Abstract

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 individuals using a protein microarray assay. The findings were also compared to previous studies. Serum and saliva were collected from 48 smoking male individuals and 48 age-matched never-smoker male individuals. 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 were 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.

Highlights

  • Cigarette smoke (CS) has numerous toxic chemical constituents, which have cytotoxic, mutagenic, carcinogenic, and/or antigenic properties (1, 2)

  • An important facet of these effects is that CS causes dysregulation and impairment of B lymphocytes (6-10); nicotinic receptors are expressed by B cells (11), and long-term exposure to nicotine can suppress B cell development, proliferation and immune functions (9, 12-14)

  • Numerous studies have investigated the effects of tobacco smoking on immunoglobulin (Ig) levels using a variety of assays

Read more

Summary

Introduction

Cigarette smoke (CS) has numerous toxic chemical constituents, which have cytotoxic, mutagenic, carcinogenic, and/or antigenic properties (1, 2). The immune system is affected in a variety of ways by CS, ranging from immunosuppression and increased susceptibility to infection to promotion of inflammation and immunopathology (3) With regard to the latter, CS is the major cause of chronic obstructive pulmonary disease (COPD) (4), and smoking is a recognised risk factor for the occurrence of autoimmune diseases (5). Investigations of Ig levels in the saliva of smokers and nonsmokers have been carried out using mainly ELISA (23-29), immunodiffusion assays (30-32) or turbidimetry (33) have been used These studies have generated varying results concerning the effects of smoking on the concentrations of different Ig classes (IgG, IgA, IgM) in serum or saliva, reporting that smoking is associated with increased, decreased or unchanged Ig class concentrations compared to non-smoking controls. Few of these studies have investigated the effects of smoking on levels of IgD (20, 22): this is expressed in the upper aerodigestive tract in humans (34), which is heavily exposed to CS in smokers

Objectives
Methods
Results

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.