antigens on PMN in three different groups of MS patients. The control group included neurological patients (OND) with noninflammatory diseases. The obtained results have proved that during MS exacerbation and in the course of chronic progressive MS, PMN reveal several forms of preactivation, including significantly higher stained-TNF-alpha binding, higher expression of CD11b and CD18, as well as CD10 and CD13 antigens, in comparison with MS remission or OND. We suggest that the increased expression of these molecules on PMN of MS patients in exacerbation of the disease and to a lower degree in the course of CP-MS is a result of PMN priming, and directly prove the PMN involvement in the disease pathogenesis.
Insights
Polymorphonuclear neutrophils (PMN) show preactivation during multiple sclerosis (MS) exacerbation and chronic progressive MS. This involves increased TNF-alpha binding and expression of specific immune molecules, suggesting PMN involvement in MS pathogenesis.
Area of Science:
- Immunology
- Neuroscience
- Cell Biology
Background:
- Polymorphonuclear neutrophils (PMN) play a key role in immune responses and inflammation.
- Their specific involvement in multiple sclerosis (MS) pathogenesis has not been fully elucidated.
- Understanding PMN behavior in MS can offer insights into disease mechanisms.
Purpose of the Study:
- To investigate the expression of specific molecules on PMN in patients with multiple sclerosis (MS).
- To assess PMN binding of TNF-alpha and expression of beta2-integrins (CD11a, CD11b, CD18) and antigens CD10/CD13.
- To compare these markers in different MS disease courses (exacerbation, chronic progressive, remission) versus controls.
Main Methods:
- Flow cytometry was used to analyze PMN.
- Studied were the binding of fluorescein isothiocyanate (FITC)-stained TNF-alpha.
- Assessed expression of CD11a, CD11b, CD18, CD10 (neutral endopeptidase-NEP), and CD13 (aminopeptidase N; APN) antigens.
Main Results:
- PMN from MS patients in exacerbation and chronic progressive MS showed significantly higher stained-TNF-alpha binding compared to MS remission or other neurological diseases (OND) patients.
- Elevated expression of CD11b, CD18, CD10, and CD13 antigens was observed on PMN during MS exacerbation and chronic progressive MS.
- These changes indicate a state of preactivation in PMN during active MS disease phases.
Conclusions:
- Increased expression of studied molecules on PMN suggests PMN priming in active MS.
- Findings provide direct evidence for the involvement of PMN in the pathogenesis of multiple sclerosis.
- PMN preactivation may represent a therapeutic target for managing MS.