Investigation the effects of cigarette smoke on immunoglobulin levels in serum and saliva samples of smoker and non-Smoker subjects using antibody-microarray technology

Cigarette smoke (CS) has many damaging effects on the body, and the chronic inhalation of cigarette smoke can change immunological functions through impact on both innate and adaptive immunity. The incidences of many diseases are affected by the adverse effects of cigarette smoke on the immune system, and the induction of an inflammatory response, which affects several tissues and organs. On this basis, a comparison of smokers′ and non-smokers′ immunoglobulin levels could provide valuable insights into the mechanisms of smoking related diseases. Although the effects of cigarette smoking on humoral and cellular immunity have been investigated previously, the results have varied between the studies, and therefore more research is still required. The aim of this study was to determine whether the levels of immunoglobulin (Ig) isotypes are different in the serum and saliva of non-smoking individuals compared to smoking individuals. An examination of serum and saliva would provide information on the effects of cigarette smoke systemically and in the oral mucosa, respectively. The effects of cigarette smoke extract on B-cell secretions were also examined to establish whether cigarette smoke components can have direct effects on immunoglobulin production by B cells. In order to determine Ig isotype levels, antibody microarray techniques were established and calibrated for determining the sample concentrations of IgM, IgG, IgA and IgD. The results showed that smoking has different effects on systemic and salivary immunoglobulin levels. In the serum, smokers had decreased levels of IgG and IgD, but increased IgM and IgA levels compared to non-smokers. However, in the saliva smokers had decreased levels of IgG, IgD, and IgM, whereas there were increased levels of IgA in smokers’ saliva. As CS has been found to influence the serum and salivary levels of Ig isotypes ex-vivo, the mechanisms underlying these effects were investigated in vitro to determine whether the changes were as a result of a direct effect of the CS on B-cells. This study has shown that CS had deleterious effects on the production and the levels, of Ig isotypes. These results support the concept that CS is related to diseases, and more research is necessary in this field

Investigation the effects of cigarette smoke on immunoglobulin levels in serum and saliva samples of smoker and non-Smoker subjects using antibody-microarray technology

Cigarette smoke (CS) has many damaging effects on the body, and the chronic inhalation of cigarette smoke can change immunological functions through impact on both innate and adaptive immunity. The incidences of many diseases are affected by the adverse effects of cigarette smoke on the immune system, and the induction of an inflammatory response, which affects several tissues and organs. On this basis, a comparison of smokers′ and non-smokers′ immunoglobulin levels could provide valuable insights into the mechanisms of smoking related diseases. Although the effects of cigarette smoking on humoral and cellular immunity have been investigated previously, the results have varied between the studies, and therefore more research is still required. The aim of this study was to determine whether the levels of immunoglobulin (Ig) isotypes are different in the serum and saliva of non-smoking individuals compared to smoking individuals. An examination of serum and saliva would provide information on the effects of cigarette smoke systemically and in the oral mucosa, respectively. The effects of cigarette smoke extract on B-cell secretions were also examined to establish whether cigarette smoke components can have direct effects on immunoglobulin production by B cells. In order to determine Ig isotype levels, antibody microarray techniques were established and calibrated for determining the sample concentrations of IgM, IgG, IgA and IgD. The results showed that smoking has different effects on systemic and salivary immunoglobulin levels. In the serum, smokers had decreased levels of IgG and IgD, but increased IgM and IgA levels compared to non-smokers. However, in the saliva smokers had decreased levels of IgG, IgD, and IgM, whereas there were increased levels of IgA in smokers’ saliva. As CS has been found to influence the serum and salivary levels of Ig isotypes ex-vivo, the mechanisms underlying these effects were investigated in vitro to determine whether the changes were as a result of a direct effect of the CS on B-cells. This study has shown that CS had deleterious effects on the production and the levels, of Ig isotypes. These results support the concept that CS is related to diseases, and more research is necessary in this field

Cigarette smoking differentially affects immunoglobulin class levels in serum and saliva: An investigation and review

The aim of the present study was to compare concentrations of IgG, IgA, IgM and IgD in both serum and saliva samples from smoking and non-smoking subjects using a protein microarray assay. The findings were also compared to previous studies. Serum and saliva were collected from 48 smoking male subjects and 48 age-matched neversmoker male subjects. The protein microarray assays for detection of human IgG, IgM, IgA and IgD were established and optimized using Ig class-specific affinity purified goat anti-human Ig-Fc capture antibodies and horseradish peroxidase (HRP)- conjugated goat anti-human Ig-Fc detection antibodies. The Ig class specificity of the microarray assays was verified and the optimal dilutions of serum and saliva samples was determined for quantification of Ig levels against standard curves. We found that smoking is associated with reduced IgG concentrations and enhanced IgA concentrations in both serum and saliva. By contrast, smoking differentially affected IgM concentrations – causing increased concentrations in serum, but decreased concentrations in saliva. Smoking was associated with decreased IgD concentrations in serum, and did not have a significant effect on the very low IgD concentrations in saliva. Thus, cigarette smoking differentially affects the levels of Ig classes systemically and in the oral mucosa. Although there is variation between the results of different published studies, there is a consensus that smokers have significantly reduced levels of IgG in both serum and saliva. A functional antibody deficiency associated with smoking may compromise the body’s response to infection and result in a predisposition to the development of autoimmunity

Thymoquinone Effect on Monocyte-Derived Macrophages, Cell-Surface Molecule Expression, and Phagocytosis

Macrophages are one of the most important cells in the immune system. They act as links between innate and adaptive immunities. In this study, the aim was to examine thymoquinone effects on the immunological properties of different macrophages. Peripheral blood mononuclear cells were isolated from blood from healthy volunteers by negative selection of monocytes that had been cultured for seven days to differentiate into macrophages. Cells were cultured with or without the presence of thymoquinone (TQ), which was used in two different concentrations (50 μg/mL and 100 μg/mL. Cluster of differentiation 80 (CD80), cluster of differentiation 86 (CD86), and human leukocyte antigen DR isotype (HLA-DR) were measured by flow cytometry, and the secretion of interferon gamma (IFN-γ) and tumour necrosis factor alpha (TNF-α) was measured. Cells were also tested for their E. coli phagocytosis abilities. The data showed that the expression of HLA-DR was significantly higher in cells treated with 100 μL/mL TQ. In addition, IFN-γ concentration increased in the 100 μg/mL TQ-treated cells. The macrophage phagocytosis results showed a significant difference in 50 μg/mL TQ-treated cells compared to the controls. TQ may enhance the immunological properties of macrophages during the early stages of innate immunity by activating phagocytosis ability and by increasing the expression of HLA-DR and the secretion of IFN-γ, which may enhance the antigen-presentation capabilities of macrophages

Role of CD27 and SAMHD1 and their genetic susceptibility to COVID-19

SARS-CoV-2, which initiated the worldwide COVID-19 epidemic in 2019, has rapidly emerged and spread, resulting in significant public health challenges worldwide. The COVID-19 severity signs and their association with specific genes have been investigated to better comprehend this phenomenon. In this study, several genes were investigated to see whether they correspond with COVID-19 sickness severity. This research aims to determine and evaluate certain gene expression levels associated with the immune system, as these genes were reported to play important roles in immune control during the COVID-19 outbreak. We analyzed two immunity-linked genes: CD27 and SAMHD1 in COVID-19 patients’ samples using RT-PCR, compared them to the samples from recovered, immunized, and healthy individuals. These data were examined to determine the potential relationships between clinical patterns, illness severity, and progression, and SARS-CoV-2 infection immunology.We observed that CD27 gene expression was higher in COVID-19 vaccinated and control groups, but lower in active and recovered COVID-19 patients. On the other hand, SAMHD1 gene expression was elevated in infected and recovered COVID-19 groups. According to our study, the proteins CD27 and SAMHD1 are essential for controlling the immunological response to COVID-19. Changes in their expression levels could increase the susceptibility of patients to severe complications associated with the disease. Therefore, the gene expression level of these proteins could serve as viable prognostic markers for COVID-19

T Cells Immunophenotyping and CD38 Overexpression as Hallmarks of the Severity of COVID-19 and Predictors of Patients’ Outcomes

Background: By the end of 2019, the COVID-19 pandemic spread all around the world with a wide spectrum of clinical presentations ranging from mild to moderate to severe or critical cases. T cell subtype dysregulation is mostly involved in the immunopathogenic mechanism. The present study aimed to highlight the role of monitoring T cell subtypes and their activation (expression of CD38) in COVID-19 patients compared to healthy subjects and their role in predicting severity and patients’ outcomes. Materials: The study involved 70 adult COVID-19 confirmed cases stratified into three groups: a mild/asymptomatic group, a clinically moderate group, and a clinically severe/critical group. Flow cytometry analysis was used for the assessment of CD3+ cells for total T cell count, CD4+ cells for helper T cells (Th), CD8+ cells for cytotoxic T cells (Tc), CD4+CD25+ cells for regulatory T cells (T reg), and CD38 expression in CD4+ T cells and CD8+ T cells for T cell activation. Results: A statistically significant difference was found between COVID-19 cases and healthy controls as regards low counts of all the targeted T cell subtypes, with the lowest counts detected among patients of the severe/critical group. Furthermore, CD38 overexpression was observed in both CD4+ and CD8+ T cells. Conclusion: Decreased T cell count, specifically CD8+ T cell (Tc), with T cell overactivation which was indicated by CD38 overexpression on CD4+ and CD8+ T cells had a substantial prognostic role in predicting severity and mortality among COVID-19 patients. These findings can provide a preliminary tool for clinicians to identify high-risk patients requiring vigilant monitoring, customized supportive therapy, or ICU admission. Studies on larger patient groups are needed