Znaczenie wybranych populacji komórek immunologicznych w leczeniu zaostrzeń stwardnienia rozsianego z zastosowaniem plazmaferezy

• Authors: Mariusz Stasiołek

Title variants

EN

The role of selected immune cell populations in plasma exchange treatment of multiple sclerosis relapses

• Languages of publication: PL

Abstracts

PL

Wstęp: Stwardnienie rozsiane (łac. sclerosis multiplex - SM) jest przewlekłym demielinizacyjnym schorzeniem ośrodkowego układu nerwowego. U większości pacjentów, przynajmniej w początkowym okresie, choroba przebiega pod postacią zaostrzeń (tzw. rzutów) i remisji objawów neurologicznych. Standardem leczenia w rzucie SM jest dożylne podawanie wysokich dawek glukokortykosteroidów. Jednakże, w niewielkiej grupie pacjentów terapia ta nie przynosi pożądanych efektów klinicznych. Liczne badania wykazały, iż plazmafereza stanowi efektywną opcję terapeutyczną dla pacjentów z opornymi na glukokortykosteroidy rzutami SM. Powszechnie uważa się, że skuteczność kliniczna plazmaferezy jest wynikiem usuwania z krwi obwodowej szeregu zróżnicowanych cząsteczek czynnych immunologicznie. Niewiele wiadomo jednak, na temat wpływu plazmaferezy na komórkowe składniki układu immunologicznego. Cel pracy: Celem pracy była ocena zaangażowania komórkowych elementów układu immunologicznego w mechanizmy warunkujące skuteczność kliniczną plazmaferezy w zaostrzeniach stwardnienia rozsianego opornych na terapię glukokortykosteroidami. Badaniem zostały objęte podstawowe populacje limfocytów T (w tym limfocyty T regulatorowe), komórki NK, komórki NKT, limfocyty B oraz najważniejsze z punktu widzenia immunoregulacji subpopulacje monocytów i komórek dendrytycznych krwi obwodowej. Materiały i metody: Krew obwodowa została pobrana od pacjentów z opornym na leczenie glukokortykosteroidami rzutem SM w trzech punktach czasowych terapii plazmaferezą: przed pierwszym zabiegiem plazmaferezy, po trzecim zabiegu plazmaferezy oraz po zakończeniu cyklu plazmaferez. Pacjenci z rzutem SM wrażliwym na terapię glukokortykosteroidami oraz zdrowi ochotnicy stanowili grupy kontrolne. Populacje komórek immunologicznych analizowane były we frakcji komórek jednojądrzastych krwi obwodowej za pomocą cytometrii przepływowej ex vivo. W kolejnej części badania, czysta frakcja monocytów izolowana była z krwi obwodowej z zastosowaniem metody sortowania magnetycznego. Uzyskane w ten sposób monocyty były poddawane 48-godzinnej hodowli w warunkach stymulacji prozapalnej. Po zakończeniu hodowli, profil ekspresji powierzchniowej monocytów in vitro, obejmujący szereg molekuł kostymulacyjnych oraz cząsteczki MHC klasy II, oceniany był metodą cytometrii przepływowej. W dalszych eksperymentach produkcja cytokin prozapalnych i regulacyjnych przez komórki jednojądrzaste oraz monocyty krwi obwodowej in vitro analizowana była w nadsączach hodowlanych. Wyniki: W przebiegu terapii plazmaferezą obserwowano, równolegle do poprawy klinicznej, istotne zmniejszenie frakcji monocytów krwi obwodowej wykazujących ekspresję CD16 ex vivo. Analiza poszczególnych subpopulacji monocytów wykazała, że efekt ten był specyficzny dla subpopulacji CD14highCD16+, podczas gdy subpopulacja monocytów CD14lowCD16+ oraz frakcja „klasycznych” monocytów CD14highCD16- nie wykazywały zmian w trakcie terapii. Terapia plazmaferezą nie miała wpływu na główne populacje limfocytów (m.in. limfocyty T regulatorowe, komórki NK, komórki NKT, limfocyty B) oraz na mieloidalne i plazmacytoidalne komórki dendrytyczne krwi obwodowej. Obserwowane przed rozpoczęciem terapii zwiększenie frakcji monocytów CD14highCD16+ było czynnikiem prognostycznym dobrej odpowiedzi terapeutycznej na plazmaferezę. Natomiast, u pacjentów z negatywną odpowiedzią terapeutyczną obserwowano początkowo zmniejszoną ekspresję HLA-DR w subpopulacji „klasycznych” monocytów CD14highCD16-. Parametr ten ulegał normalizacji po zakończeniu cyklu plazmaferez, czemu towarzyszyła zwiększona sekrecja TNF-α przez monocyty in vitro. W badaniu nie wykazano wpływu terapii plazmaferezą na profil sekrecji całkowitej frakcji komórek jednojądrzastych krwi obwodowej. Wnioski: Uzyskane wyniki dowodzą istotnego wpływu plazmaferezy na strukturę i funkcję komórek krwi obwodowej pacjentów z opornym na glukokortykosteroidy zaostrzeniem SM. Zróżnicowanie efektów immunologicznych plazmaferezy w zależności od odpowiedzi klinicznej na terapię sugeruje istnienie w SM złożonych i niejednorodnych mechanizmów zaburzeń wrażliwości na glukokortykosteroidy. Poczynione w badaniu obserwacje mogą przyczynić się do lepszego zrozumienia efektów klinicznych plazmaferezy w terapii rzutów SM, jak również znaleźć zastosowanie w badaniach nad zagadnieniem oporności na glukokortykosteroidy w chorobach zapalnych.

EN

Introduction: Multiple sclerosis (MS) is a chronic demyelinating disorder of the central nervous system. In the majority of patients the disease is characterized, at least in the early phase, by relapsing-remitting clinical course. The standard therapy of MS relapse consist of high dose intravenous glucocorticoid treatment. However, in a small group of MS patients this therapy brings no clinical improvement. Numerous studies showed that plasma exchange is an effective therapeutic option for patients with glucocorticoidresistant MS relapse. Elimination of multiple humoral factors has been postulated as a possible therapeutic mechanism of plasma exchange. However, the influence of plasma exchange on cellular immunity remains poorly understood. Aim of the study: The aim of this study was to assess the involvement of cellular immunity in clinical efficacy of plasma exchange as therapy for multiple sclerosis patients suffering from relapses resistant to glucocorticoid pulse therapy. The analysis encompassed main T cell populations (including regulatory T cells), NK cells, NKT cells, B cells and the most important for immunoregulatory processes monocyte and dendritic cell subpopulations. Materials and methods: Peripheral blood was obtained from MS patients suffering from glucocorticoid-resistant relapses at three consecutive time-points of plasma exchange treatment: before the first plasma exchange, after the third plasma exchange and after completion of plasma exchange therapy. Patients with MS relapse with good response to glucocorticoid pulse therapy and healthy individuals served as controls. Peripheral blood mononuclear cells were obtained and immune cell subsets were investigated by flow cytometry ex vivo. In further experiments, the pure monocyte population was isolated from peripheral blood by magnetic sorting. Isolated monocytes were cultured 48 hours under inflammatory conditions. After completion of culture period, surface expression profile of monocytes in vitro, including various co-stimulatory and MHC class II molecules, was assessed by flow cytometry. The secretion of pro-inflammatory and regulatory cytokines by peripheral blood mononuclear cells and monocytes in vitro was analyzed in culture supernatants. Results: The percentage of monocytes expressing CD16 decreased significantly over the course of PE treatment. The effect was specific for the CD14highCD16+ monocyte subpopulation, whereas the CD14lowCD16+ and the “classical” CD14highCD16- subpopulations showed no differences during the treatment. Plasma exchange did not influence the main lymphocyte populations (including regulatory T cells, NK or NKT cells, B cells) and dendritic cell subtypes. A baseline increase in the percentage of CD14highCD16+ monocytes was predictive for a good therapeutic response to plasma exchange treatment. In contrast, PE non-responders were characterized at baseline by lower expression of HLA-DR in CD14highCD16- monocytes. This parameter normalized after completion of plasma exchange, paralleled by increased TNF-α secretion by monocytes in culture. The secretion profile of peripheral blood mononuclear cells was not influenced by plasma exchange therapy. Conclusions: Results obtained in the study demonstrate a significant influence of plasma exchange on the structure and function of immune cells in peripheral blood of patients with glucocorticoid-resistant MS relapse. The diversity of immune effects of plasma exchange depending on the clinical response to therapy suggests complex and inhomogeneous mechanisms of glucocorticoid resistance in MS. These observations may be of particular importance for understanding of clinical effectiveness of plasma exchange in MS relapse as well as for the problem of glucocorticoid sensitivity in inflammatory disorders.

Keywords

EN

Plazmafereza; komórki immunologiczne; stwardnienie rozsiane

Discipline

• MEDICINE: MEDICINE

• Publisher: Łódzkie Towarzystwo Naukowe
• Journal: Folia Medica Lodziensia
• Year: 2011
• Volume: 38
• Issue: suplement 1
• Pages: 5-124

Contributors

author

Mariusz Stasiołek

• Klinika Endokrynologii i Chorób Metabolicznych, Instytut Centrum Zdrowia Matki Polki

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