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Polymorphonuclear Cell Functional Impairment in Relapsing Remitting Multiple Sclerosis Patients: Preliminary Data
Valeria Allizond1, Sara Scutera2, Silvia Rossi2
1Bacteriology and Mycology Laboratory, Department of Public Health and Pediatrics, University of Torino, Turin, Italy.
Abstract:
Multiple Sclerosis patients run an increased risk of microbial infections, which leads to high rates of hospitalization and infection-related mortality. Although immunotherapy may increase infection risk in some cases, data as to the relationship among microbial factors, immunotherapy and alterations in the innate immunity of these patients are still scanty. On these grounds, this interdisciplinary study aims at investigating the role the functional activity of polymorphonuclear cells (PMNs) play in relapsing remitting multiple sclerosis at different stages. The in vitro ability of PMNs from patients, either untreated or treated with immunosuppressant or immunomodulatory drugs to kill Klebsiella pneumonia or Candida albicans, were investigated and compared to PMNs from healthy subjects. The release of various cytokines was also assessed, as was the production of reactive oxygen species and their ability to regulate apoptosis after microbial stimulation. Our results indicate that although patients have a normal number of PMNs, they have a statistically significant (p<0.05) reduction in intracellular killing activity. Although variations are strongly related to the therapeutic management of patients, they are independent from their disease stage. As no statistically significant differences were observed between patients and controls in cytokine release values, reactive oxygen species production or apoptosis, we came to the conclusion that other factors may be involved. Supportive validation of these results from further studies might well help in identifying a subset of patients at high risk of infection who could benefit from a closer follow-up and/or antibiotic prophylaxis.
Insights
Multiple Sclerosis patients exhibit reduced polymorphonuclear cell (PMN) antimicrobial activity, increasing infection risk. This impairment is linked to therapy, not disease stage, suggesting targeted interventions for high-risk individuals.
Area of Science:
- Immunology
- Infectious Diseases
- Neurology
Background:
- Multiple Sclerosis (MS) patients face higher risks of microbial infections, leading to significant morbidity and mortality.
- The interplay between MS, microbial factors, immunotherapy, and innate immune system alterations remains incompletely understood.
- Polymorphonuclear cells (PMNs) are crucial in innate immunity against microbial pathogens.
Purpose of the Study:
- To investigate the functional activity of PMNs in patients with relapsing-remitting MS.
- To assess the impact of disease stage and therapeutic management on PMN antimicrobial functions.
- To explore the relationship between PMN activity, microbial killing, cytokine release, reactive oxygen species (ROS) production, and apoptosis.
Main Methods:
- In vitro assessment of PMN's ability to kill Klebsiella pneumoniae and Candida albicans.
- Comparison of PMN function between MS patients (untreated and treated) and healthy controls.
- Measurement of cytokine release, ROS production, and apoptosis regulation following microbial stimulation.
Main Results:
- MS patients demonstrated a statistically significant reduction in intracellular PMN killing activity (p<0.05) despite normal PMN counts.
- Impaired PMN function was strongly associated with therapeutic management but independent of MS disease stage.
- No significant differences were observed in cytokine release, ROS production, or apoptosis regulation between patients and controls.
Conclusions:
- Reduced PMN intracellular killing activity is a key factor contributing to increased infection susceptibility in MS patients.
- Therapeutic interventions, rather than disease progression, appear to influence PMN dysfunction.
- Further research may identify high-risk patients who could benefit from closer monitoring and prophylactic strategies.
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