scholarly journals Leucocytes and Th-associated cytokine profile of HIV-leishmaniasis coinfected patients attending the Abuja Teaching Hospital, Nigeria

2020 ◽  
Vol 89 (1) ◽  
pp. e408
Author(s):  
Idris Nasir Abdullahi ◽  
Anthony Uchenna Emeribe ◽  
Hafeez Aderinsayo Adekola ◽  
Habiba Yahaya Muhammad ◽  
Abdurrahman El-fulaty Ahmad ◽  
...  
Keyword(s):  
Teaching Hospital ◽  
Leishmania Donovani ◽  
Cell Counts ◽  
Tnf Α ◽  
Group 3 ◽  
Group 2 ◽  
Cell Subpopulations ◽  
Healthy Persons ◽  
Group 1 ◽  
Apparently Healthy

Introduction. T helper cells (Th)-1 and -2 cytokines homeostasis control or predict clinical outcome of infected persons, especially those with HIV/AIDS. This case-control study evaluated the leucocyte differentials, TNF-α, IL-2 and -10 levels, among HIV-infected persons with serological evidence of leishmaniasis attending the University of Abuja Teaching Hospital, Nigeria. Material and Methods. This study involved blood samples from 28 HIV-infectedwith Leishmania donovani rK39 and IgG positive (group 1), 30 age- and sex-matched HIV-infected individuals without Leishmania antibodies (group 2) and 30 apparently healthy persons without HIV and Leishmania antibodies (group 3). Full blood counts, TNF-α, IL-2 and IL-10 levels were analysed using an automated haematology analyser and ELISA, respectively. Structured questionnaires were used to collate biochemical and clinical data from participants. Results. Ten (35.7%) participants in group 1 were on ART, 15 (50%) in group 2 were on ART, while group 3 were ART naïve. There were significantly higher values in basophil (4.4 ± 2.5%) and eosinophil counts (12.9 ± 3.8%) in HIV/Leishmania coinfected persons (p˂0.005), whereas other white cell subpopulations were significantly lower in the HIV/Leishmania coinfected participants (p˂0.05). There were significantly reduced CD4+ T cell counts (119 ± 26 vs 348 ± 63 vs 605 ± 116 cells/mm3), TNF-α (36.82 ± 8.21 vs 64.67 ± 12.54 vs 254.98 ± 65.59 pg/mL) and IL-2 levels (142.14 ± 20.91 vs 507.6 ± 84.42 vs 486.62 ± 167.87 pg/mL) among HIV/Leishmania coinfected participants compared to group 2 and group 3 participants, respectively. However, higher IL-10 levels (80.35 ± 14.57 pg/mL) were detected in HIV/Leishmania coinfected participants compared to the HIV mono-infected (62.2 ± 10.43 pg/mL) and apparently healthy persons (23.97 ± 4.88 pg/mL; p˂0.001). Conclusion. Eosinophil and basophil counts, and serum IL-10 level were high in HIV/Leishmania coinfected patients demonstrating parasite-induced hypersensitivity and immunosuppression.

scholarly journals Cell Loss from the Nucleus Basalis of Meynert in Alzheimer's Disease

1986 ◽  
Vol 13 (S4) ◽  
pp. 435-440 ◽  
Author(s):  
R. Doucette ◽  
M. Fisman ◽  
V.C. Hachinski ◽  
H. Mersky
Keyword(s):  
Paraffin Section ◽  
Neuronal Loss ◽  
Cell Loss ◽  
Nucleus Basalis ◽  
Nucleus Basalis Of Meynert ◽  
Cell Counts ◽  
Group 3 ◽  
Group 2 ◽  
Death Group ◽  
Group 1

Abstract:We examined the degree of neuronal loss from the nucleus basalis of Meynert (nbM) in two groups of Alzheimer patients differing in the degree of intellectual impairment. Significant cell loss from the nbM was found only in the more severely demented group of patients. Mean cell counts (per lOu, paraffin section) were compiled separately for the anterior, intermediate and posterior subdivisions of the human nbM in three groups of subjects: Group 1 (N = 4) was severely demented and was untestable on the Extended Scale for Dementia (ESD) for at least the last two years of life; Group 2 (N = 4) was less demented and had completed at least one ESD test within 12 months of death; Group 3 (five controls) had died of non-neurological causes. In Group 2 there was a small (but insignificant) trend toward cell loss in the anterior subdivision, and a normal complement of neurons in both the intermediate and posterior subdivisions. There was, however, significant cell loss from all subdivisions of Group 1. How these cell counts may relate to the severity of the dementia is discussed.

Abstract 196: The Characteristics of Patients with Kawasaki disease Presented with Fever and Cervical Lymphadenopathy at Admission

Circulation ◽  
2015 ◽  
Vol 131 (suppl_2) ◽  
Author(s):  
yeo hyang kim ◽  
Chae Ok Shin ◽  
Myung Chul Hyun ◽  
Dong Seok Lee
Keyword(s):  
Intravenous Immunoglobulin ◽  
Cervical Lymphadenopathy ◽  
Systemic Steroid ◽  
Line Treatment ◽  
Cell Counts ◽  
Blood Cell Counts ◽  
Group 3 ◽  
Group 2 ◽  
White Blood Cell Counts ◽  
Group 1

Purpose: Of the principal diagnostic criteria of Kawasaki disease (KD), cervical lymphadenopathy is the least common. However, it may be misdiagnosed as bacterial cervical lymphadenitis. We evaluated the characteristics of patients with KD presenting with only fever and cervical lymphadenopathy at admission. Methods: This study enrolled patients diagnosed KD from January 2013 to May 2014. All of patients were divided to three groups: group 1 had only fever and cervical lymphadenopathy at admission; group 2 had typical manifestations with cervical lymphadenopathy; group 3 had typical manifestations without cervical lymphadenopathy. Results: Ninety eight patients (group 1 in 13, group 2 in 31, group 3 in 54) were examined. The median age of group 1 was significantly older than group 2 and 3 ( P =0.001). The duration of fever before admission at our hospital was more prolonged in group 1 than in group 2 and 3 ( P =0.001). In comparison between groups, the laboratory results at the admission day were not significantly different. However, group 1 showed significantly elevated white blood cell counts, elevated neutrophil counts, and decreased lymphocyte counts after first intravenous immunoglobulin administration ( P =0.001, P =0.001, and P =0.003). The frequency of additional intravenous immunoglobulin treatment did not have significant difference. Group 1 had significantly increased duration of hospitalization, and frequency of second line treatment such as systemic steroid or infliximab than group 2 and 3 ( P =0.000, P =0.024, and P =0.007). The development of a coronary artery dilatation (z score >2.5) was higher in group 1 than in group 3 ( P =0.008). Conclusions: KD with cervical lymphadenopathy as main presentation indicates a severe form of KD associated with increased risks of second line treatment such as systemic steroid or infliximab and coronary artery dilatation. KD should be suspected in the older children with antibiotics non-responsive, prolonged fever and cervical lymphadenopathy. For differentiation between responder and non-responder for first line treatment, white blood cell counts and their subset after first intravenous immunoglobulin administration may be beneficial.

scholarly journals Acute Phase Effect of Memantine Hydrochloride in Experimental Peripheral Nerve Injury

2019 ◽  
Vol 08 (02) ◽  
pp. 113-118
Author(s):  
Hakan AK ◽  
Iskender Samet Daltaban ◽  
Sevilay Vural
Keyword(s):  
Peripheral Nerve ◽  
Nerve Injury ◽  
Peripheral Nerve Injury ◽  
Group 4 ◽  
Tnf Α ◽  
Group 3 ◽  
The Mean ◽  
Cox 2 ◽  
Group 2 ◽  
Group 1

Abstract Aim In this experimental study, we aimed to investigate possible healing effects of memantine hydrochloride, an N-methyl-d-aspartate (NMDA) antagonist, with clinical, biochemical, and histopathologic methods on acute peripheral nerve injury (PNI). Material and Method Forty-eight adult Wistar albino rats were divided into four groups (n = 12). The groups were arranged as sham-operated group (group 1), acute compression model group (group 2), trauma + low-dose memantine group (group 3), and trauma + high-dose memantine group (group 4). Memantine was administered intraperitoneally for 7 days. Subjects were sacrificed after the measurement of the sciatic nerve function index (SNFI) on the eighth day. Cyclooxygenase 2 (COX-2) and tumor necrosis factor-α (TNF-α) levels were measured in nerve tissues. Histopathologic evaluation was performed by electron microscopy. Results The mean sciatic function index (SFI) scores of groups 1 to 4 were +3.27 (standard deviation [SD] ±4.66),–18.2 (SD = ±11.7),–8.5 (SD = ±7.5), and–2.5 (SD = ±9), respectively. The mean COX-2 values were 0.98 ng/mL (SD = ±0.51), 1.89 ng/mL (SD = ±0.22), 1.39 ng/mL (SD = ±0.36), and 1.35 ng/mL (SD = ±0.59), respectively. TNF-α values were 0.09 pg/mL (SD = ±0.23), 1 pg/mL (SD = ±0.96), 0.46 pg/mL (SD = ±0.55), and 0.48 pg/mL (SD = ±0.78), respectively. Group 1 showed normal histologic findings. Group 2 showed marked edema particularly in large-diameter myelins. Myelin configurations were detected in large myelinated axons in group 3. The number of mast cells in endoneurium was high in group 4. Conclusion The efficacy of memantine in the acute phase of PNI appears to be significant according to the SNFI and biochemical tests. However, histologic findings suggest that high doses of memantine have a negative effect on PNI.

scholarly journals Endotoxin and ischemic preconditioning: TNF-α concentration and myocardial infarct development in rabbits

1999 ◽  
Vol 277 (6) ◽  
pp. H2470-H2475 ◽  
Author(s):  
Sergej Belosjorow ◽  
Rainer Schulz ◽  
Hilmar Dörge ◽  
F. Ulrich Schade ◽  
Gerd Heusch
Keyword(s):  
Ischemic Preconditioning ◽  
Myocardial Infarct ◽  
Ischemia Reperfusion ◽  
Ischemia And Reperfusion ◽  
Area At Risk ◽  
Tnf Α ◽  
Maximum Inhibition ◽  
Group 3 ◽  
Group 2 ◽  
Group 1

Ischemic preconditioning (IP) and prior exposure to lipopolysaccharides (LPS) reduce infarct size (IS) and serum tumor necrosis factor-α (TNF-α) concentration resulting from myocardial ischemia-reperfusion in rabbits. The decrease in TNF-α might relate to an induced TNF-α inhibitory serum activity (TNF-α-ISA). We analyzed TNF-α and TNF-α-ISA during 30 and 180 min ischemia and reperfusion, respectively, in anesthetized rabbits either untreated ( group 1, n = 7), preconditioned (5 and 10 min ischemia and reperfusion, respectively, group 2, n = 9), or exposed to LPS 72 h before ischemia ( group 3, n = 9). TNF-α-ISA was assessed by coincubating LPS-stimulated rabbit blood with serum of groups 1–3 and measuring TNF-α (WEHI assay). With a comparable area at risk, IS in group 1 was 36.9 ± 11.1 (SD)%, and it was reduced to 13.1 ± 11.6% and 17.3 ± 11.3% (both P < 0.05) in groups 2 and 3, respectively. TNF-α was increased during ischemia-reperfusion in group 1 but remained unchanged in rabbits subjected to IP or LPS. TNF-α-ISA was detected during ischemia-reperfusion in group 2 (29% and 38% of maximum inhibition, respectively) and during baseline, ischemia and reperfusion in group 3 (51%, 46%, 48% of maximum inhibition, respectively) but was absent in group 1. Cardioprotection by IP and LPS is associated with a reduced TNF-α and an induced TNF-α-ISA during ischemia-reperfusion.

scholarly journals Extracorporeal Shock Wave Therapy Protected the Functional and Architectural Integrity of Rodent Urinary Bladder against Ketamine-Induced Damage

Biomedicines ◽  
2021 ◽  
Vol 9 (10) ◽  
pp. 1391
Author(s):  
Yen-Ta Chen ◽  
Kuan-Hui Huang ◽  
John Y. Chiang ◽  
Pei-Hsun Sung ◽  
Chi-Ruei Huang ◽  
...  
Keyword(s):  
Urinary Bladder ◽  
Cyclophilin D ◽  
Group 4 ◽  
Extracorporeal Shock Wave ◽  
Tnf Α ◽  
Bladder Contraction ◽  
Group 3 ◽  
Group 2 ◽  
Cell Stress Response ◽  
Group 1

This study tested the hypothesis that extracorporeal-shock-wave (ECSW) protected the functional and anatomical integrity of rat urinary-bladder against ketamine-induced damage. In in vitro study, the rat bladder smooth muscle cells (RBdSMCs) were categorized into G1 (sham-control), G2 (RBdSMCs + menadione), G3 (RBdSMCs + ECSW) and G4 (RBdSMCs + menadione + ECSW). The results showed protein expressions of oxidative-stress/mitochondrial-damaged biomarkers (NOX-1/NOX-2/oxidized protein/cytosolic-cytochrome-C/cyclophilin-D), inflammatory markers (MyD88/TRAF6/p-IKB-α/NF-κB/TNF-α/IL-6/IL-1ß/MMP-9/iNOS), and cell-stress response signalings (ASK1/p-MKK4/p-MKK7/ERK1/2//p-JNK/p-p38/p-53) were significantly increased in G2 than in G1 and G3, and those were significantly reversed in G4 (all p < 0.0001). Adult-male SD rats (n = 24) were equally categorized into group 1 (sham-control), group 2 (ketamine/30 mg/kg/daily i.p. injection for four weeks), group 3 [ketamine/30 mg/kg + ECSW/optimal energy (0.12 mJ/mm2/120 impulses/at 3 h and days 3/7/14/21/28 after ketamine administration)] and group 4 [(ketamine/30 mg/kg + ECSW/higher energy (0.16 mJ/mm2/120 impulses)] and animals were euthanized by day 42. The results showed the urine levels of pro-inflammatory cytokines (TNF-α/IL-6) were lowest in group 1, highest in group 2 and significantly higher in group 3 than in group 4 at days 1/7/14/28 (all p < 0.0001). The duration of urinary bladder contraction was lowest in group 2, highest in group 1 and significantly higher in group 4 than in group 3, whereas the maximal pressure of urinary bladder exhibited an opposite pattern of bladder contraction among the groups (all p < 0.0001). The histopathological findings of fibrosis/inflammation/keratinization and protein expressions of oxidative-stress/mitochondrial-damaged biomarkers (NOX-1/NOX-2/oxidized protein/cytosolic-cytochrome-C/cyclophilin-D), and inflammatory (TLR-2/TLR-4/MyD88/TRAF6/p-IKB-α/NF-κB/TNF-α/IL-1ß/MMP-9/iNOS) and cell-stress response (ASK1/p-MKK4/p-MKK7/ERK1/2//p-JNK/p-p38) signalings and apoptotic/fibrotic biomarkers (cleaved-caspas3/cleaved-PARB/Smad3/TFG-ß) exhibited an identical pattern of urine proinflammatory cytokine among the groups (all p < 0.0001). ECSW effectively attenuated ketamine-induced bladder damage and dysfunction.

The Association Between Vitamin D and Inflammation in Sickle Cell Disease

Blood ◽  
2014 ◽  
Vol 124 (21) ◽  
pp. 4923-4923
Author(s):  
Selma Unal ◽  
Yesim Oztas ◽  
Gulcin Eskandari ◽  
Lulufer Tamer Gumus ◽  
Ozgunes Nuriman
Keyword(s):  
Vitamin D ◽  
Steady State ◽  
Healthy Children ◽  
Cell Disease ◽  
Vitamin D Levels ◽  
Tnf Α ◽  
Normal Vitamin ◽  
Group 3 ◽  
Group 2 ◽  
Group 1

Abstract Sickle Cell Disease (SCD) is characterized by periodic vaso-occlusive crises, chronic hemolysis and frequent infections that are accompanied by pain and organ damage. Inflammation has substantial role in SCD pathogenesis. Patients exhibit elevated leukocyte counts, abnormal activation of granulocytes, monocytes, and endothelial cells, and increased levels of multiple inflammatory mediators. Vitamin D, a secosteroid hormone synthesized in the skin or derived from nutritional sources, serves a variety of functions that include immunomodulation, bone homoeostasis and wound healing. Deficiency of vitamin D has been linked to autoimmune diseases, carcinogenesis, and importantly, different inflammatory diseases. Vitamin D deficiency is seen frequently in patients with SCD. However, relationship between inflammation and vitamin D deficiency in SCD pathogenesis has not been investigated, yet. In this study, we aimed to investigate the relation between vitamin D levels and inflammation in children with SCD. For this purpose, 64 patients with SCD, 21 SCD trait, and 21 healthy controls were included in this study. The local ethics committee approved the study and informed consent was obtained from the children and parents. Vitamin D status was expressed as low, if plasma vitamin D levels were lower than 20 ng/ml. The SCD patients were grouped as Group 0 which includes steady state patients with low vitamin D levels (n=21), Group 1 which includes vaso-occlusive crisis patients with low vitamin D levels (n=18), Group 2 which includes steady state patients with normal vitamin D levels (n=16), Group 3 which includes vaso-occlusive crisis patients with normal vitamin D levels (n=9). The SCD trait patients were grouped in Group 4 and healthy children were grouped in Group 5. Levels of vitamin D and inflammatory parameters were determined in all groups; bone parameters were studied in SCD patients and SCD traits. WBC count and levels of CRP, IL-2, IL-4, IL-6, IL-10, IL-12, TNF-α and IFN-γ were determined as inflammatory markers. Vitamin D levels lower than 20 ng/ml were found in 61% of SCD patients, in 33% of SCD traits and in 84% of healthy children. We could not find any relation between vitamin D levels and WBC, CRP and bone markers in SCD patients. Vitamin D is correlated to TNF-α in Group 0 (R=0.589 and P=0.005), to IL-10 in Group 1 (R=0.612 and P=0.046), to IL-12 in Group 2 (R=-0.549 and P=0.028) and to IL-4 (R=0.695 and P=0.038) and IL-6 (R=0.865 and P=0.003) in Group 3. TNF-α levels were higher in the groups who had vaso-occlusive crises (Group 1 and 3) than the groups who were at steady state (Group 0 and 2). Vaso-occlusive crisis are the result of interactions between sickle erythrocytes, inflammatory cytokines and endothelium. Deficiency of vitamin D that has effects on endothelial dysfunction and cytokines, has possibly contributed to the pathogenesis of SCD. However, we could not show a concrete association between vitamin D and inflammation, possibly there are other molecules or markers modulating this association. Additionally our patient number may not be high enough to show this association. Our study is valuable for it's the first study on investigating the possible association between vitamin D and inflammation in SCD. Research on this topic should be continued with larger groups and novel biomarkers. Disclosures No relevant conflicts of interest to declare.

scholarly journals Association between HSPA1B, S100B, and TNF genes polymorphisms and risks of chronic mercury poisoning

2021 ◽  
pp. 126-132
Author(s):  
Yu.I. Chernyak ◽  
Keyword(s):  
Genetic Interaction ◽  
Rflp Analysis ◽  
Population Group ◽  
Mercury Vapor ◽  
Recessive Model ◽  
Mercury Poisoning ◽  
Tnf Α ◽  
Group 3 ◽  
Group 2 ◽  
Group 1

We examined association between HSPA1B (+1267A/G, rs1061581), TNF-α (–308G/A, rs1800629), and S100B (C/T, rs9722) genes polymorphisms and chronic mercury poisoning (CMP). PCR-RFLP analysis was used to examine a cohort consisting of 128 workers who were chronically exposed to mercury vapor; workers were distributed into two groups. The group 1 was made up of workers with long working experience who didn’t have CMP (n = 46), the group 2 included patients with long-term CMP period (n = 82). In addition, we estimated frequencies of rs1061581genotypes in 298 practically healthy men from regional sub-population (group 3). HSPA1B (+1267A/G) polymorphic variant was established to have more frequent carriage of both minor G allele (р = 0.003) and a rare GG homozygote (р = 0.005) in the group 2 against the group 1. 23.2 % patients from the group 2 turned out to have GG genotype and CMP was diagnosed in 95 % people who had it. We didn’t detect any differences in genotypes distribution among people from the examined occupational cohort (groups 1 and 2) against the group 3. GG-HSP1AB (+1267A/G) homozygous genotype was shown to be associated with CMP risks (OR = 13.57, p < 0.0001, recessive model). Haplotype G–G (rs1061581–rs1800629) carriers were established to run 2.6 higher risks of CMP occurrence (р = 0.0098), and there was a significant linkage disequilibrium D' = 0.459 (р = 0.0004) between a pair of the abovementioned polymorphic loci. These data indicate that there is genetic interaction between HSPA1B (+1267A/G) and TNF-α (–308G/A) loci in the examined cohort. Overall, these results indicate that carriers of GG-HSPA1B (+1267A/G) genotype run high predictive risks of CMP occurrence.

scholarly journals Changes in the immunomorphological indicators of the placenta in women with exacerbation of cytomegalovirus infection in the second trimester of pregnancy complicated by chronic placental insufficiency

2021 ◽  
pp. 80-85
Author(s):  
I. N. Gorikov ◽  
I. A. Andrievskaya
Keyword(s):  
Cytomegalovirus Infection ◽  
Placental Insufficiency ◽  
Second Trimester ◽  
Chorionic Villi ◽  
Group 4 ◽  
Terminal Villi ◽  
Tnf Α ◽  
Group 3 ◽  
Group 2 ◽  
Group 1

Aim. To assess the change of immunomorphological parameters in the placenta in women with exacerbation of cytomegalovirus infection (CMVI) in the second trimester of pregnancy, complicated by chronic placental insufficiency.Materials and methods. The concentration of TNF-α in the homogenate of 120 placentas and the histometric parameters of chorionic villi were determined in patients who underwent latent CMVI and exacerbation of CMVI in the second trimester of gestation. Group 1 included 30 placentas from seronegative women with a physiological course of pregnancy, group 2 included 30 placentas from patients with latent CMVI and chronic compensated placental insufficiency, group 3 – 30 placentas from women with exacerbation of CMVI and chronic compensated placental insufficiency; and group 4 – 30 placentas from pregnant women with exacerbation of CMVI and chronic subcompensated placental insufficiency.Results. In the 1st group in the placenta homogenate the concentration of TNF-α was 16.8±1.86 pg/mL; the number of villi with a diameter of 30-50 microns was 25.4±2.08%, with a diameter of 60-90 microns – 64.4±2.43% and with a diameter of more than 90 microns – 10.2±0.88%; the number of terminal villi with 1-3 capillaries was 27.0±2.29%, with 4- 6 capillaries – 42.1±2.02%, with 7-10 capillaries – 23.9±1.58% and villi with more than 10 capillaries – 7.0±0.79%. In group 2, the concentration of TNF-α in the placenta homogenate was amounted to 22.1±2.06 pg/mL (p>0.05); among the villi, anatomical forms with a diameter of 30-50 μm (p<0.01) were found 1.41 times more often, and villi with a diameter of 60-90 μm (p<0.01) were 1.19 times less common; the number of villi with 4-6 capillaries decreased by 1.21 times (p<0.05) and the number of villi with 7-10 capillaries increased by 1.43 times (p<0.001). In the placentas of group 3, compared with group 2 in the homogenate, there was an increase in the concentration of TNF-α to 60.2±3.47 pg/mL (p<0.001) against the background of a decrease in the concentration of villi with a diameter of 30-50 μm to 26.4±2,61% (p<0.05), villi with 7-10 capillaries up to 20.7±1.53% (p<0.001) and an increase in the number of villi with 1-3 capillaries up to 34.8±3.05% (p<0.05). In the placental homogenate of group 4, compared with group 3, the concentration of TNF-α (p<0.05) increased 1.31 times, the number of villi with a diameter of 60-90 μm increased to 70.2±1.59%, (p<0,01) and villi with 1- 3 capillaries to 46.8±3.76% (p<0.05) with a decrease in the number of villi with a diameter of 30-50 μm to 18.9±1.69% (p<0,05), with 7-10 capillaries up to 13.3±1.36% (p<0.001) and with 10 or more capillaries – up to 3.9±0.43% (p<0.01).Conclusion. In women with exacerbation of CMVI in the second trimester of pregnancy and the development of chronic subcompensated placental insufficiency, inhibition of the growth and angiogenesis of terminal villi is observed against the background of the maximum concentration of TNF-α in the medium.

Lymphocyte Subsets In Chronic Gvhd – a Key Role for B Cells?

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 2311-2311
Author(s):  
Inken Hilgendorf ◽  
Brigitte Mueller-Hilke ◽  
Guenther Kundt ◽  
Ernst Holler ◽  
Petra Hoffmann ◽  
...  
Keyword(s):  
B Cells ◽  
B Cell ◽  
Chronic Gvhd ◽  
Memory B Cells ◽  
Blood Samples ◽  
Cell Counts ◽  
Group 3 ◽  
Group 2 ◽  
B Cell Subsets ◽  
Group 1

Abstract Abstract 2311 Background: Chronic graft-versus host disease (cGVHD) features certain similarities with autoimmune diseases. The pathogenesis of cGVHD after allogeneic hematopoietic stem cell transplantation (alloHSCT), however, is poorly understood. Methods: Peripheral blood samples from 52 pts with active (median day 976, range 177–2773) (group 1), 28 pts with resolved (median day 1207, range 147–2849) (group 2) and 18 pts without cGVHD (median day 1015, range 124–2655) (group 3) were analysed for T and B cell subsets by FACS. 47 pts were transplanted from matched related donors, 40 pts from matched and 11 from mismatched unrelated donors. In addition, blood samples from 20 patients with and 10 patients without history of cGVHD were tested for: antinuclear antibody (ANA), anti-neutrophil cytoplasmatic antibody (ANCA), antimitochondrial antibody (AMA), anti-smooth-muscle antibody (ASMA) and double stranded DNA (dsDNA). Chronic GVHD was evaluated using criteria and guidelines of the National Institute of Health (mild n=16, moderate=18, severe n=18). Results: The absolute CD19+ B cell counts (median in 109/l) in pts with active chronic GVHD (0.03; range 0–2.59) were subnormal and lower than in pts of group 2 (0.140; range 0.001–0.856; p 0.019) and group 3 (0.175; range 0.20–0.553; p 0.002). Significant differences in absolute numbers of the CD27− B cell compartment, including immature (CD19+ CD27− CD38++CD20+IgM+) and transitional B cells (CD19+ CD27− CD38++CD10+CD20+IgM+), (median in 109/l: group1: 0.015; range 0–0.499 vs. group 2: 0.090; range 0–0.667 or vs. group 3: 0.158; range 0.02–0.52; both p<0.001) as well as class switched memory B cells (median in 106/l: 0.045; range 0–96.00 vs. 3.40; range 0–69.35; p 0.032 or vs. 7.40; range 0–56.83; p 0.003) were observed between the groups. Of interest, the CD 27+IgD+IgM+ B cell subpopulation (median in 106/l) is lacking in pts with active cGVHD (0; range 0–1.35) in contrast to patients with resolved (0.43, range 0–17.47; p<0.001) or pts who never experienced cGVHD (1.69; range 0–10.00; p<0.001). The counts of CD8+ T cells (median in 109/l) were significantly lower in pts of group 1 (0.257, range 0.01–1.76) compared to pts of group 2 (0.373; range 0 –1.96; p 0.010) or group 3 (0.545; range 0.06–1.61; p 0.027). No significant differences in CD4+ T cell counts (median in 109/l: 0.274 vs. 0.355 vs. 0.293) including naïve and memory CD4+ T cells as well as regulatory CD25+CD4+ FoxP3+ T cell counts (median in 106/l: 8.11 vs. 6.55 vs. 9.72) were observed between the three groups. In patients with cGVHD ANA was positive in 35% (7/20), ASMA in 20% (4/20) and AMA in 5% (1/20). ANA was positive in 36% (4/11) and ASMA in 27% (3/11) of patients without cGVHD. AMA and dsDNA were negative in all patients without cGVHD and ANCA was negative in all tested patients. 10% (3/31) of patients showed more than one autoantibody. Conclusion: Our data confirm a close association of diminished B cell counts with cGVHD while no difference of the tested autoantibodies was observed between pts with and without cGVHD. The lack of CD 27+IgD+IgM+ B cells in pts with cGVHD indicates functional asplenia in these pts, because IgM+ memory B cells are dependent upon a functional spleen for their generation and/or survival. Analysis of B cell subsets can provide a diagnostic tool for monitoring cGVHD activity but requires prospective evaluation. Disclosures: No relevant conflicts of interest to declare.

scholarly journals The effect of immunomodulators on various markers of the acute inflammation phase in patients with mild community-acquired pneumonia

2021 ◽  
Vol 99 (4) ◽  
pp. 36-43
Author(s):  
M. P. Kostinov ◽  
V. V. Gaynitdinova ◽  
S. V. Kazharova ◽  
V. N. Zorina ◽  
V. B. Polischuk ◽  
...  
Keyword(s):  
Acute Inflammation ◽  
Community Acquired Pneumonia ◽  
Control Group ◽  
Blood Levels ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Tnf Α ◽  
Group 3 ◽  
Group 2 ◽  
Group 1

The objective: to study the effect of immunomodulators on markers of the acute inflammation phase in patients with mild community-acquired pneumonia (CAP).Subjects and methods. Patients (n = 64) with mild CAP (39.62 ± 9.82 years, CRB – 650.15 ± 0.04 scores) were enrolled in the study. The patients were divided into 2 groups: Group 1 (control) received only standard CAP therapy; in the other two groups, immunomodulators were prescribed simultaneously with standard therapy: in Group 2 – bacterial lysate (BL), in Group 3 – azoximer bromide (AB). In the patients, the blood levels of IL-6, TNF-α, C-reactive protein (CRP), lactoferrin were tested before treatment (day 1), and on days 13 and 60 of observation.Results. The initial levels of TNF-α, IL-6, CRP and lactoferrin in the patients were statistically significantly higher above normal ones. A significant decrease in the levels of TNF-α, IL-6, CRP was found in all patients on the 13th and 60th days of observation compared to the 1st day, the maximum reduction was observed in the patients receiving immunomodulators. The biggest decrease in the level of lactoferrin on the 60th day of observation was noted in the group of patients taking BL. The changes in the rate of TNF-α and IL-6 levels decrease on the 13th and 60th days were also statistically significantly more pronounced (compared to the control group). The changes in the rate of decreasing from the baseline on the 13th and 60th days in TNF-α in the BL Group made 44 [-64; -32]% and 85 [-89; -82]%; in the AB Group – 28 [-40; -20]% and 82 [-86; -80]%; in IL-6 in the BL group – 32 [-40; -18]% and 86 [-90; -85]%, in the AB group – 45 [-53; -38]% and 86 [-88; -84]%. In the control group, this parameter for TNF-α was 18 [-32; -8]% and 64 [-78; -56]%, for IL-6 – 11 [-20; -1]% and 75 [-81; -74]%.Conclusion. The addition of immunomodulators (BL, AB) to the therapy of patients with mild CAP results in statistically significant decrease in the blood levels of biomarkers of the acute inflammation phase on the 13th and 60th days.

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