scholarly journals Immunophenotyping of circulating mononuclear cells in active pulmonary tuberculosis

2018 ◽  
Vol 12 (12) ◽  
pp. 1073-1078
Author(s):  
Amany Elkholy ◽  
Mirvat El Anany ◽  
Ghada Mohamed Ezzat ◽  
Fadwa Abd El Reheem ◽  
Assem Fouad Elessawy
Keyword(s):  
T Cells ◽  
B Lymphocytes ◽  
Disease Severity ◽  
Defense Mechanisms ◽  
Mononuclear Cells ◽  
Immune Defense ◽  
Skin Tests ◽  
Active Pulmonary Tuberculosis ◽  
Mild Disease ◽  
Regulatory Lymphocytes

Introduction: Interpreting the interactions between M. tuberculosis and the host innate and adaptive immune defense mechanisms is mandatory for understanding the pathogenesis of active pulmonary TB (APTB). The aim was to describe the distribution of mononuclear cells in APTB and their relation to disease severity. Methodology: A case-control study of peripheral blood CD4+ T cells, CD8+ T cells, B-lymphocytes, NK cells, T regulatory lymphocytes (Tregs) and monocytes by flow cytometry. The patients had clinical presentations of APTB, positive tuberculin skin tests, acid-fast bacilli smears and sputum cultures using BACTEC 960. Results: There was a significant decrease in the haemoglobin level and the absolute lymphocytic count (p < 0.01), while both the neutrophil count and erythrocyte sedimentation rate showed significant increase in the APTB patients compared to HC with p-values < 0.001 and < 0.0001 respectively. Both the CD4+/CD8+ ratio and the percentages of CD3−CD19+ cells were significantly lower in APTB patients (p = 0.03 and p = 0.005 respectively). The percentages of CD4+, CD8+, CD3−CD19+, CD14+, and CD3−CD (16+56)+ cells showed no significant differences, when comparing either disease severity groups, or cavitated and non-cavitated groups of APTB patients. There was significant increase in the CD4+25+ lymphocytes in the advanced APTB patients than in the mild disease group (p < 0.05). Conclusions: B-lymphocytes and CD4/CD8 ratios were significantly lower in the APTB patients than controls with no association with disease severity. CD4+ CD25+hi Tregs were significantly higher in the advanced versus mild groups.

PSK and Trx80 inhibit B-cell growth in EBV-infected cord blood mononuclear cells through T cells activated by the monocyte products IL-15 and IL-12

Blood ◽  
2005 ◽  
Vol 105 (4) ◽  
pp. 1606-1613 ◽  
Author(s):  
Anquan Liu ◽  
Jack L. Arbiser ◽  
Arne Holmgren ◽  
George Klein ◽  
Eva Klein
Keyword(s):  
T Cells ◽  
Cord Blood ◽  
B Cell ◽  
B Lymphocytes ◽  
Cell Activation ◽  
Mononuclear Cells ◽  
Nk Cell ◽  
Barr Virus ◽  
Epstein Barr

AbstractEpstein-Barr virus (EBV)–specific immunologic memory is not transferred from mother to child. In vitro infection of cord blood cells can therefore readily lead to the outgrowth of transformed B lymphocytes. We found that the immunomodulator polysaccharide K (PSK) or the mitogenic cytokine truncated thioredoxin (Trx80) inhibited the EBV-induced B-cell proliferation. Using signaling lymphocytic activation molecule (SLAM)–associated protein (SAP) induction as a sign for T- and natural killer (NK) cell activation, we could follow it without any need for cell separation because neither macrophages nor B lymphocytes express SAP. The results suggest the following scenario: EBV infected and activated B lymphocytes. Upon interacting with these cells, T cells became posed for responding to cytokines produced by monocytes. Both PSK and Trx80, which is a secreted C-terminally truncated thioredoxin, activated the monocytes, which then produced cytokines in the presence of the primed T cells. PSK induced interleukin-15 (IL-15), while Trx80 induced IL-12 production. Both cytokines activated the T cells for function. Phosphatidylinositol 3–(PI 3)–kinase and reactive oxygen species (ROSs) were involved in the PSK-induced activation of monocytes. Restimulation of the cultures with EBV-transformed B cells generated specific cytotoxic activity.

scholarly journals Flagellum-Mediated Biofilm Defense Mechanisms of Pseudomonas aeruginosa against Host-Derived Lactoferrin

2009 ◽  
Vol 77 (10) ◽  
pp. 4559-4566 ◽  
Author(s):  
Jeff G. Leid ◽  
Mathias Kerr ◽  
Candice Selgado ◽  
Chelsa Johnson ◽  
Gabriel Moreno ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Defense Mechanisms ◽  
Mononuclear Cells ◽  
Immune Defense ◽  
Bacterial Biofilm ◽  
Necrosis Factor Alpha ◽  
Bacterial Killing ◽  
Tnf Α ◽  
High Doses ◽  
Biofilm Development

ABSTRACT Chronic infection with the gram-negative organism Pseudomonas aeruginosa is a leading cause of morbidity and mortality in human patients, despite high doses of antibiotics used to treat the various diseases this organism causes. These infections are chronic because P. aeruginosa readily forms biofilms, which are inherently resistant to antibiotics as well as the host's immune system. Our laboratory has been investigating specific mutations in P. aeruginosa that regulate biofilm bacterial susceptibility to the host. To continue our investigation of the role of genetics in bacterial biofilm host resistance, we examined P. aeruginosa biofilms that lack the flgK gene. This mutant lacks flagella, which results in defects in early biofilm development (up to 36 h). For these experiments, the flgK-disrupted strain and the parental strain (PA14) were used in a modified version of the 96-well plate microtiter assay. Biofilms were challenged with freshly isolated human leukocytes for 4 to 6 h and viable bacteria enumerated by CFU. Subsequent to the challenge, both mononuclear cells (monocytes and lymphocytes) and neutrophils, along with tumor necrosis factor alpha (TNF-α), were required for optimal killing of the flgK biofilm bacteria. We identified a cytokine cross talk network between mononuclear cells and neutrophils that was essential to the production of lactoferrin and bacterial killing. Our data suggest that TNF-α is secreted from mononuclear cells, causing neutrophil activation, resulting in the secretion of bactericidal concentrations of lactoferrin. These results extend previous studies of the importance of lactoferrin in the innate immune defense against bacterial biofilms.

scholarly journals COVID-19 Vaccines for HIV-Infected Patients

Viruses ◽  
2021 ◽  
Vol 13 (10) ◽  
pp. 1890
Author(s):  
Maria M. Plummer ◽  
Charles S. Pavia
Keyword(s):  
T Cells ◽  
Defense Mechanisms ◽  
Etiologic Agent ◽  
Immune Defense ◽  
Microbial Pathogens ◽  
Protective Measure ◽  
People Living With Hiv ◽  
Reverse Transcriptase Enzyme ◽  
Molecular Tests ◽  
Hiv Aids

Nearly 40 years have passed since the initial cases of infection with the human mmunodeficiency virus (HIV) were identified as a new disease entity and the cause of acquired immunodeficiency disease (AIDS). This virus, unlike any other, is capable of causing severe suppression of our adaptive immune defense mechanisms by directly infecting and destroying helper T cells leading to increased susceptibility to a wide variety of microbial pathogens, especially those considered to be intracellular or opportunistic. After T cells are infected, HIV reproduces itself via a somewhat unique mechanism involving various metabolic steps, which includes the use of a reverse transcriptase enzyme that enables the viral RNA to produce copies of its complementary DNA. Subsequent physiologic steps lead to the production of new virus progeny and the eventual death of the invaded T cell. Fortunately, both serologic and molecular tests (such as PCR) can be used to confirm the diagnosis of an HIV infection. In the wake of the current COVID-19 pandemic, it appears that people living with HIV/AIDS are equally or slightly more susceptible to the etiologic agent, SARS-CoV-2, than the general population having intact immune systems, but they may have more serious outcomes. Limited clinical trials have also shown that the currently available COVID-19 vaccines are both safe and effective in affording protection to HIV/AIDS patients. In this review, we further explore the unique dynamic of HIV/AIDS in the context of the worldwide COVID-19 pandemic and the implementation of vaccines as a protective measure against COVID-19, as well as what immune parameters and safeguards should be monitored in this immunocompromised group following vaccination.

scholarly journals In-depth phenotyping of human peripheral blood mononuclear cells in convalescent COVID-19 patients following a mild versus severe disease course

2020 ◽  
Author(s):  
Chang-Feng Chu ◽  
Florian Sabath ◽  
Shan Sun ◽  
Ying-Yin Chao ◽  
Christina E. Zielinski
Keyword(s):  
T Cells ◽  
Disease Severity ◽  
Peripheral Blood Mononuclear Cells ◽  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Disease Course ◽  
Peripheral Blood Mononuclear ◽  
Adaptive Immune ◽  
Immune Signatures ◽  
Blood Mononuclear Cells

AbstractBackgroundCovid-19, the disease caused by infection with SARS-CoV-2, has developed to a pandemic causing more than 239, 000 deaths worldwide as of 6th May according to the World Health Organization (WHO). It presents with a highly variable disease course ranging from a large proportion of asymptomatic cases to severe respiratory failure in 17-29% of cases even in the absence of apparent comorbidities 1, 2. This implies a diverse host immune response to SARS-CoV-2. The immunological characteristics underlying these divergent disease courses, however, still remain elusive. While insights into abrogations of innate immunity begin to emerge, adaptive immune responses towards SARS-CoV-2 are poorly investigated, although they serve as immune signatures of protection and vaccine responses. We therefore set out to characterize immune signatures of convalescent COVID-19 patients stratified according to their disease severity.MethodsWe performed high-dimensional flow cytometric profiling of peripheral blood mononuclear cells of convalescent COVID-19 patients who we stratified according to their disease severity by a physician-assisted questionnaire based assessment of COVID-19 symptoms.ResultsSurprisingly, we did not observe any difference in the relative proportions of any major immune cell type in convalescent patients presenting with different severity of COVID-19 disease except for a reduction in monocytes. The frequency of Tnaive T cells was significantly reduced in CD4+ and CD8+ T cells, whereas other T cell differentiations states (TCM, TEM, TEMRA) remained relatively unaffected by COVID-19 severity as assessed approximately two weeks after infection.ConclusionsIn our COVID-19 patient cohort, which is characterized by absence of comorbidities and therapeutic interventions other than symptomatic antipyretics, the immunophenotype is similar irrespective of a highly variable disease severity. Convalescence is therefore associated with a rather uniform immune signature. Abrogations, which were previously identified in the innate and adaptive immune compartment of COVID-19 patients should be scrutinized for direct associations with a preconditioned immune system shaped and made vulnerable for SARS-CoV-2 by preexisting comorbidities.

scholarly journals An untargeted metabolomic approach to identify antiviral defense mechanisms in memory leukocytes secreting in vitro IgG anti-SARS-Cov-2

2021 ◽  
Author(s):  
Anna Maria Timperio ◽  
Federica Gevi ◽  
Giuseppina Fanelli ◽  
Veronica Lelli ◽  
Gianpaolo Zarletti ◽  
...  
Keyword(s):  
Defense Mechanisms ◽  
Mononuclear Cells ◽  
Inflammatory Responses ◽  
Cell Metabolism ◽  
Immune Defense ◽  
Igg Antibody ◽  
Peripheral Blood Mononuclear ◽  
Multiple Organs ◽  
Metabolic Activities

Available knowledge shows that individuals infected by SARS-CoV-2 undergo an altered metabolic state in multiple organs. Metabolic activities are directly involved in modulating the immune responses against infectious diseases, yet our understanding remains limited on how host metabolism relates with inflammatory responses. To better elucidate the underlying biochemistry of leukocytes response, we focused our analysis on the possible relationships between SARS-CoV-2 post-infection stages and distinct metabolic pathways. Indeed, in cultures of peripheral blood mononuclear cells (PBMC, n=48) obtained 60-90 days after infection and showing in vitro IgG antibody memory for spike-S1 antigen (n=19), we observed a significant altered metabolism of tryptophan and urea cycle pathways. This work for the first time identifies metabolic routes in cell metabolism possibly related to later stages of immune defense against SARS-Cov-2 infection, namely when circulating antibodies may be absent, but an antibody memory is present. The results suggest a reprogramming of leukocyte metabolism after viral pathogenesis through activation of specific amino acid pathways possibly related to protective immunity against SARS-CoV-2.

scholarly journals Single-cell RNA-seq and V(D)J profiling of immune cells in COVID-19 patients

2020 ◽  
Author(s):  
Xiaoying Fan ◽  
Xiangyang Chi ◽  
Wenji Ma ◽  
Suijuan Zhong ◽  
Yunzhu Dong ◽  
...  
Keyword(s):  
T Cells ◽  
B Cells ◽  
Virus Infection ◽  
Single Cell ◽  
B Lymphocytes ◽  
Immune Cells ◽  
Mononuclear Cells ◽  
Plasma Cells ◽  
Inflammatory Responses ◽  
Peripheral Blood Mononuclear

Coronavirus disease 2019 (COVID-19) has caused over 220,000 deaths so far and is still an ongoing global health problem. However, the immunopathological changes of key types of immune cells during and after virus infection remain unclear. Here, we enriched CD3+ and CD19+ lymphocytes from peripheral blood mononuclear cells of COVID-19 patients (severe patients and recovered patients at early or late stages) and healthy people (SARS-CoV-2 negative) and revealed transcriptional profiles and changes in these lymphocytes by comprehensive single-cell transcriptome and V(D)J recombination analyses. We found that although the T lymphocytes were decreased in the blood of patients with virus infection, the remaining T cells still highly expressed inflammatory genes and persisted for a while after recovery in patients. We also observed the potential transition from effector CD8 T cells to central memory T cells in recovered patients at the late stage. Among B lymphocytes, we analyzed the expansion trajectory of a subtype of plasma cells in severe COVID-19 patients and traced the source as atypical memory B cells (AMBCs). Additional BCR and TCR analyses revealed a high level of clonal expansion in patients with severe COVID-19, especially of B lymphocytes, and the clonally expanded B cells highly expressed genes related to inflammatory responses and lymphocyte activation. V-J gene usage and clonal types of higher frequency in COVID-19 patients were also summarized. Taken together, our results provide crucial insights into the immune response against patients with severe COVID-19 and recovered patients and valuable information for the development of vaccines and therapeutic strategies.

scholarly journals Alterations in the phenotype of hairy cells during culture in the presence of PHA: requirement for T cells

Blood ◽  
1982 ◽  
Vol 59 (5) ◽  
pp. 895-899 ◽  
Author(s):  
CP Worman ◽  
PC Beverley ◽  
JC Cawley
Keyword(s):  
T Cells ◽  
Hairy Cell Leukemia ◽  
Mononuclear Cells ◽  
Cultured Cells ◽  
Phenotypic Change ◽  
Cell Contact ◽  
Hairy Cell ◽  
Cell Leukemia ◽  
Peripheral Blood Mononuclear ◽  
Hairy Cells

Abstract Culture studies of peripheral blood mononuclear cells from 7 entirely typical cases of hairy cell leukemia showed that after culture in the presence of PHA for 2--5 days, the predominant cell type changed from E- SIg+ CIg+ gamma FcR+ muFcR+ hairy cells to an E+ SIg- CIg- gamma FcR- muFcR- population of transformed cells derived from hairy cells. Depletion and readdition experiments demonstrated that cell-to-cell contact with T cells was necessary for the phenotypic change, while several observations indicated that the E+ population was not derived from T cells present before culture. The E positivity of the cultured cells was shown to be due to the possession of E receptor not acquired from the culture fluid, but the cells differed from true T cells in lacking both mature and immature T-cell antigens. The relevance of these in vitro observations to the continuing controversy concerning the nature of the hairy cell and to the in vivo fluctuations in immunologic phenotype not infrequently observed in hairy cell leukemia is briefly discussed.

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