Abstract
BackgroundAlthough the onset of inflammatory cascades may profoundly influence the nature of antibody responses, the interplay between inflammatory and humoral (antibody) immune markers remains unclear. Thus, we explored the reciprocity between the humoral immune system and inflammation and assessed how external socio-demographic factors may influence these interactions. From the AMORIS cohort, 5513 individuals were identified with baseline measurements of serum humoral immune [immunoglobulin G, A & M (IgG, IgA, IgM)] and inflammation (C-reactive protein (CRP), albumin, haptoglobin, white blood cells (WBC), iron and total iron-binding capacity) markers measured on the same day. Correlation analysis, principal component analysis and hierarchical clustering were used to evaluate biomarkers correlation, variation and associations. Multivariate analysis of variance was used to assess associations between biomarkers and educational level, socio-economic status, sex and age.ResultsFrequently used serum markers for inflammation, CRP, haptoglobin and white blood cells, correlated together. Hierarchical clustering and principal component analysis confirmed the interaction between these main biological responses, showing an acute response component (CRP, Haptoglobin, WBC, IgM) and adaptive response component (Albumin, Iron, TIBC, IgA, IgG). A socioeconomic gradient associated with worse health outcomes was observed, specifically low educational level, older age and male sex were associated with serum levels that indicated infection and inflammation.ConclusionsThese findings indicate that serum markers of the humoral immune system and inflammation closely interact in response to infection or inflammation. Clustering analysis presented two main immune response components: an acute and an adaptive response, comprising markers of both biological pathways. Future studies should shift from single internal marker assessment to multiple humoral and inflammation serum markers combined, when assessing risk of clinical outcomes such as cancer.
Highlights
The onset of inflammatory cascades may profoundly influence the nature of antibody responses, the interplay between inflammatory and humoral immune markers remains unclear
The study population consisted of 5513 participants whom had all serum markers of the humoral immune system and inflammation measured on the same day
83.98% of the individuals had no diseases recorded at the time the measurements were taken, which implies the healthy status of the study population
Summary
The onset of inflammatory cascades may profoundly influence the nature of antibody responses, the interplay between inflammatory and humoral (antibody) immune markers remains unclear. Macrophages conduct the defence against bacteria and fungi, and by acting as antigen-presenting cells to trigger adaptive immunity and as effector cells in antibody-dependent cellular cytotoxicity (ADCC) and phagocytosis (ADCP). The adaptive immune system consists of cell mediated and humoral (antibody) immunity and can respond to protect from pathogens. Activation of humoral immunity can manifest in the form of serum antibodies, of different classes, including IgM, IgA, IgG and IgE, produced by plasma B cells. Mature class-switched and affinity-matured antibodies can recognise antigens with high affinity, engage immune effector cells to mediate pathogen ADCC and ADCP, and trigger the complement cascade leading to effective elimination of infection [4]. Cell mediated immunity relies on the direct cytotoxic activity of specific immune cells, such as cytotoxic T cells, in conjunction with various immune cells and components [2]
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