THE p olym or ph on uclear n eutr op h ils (PMN) po s s e s s s ufficie n t p ote ntial to affect both im m un e r es p o ns e an d in flam m ation , h o w e ver it h as no t been yet de s cribed in th e co urs e of m ultip le s cler o s is (MS). IntroductionMultiple sclerosis (MS) is a dise as e in w hich multifoc al inflammation and damage of the blood -brain barrier and myelin sheath are salie nt pathologic features. Overw he lming evidenc e demons trates that MS is a pre dominantly T-c ell and monoc yte/mac rophageme diated autoimmune disorde r.1 ,2 Polymorphonuclear ne utrop hils (PMN) have not be en considere d as a ce ll population participating in it.3 PMN can how e ver ex pre ss immunore gulatory abilities, that has not be en ye t de sc ribe d in the c ourse of MS. Activated in vitro PMN produc e a numbe r of immune mediators including cytokines like IL-1b , IL-4, IL-6, IL-8, IL-10, IL-12, TNF, TGF-b 1. 4 ,5 There fore the re gulatory functions of these ce lls may be postulate d in the c ourse of MS. PMN in the pe ripheral blood (PB) of MS patients can be primed mainly by inflammatory cytokine s like IL-1, INF-g , or by TNF-a sec re te d by mononuclear ce lls. Hypothetically PMN priming or activation in PB of MS patients may dep end also on compleme nt (especially C5a) immunologic al c omplex es, or certain me tabolite s of the arachidonic ac id (LTB 4 , PAF).Priming re sults in the enhanced ex p re ssion on PMN of re cep tors for chemokines and other chemotactic pep tide s, 6 priming also enhance s the ex pre ssion of CD11b/CD18 molecules on PMN c ell surface 7,8 w hich re sults in the indire ct ac tivation of PMN.9,10 In the pre sente d pap er w e have suggeste d that PMN priming can be obse rved in MS patie nts p eriphe ral blood. Patients and methodsPatients (34 total; 19 w omen and 15 men, aged 22-56 years) w ere se lecte d w ith a clinic ally definitive diagnosis of MS 1 1 and w ith Kurtzke Ex panded Disability Status Scale 12 scores 5 or few er and categorized as having the re lapsing-re mitting MS (RR-MS) course for at least 5 years but curre ntly in re mission (REM) (n =13), as having either sec ondary CP-MS for at least 2 ye ars (n =13) or RR-MS and currently ex pe riencing clinical ex ace rbation (REL) of the disease (n = 12). Ex acerbations w ere defined as the appearance of new symptoms or significant w orsening of the old ones, attributabl e to MS, for at least 24 hours w ithout any fever.The control group c onsiste d of patients w ith other ne urologic al diseas es (OND) (14 total; nine w omen and five men, aged from 24 to 37 ye ars), including those w ith vasomotor headache (n = 8) and ischialgia (n = 6). Sample collectionThe studies w e re performed on PMN of the p eripheral venous blood, c ollec te d into heparin-containin g tubes (10 U/ml).0962-9351/98/050335-04 $9.00 © 1998 Carfax Publishing Ltd 335 Research PaperMediators of Inflammation, 7, 335-338 (1998) TNF labelling with fluorescein isothiocyanate (FITC)The synthesis and biological analysis of the TNF molecules w ere pe rfor...
CD13 Ag and CD11a, CD11b, CD18 molecule expression on peripheral blood mononuclear cells (PBMC) were studied as these cells' adherent or transendothelial migration properties in three different multiple sclerosis (MS) patients groups (total 38): with clinically active MS (acute exacerbation of MS and primary chronic progressive MS (CP-MS)) and with MS remission. The control group consisted of patients, suffering from other non-inflammatory neurological diseases (OND). The results of our study suggest that CD11a/CD18 molecules expression on PB lymphocytes, although higher on these cells' surface in the course of MS as compared to OND, does not differentiate clinical forms of MS. CD11a molecule expression on monocytes did not differ significantly in all tested MS patient groups in comparison to OND. Although the expression of CD11b/CD18 molecules on monocytes' surface shows their activation in the course of MS, it does not differentiate them either. However, CD13 Ag of APN expression on PBMC surface may be an immunological marker of MS clinical form. CD13 Ag expression may also be a sensitive marker of these cells' transendothelial migration properties.
The aim of this study was to investigate whether the restriction in neck rotation and increased neck muscle tension could be causally related to vertigo and dizziness. Material and Methods: Seventy-one patients reporting vertigo and/or imbalance were divided into 2 groups: 45 subjects with unilateral restriction (R+) and 26 without restriction (R-) of cervical rotation and muscle tension in the clinical flexion-rotation test. The normal caloric test was the inclusion criterion. The control group comprised 36 healthy volunteers with no history of vertigo. The vestibulo-ocular reflex (VOR) and the cervico-occular reflex (COR) were measured through the videonystagmography (VNG) sinusoidal pendular kinetic test in the conditions of not inactivated head and immobilized head, respectively. The VNG-head torsion test (VNG-HTT) nystagmus was recorded. Results: Among the reported complaints, neck stiffness, headaches and blurred vision were more frequent in the R+ group than in both the R-group and the control group. VNG revealed an increased COR gain and the presence of VNG-HTT nystagmus in the R+ group only. Similarly, only in the R+ group a positive relationship between COR and VOR was observed. Conclusions: Patients with asymmetric restriction in neck rotation and increased neck muscle tension reveal the tendency to have an increased response of the vestibular system, along with co-existing COR upregulation. Further research is needed to investigate the relationships between the activation of cervical mechanoreceptors and dizziness pathomechanisms.
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