scholarly journals Low-Dose Steroid Therapy Is Associated with Decreased IL-12 Production in PBMCs of Severe Septic Patients

2016 ◽  
Vol 2016 ◽  
pp. 1-8
Author(s):  
Huang-Pin Wu ◽  
Chi-Chung Shih ◽  
Duen-Yau Chuang ◽  
Tien-Hsing Chen
Keyword(s):  
Steroid Therapy ◽  
Low Dose ◽  
Mononuclear Cells ◽  
Human Leukocyte ◽  
Mortality Rates ◽  
Peripheral Blood Mononuclear ◽  
Leukocyte Antigen ◽  
Hla Dr ◽  
Relationship Of ◽  
The Relationship

Background.Sepsis-induced immunosuppression may result in higher mortality rates in patients.Methods. We examined the relationship of cytokine responses from stimulated peripheral blood mononuclear cells (PBMCs) and monocyte human leukocyte antigen-DR (HLA-DR) expression (days 1 and 7) with low-dose steroid therapy in 29 septic patients. Patients were treated according to the guidelines. Thirty healthy controls were enrolled for validation.Results. Eighteen patients were prescribed low-dose steroids and 11 were not. Interleukin- (IL-) 12 responses in patients without low-dose steroid therapy on days 1 and 7 were higher than those with low-dose steroid therapy. Compared to day 1, IL-12 responses significantly increased on day 7 in patients without low-dose steroid therapy. After regression analysis, the change in the IL-12 response from day 7 to day 1 was found to be independently associated with the low-dose steroid therapy. There was no difference in monocyte HLA-DR expression between patients treated with and without low-dose steroid on day 1 or 7. No change in monocyte HLA-DR expression from day 7 to day 1 was observed in patients with or without low-dose steroid therapy.Conclusion. Decreased IL-12 response was associated with the low-dose steroid therapy in PBMCs of septic patients.

scholarly journals Cytokine influence on killing of fresh chronic lymphocytic leukemia cells by human leukocytes

Blood ◽  
1991 ◽  
Vol 77 (12) ◽  
pp. 2707-2715 ◽  
Author(s):  
D Cemerlic ◽  
B Dadey ◽  
T Han ◽  
L Vaickus
Keyword(s):  
Chronic Lymphocytic Leukemia ◽  
Mononuclear Cells ◽  
Protein A ◽  
Human Leukocyte ◽  
Lymphocytic Leukemia ◽  
Target Antigen ◽  
Peripheral Blood Mononuclear ◽  
Ifn Gamma ◽  
Hla Dr

Abstract The feasibility of combining the Lym-1 monoclonal antibody (MoAb) with interferon-gamma (IFN-gamma) in the treatment of chronic lymphocytic leukemia (CLL) was evaluated. We used an in vitro tumor lysis model that incorporated fresh CLL cells from 21 different patients as targets for two distinct normal human leukocyte effector subsets, neutrophils, and peripheral blood mononuclear cells (PBMCs). Lym-1 antigen (Lym-1- Ag) expression varied greatly and did not correlate with the expression of other CLL-associated antigens such as CD5, CD19, or HLA-DR. CLL cells were not lysed by neutrophils alone or with IFN-gamma in the absence of Lym-1. Neutrophil Lym-1-dependent cytotoxicity (ADCC) in the absence of IFN-gamma was weak and inconsistent. IFN-gamma exposure induced MoAb-dependent lysis of 80% of 21 CLL targets and resulted in an eightfold augmentation of neutrophil ADCC against the remainder. Cytotoxicity correlated directly and positively with Lym-1-Ag expression. Confirmation of the need for interaction between neutrophil IgG Fc receptors (Fc gamma Rs) and the Fc portion of the Lym-1 MoAb was obtained by demonstrating that purified Staphylococcus aureus Protein A (SpA) inhibited ADCC. IFN-gamma exposure caused no consistent alternations in Lym-1-Ag expression on CLL cells so that target antigen upregulation was unlikely to account for augmentation of neutrophil ADCC. PBMCs alone, exposed to interkeukin-2 (IL-2) or IFN-gamma, or with Lym-1 in the presence or absence of IL-2 or IFN-gamma were unable to lyse CLL targets. PBMCs were able to kill Raji Burkitt lymphoma cells in conjunction with Lym-1, so their ability to interact with Lym- 1-coated targets and their lytic functions appeared intact. These results emphasize the importance of examining fresh tumor cells with different leukocyte effector subsets before designing a clinical trial that combines a therapeutic MoAb with a cytokine.

scholarly journals Reiter’s syndrome - disease of young men: Analysis of 312 patients

2014 ◽  
Vol 67 (7-8) ◽  
pp. 222-230 ◽  
Author(s):  
Jaroslav Bojovic ◽  
Natasa Strelic ◽  
Ljiljana Pavlica
Keyword(s):  
Synovial Fluid ◽  
Human Leukocyte Antigen ◽  
Reactive Arthritis ◽  
Mononuclear Cells ◽  
Clinical Manifestations ◽  
Human Leukocyte ◽  
Multisystem Disease ◽  
Peripheral Blood Mononuclear ◽  
Leukocyte Antigen ◽  
Number Of Patients

Introduction. Reiter?s syndrome is reactive arthritis occurring after acute urogenital (urethritis, cervicitis) or enterocolitis infections. The associated ophthalmological and/or mucocutaneous changes are full clinical manifestations of this disease. This paper was aimed at analyzing clinical and radiological characteristics and findings of possible etiological factors and protocol for Reiter?s syndrome therapy. Material and Methods. Of 312 patients included in the study, 279 were men and 33 were women, the ratio between them being 8.5:1. The disease was diagnosed based on clinical evidence of two basic characteristics of Reiter?s syndrome: arthritis preceded by acute urogenital or enteral infection. Results. Urogenital and enterocolitic form of disease was found in 242 (77.5%) and 52 (16.5%) patients, respectively; whereas the initial cause was not discovered in 18 patients (6%). Three or two main signs of Reiter?s syndrome were present in approximately the same number of patients (41.7% and 44.2%), whereas all four signs of disease were present in 14.1% of the patients. Acute or sub-acute form was present in 40.5%, while recurrent and chronic disease was diagnosed in 31% and 28.5% of the patients, respectively. The most frequent clinical manifestation of this disease was on the locomotor system as asymmetrical oligoarthritis localized in lower extremities, present in 69.4% of the patients. Chlamydia trachomatis was found in the synovial fluid in 54% of patients (20/37), ureaplasma or mycoplasma was isolated in the synovial tissue of 73.1% of patients (30/41) and in the peripheral blood mononuclear cells in 93.2% of patients (41/44). Human leukocyte antigen B27 was present in 83.3% of patients. Conclusion. Reiter?s syndrome is a multisystem disease, predominantly occurring in human leukocyte antigen B27 positive young males. The fact that the causative agents are found in the synovial membrane or synovial fluid is indicative of infectious rather than reactive arthritis.

scholarly journals Systems biological assessment of immunity to mild versus severe COVID-19 infection in humans

Science ◽  
2020 ◽  
Vol 369 (6508) ◽  
pp. 1210-1220 ◽  
Author(s):  
Prabhu S. Arunachalam ◽  
Florian Wimmers ◽  
Chris Ka Pun Mok ◽  
Ranawaka A. P. M. Perera ◽  
Madeleine Scott ◽  
...  
Keyword(s):  
Mononuclear Cells ◽  
Mammalian Target Of Rapamycin ◽  
Myeloid Cells ◽  
Human Leukocyte ◽  
Oncostatin M ◽  
Biological Assessment ◽  
Interferon Α ◽  
Type I ◽  
Peripheral Blood Mononuclear ◽  
Hla Dr

Coronavirus disease 2019 (COVID-19) represents a global crisis, yet major knowledge gaps remain about human immunity to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). We analyzed immune responses in 76 COVID-19 patients and 69 healthy individuals from Hong Kong and Atlanta, Georgia, United States. In the peripheral blood mononuclear cells (PBMCs) of COVID-19 patients, we observed reduced expression of human leukocyte antigen class DR (HLA-DR) and proinflammatory cytokines by myeloid cells as well as impaired mammalian target of rapamycin (mTOR) signaling and interferon-α (IFN-α) production by plasmacytoid dendritic cells. By contrast, we detected enhanced plasma levels of inflammatory mediators—including EN-RAGE, TNFSF14, and oncostatin M—which correlated with disease severity and increased bacterial products in plasma. Single-cell transcriptomics revealed a lack of type I IFNs, reduced HLA-DR in the myeloid cells of patients with severe COVID-19, and transient expression of IFN-stimulated genes. This was consistent with bulk PBMC transcriptomics and transient, low IFN-α levels in plasma during infection. These results reveal mechanisms and potential therapeutic targets for COVID-19.

scholarly journals Cytokine influence on killing of fresh chronic lymphocytic leukemia cells by human leukocytes

Blood ◽  
1991 ◽  
Vol 77 (12) ◽  
pp. 2707-2715
Author(s):  
D Cemerlic ◽  
B Dadey ◽  
T Han ◽  
L Vaickus
Keyword(s):  
Chronic Lymphocytic Leukemia ◽  
Mononuclear Cells ◽  
Protein A ◽  
Human Leukocyte ◽  
Lymphocytic Leukemia ◽  
Target Antigen ◽  
Peripheral Blood Mononuclear ◽  
Ifn Gamma ◽  
Hla Dr

The feasibility of combining the Lym-1 monoclonal antibody (MoAb) with interferon-gamma (IFN-gamma) in the treatment of chronic lymphocytic leukemia (CLL) was evaluated. We used an in vitro tumor lysis model that incorporated fresh CLL cells from 21 different patients as targets for two distinct normal human leukocyte effector subsets, neutrophils, and peripheral blood mononuclear cells (PBMCs). Lym-1 antigen (Lym-1- Ag) expression varied greatly and did not correlate with the expression of other CLL-associated antigens such as CD5, CD19, or HLA-DR. CLL cells were not lysed by neutrophils alone or with IFN-gamma in the absence of Lym-1. Neutrophil Lym-1-dependent cytotoxicity (ADCC) in the absence of IFN-gamma was weak and inconsistent. IFN-gamma exposure induced MoAb-dependent lysis of 80% of 21 CLL targets and resulted in an eightfold augmentation of neutrophil ADCC against the remainder. Cytotoxicity correlated directly and positively with Lym-1-Ag expression. Confirmation of the need for interaction between neutrophil IgG Fc receptors (Fc gamma Rs) and the Fc portion of the Lym-1 MoAb was obtained by demonstrating that purified Staphylococcus aureus Protein A (SpA) inhibited ADCC. IFN-gamma exposure caused no consistent alternations in Lym-1-Ag expression on CLL cells so that target antigen upregulation was unlikely to account for augmentation of neutrophil ADCC. PBMCs alone, exposed to interkeukin-2 (IL-2) or IFN-gamma, or with Lym-1 in the presence or absence of IL-2 or IFN-gamma were unable to lyse CLL targets. PBMCs were able to kill Raji Burkitt lymphoma cells in conjunction with Lym-1, so their ability to interact with Lym- 1-coated targets and their lytic functions appeared intact. These results emphasize the importance of examining fresh tumor cells with different leukocyte effector subsets before designing a clinical trial that combines a therapeutic MoAb with a cytokine.

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