International forum. an investigation of iron status in blood donors

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ABO blood group type does not influence the level of SARS-CoV-2 antibody response in convalescent plasma donors

AbstractThe association of ABO blood group types with the COVID-19 disease has been confirmed by several studies, with the blood group A-type patients being more susceptible and prone to more severe clinical course of disease. Similarly, some authors explored the association of ABO-types and the levels of anti-SARS-CoV-2 antibodies in convalescents. The recent reports mostly support a theory that non-O blood group convalescents present with higher levels of anti-SARS-CoV-2 antibodies. Since these findings were based on small convalescent cohorts, we quantified the anti-SARS-CoV-2 antibodiy levels in four larger cohorts of total 3185 convalescent plasma donors with three commercial serological tests and one standard neutralizing antibody test. The majority of donors had undergone a mild form of disease and the median time of sampling was 66 days after the onset of COVID-19 symptoms. None of the antibody quantitation methods showed an association of the ABO blood group types with the level of anti-SARS-CoV-2 antibodies. The same result is evident in the group of vaccinated individuals (n=370) as well as in the groups stratified into three post-COVID-19 periods (0-60, 60-120, and 120-180 days). In conclusion we can state that the ABO blood group type does not influence the level of SARS-CoV-2 antibody response in COVID-19 convalescent plasma donors.</jats:p

Naturally occurring antibodies against serum amyloid A reduce IL-6 release from peripheral blood mononuclear cells

<div><p>Serum amyloid A (SAA) is a sensitive inflammatory marker rapidly increased in response to infection, injury or trauma during the acute phase. Resolution of the acute phase and SAA reduction are well documented, however the exact mechanism remains elusive. Two inducible SAA proteins, SAA1 and SAA2, with their variants could contribute to systemic inflammation. While unconjugated human variant SAA1α is already commercially available, the variants of SAA2 are not. Antibodies against SAA have been identified in apparently healthy blood donors (HBDs) in smaller, preliminary studies. So, our objective was to detect anti-SAA and anti-SAA1α autoantibodies in the sera of 300 HBDs using ELISA, characterize their specificity and avidity. Additionally, we aimed to determine the presence of anti-SAA and anti-SAA1α autoantibodies in intravenous immunoglobulin (IVIg) preparations and examine their effects on released IL-6 from SAA/SAA1α-treated peripheral blood mononuclear cells (PBMCs). Autoantibodies against SAA and SAA1α had a median (IQR) absorbance OD (A₄₅₀) of 0.655 (0.262–1.293) and 0.493 (0.284–0.713), respectively. Both anti-SAA and anti-SAA1α exhibited heterogeneous to high avidity and reached peak levels between 41–50 years, then diminished with age in the oldest group (51–67 years). Women consistently exhibited significantly higher levels than men. Good positive correlation was observed between anti-SAA and anti-SAA1α. Both anti-SAA and anti-SAA1α were detected in IVIg, their fractions subsequently isolated, and shown to decrease IL-6 protein levels released from SAA/SAA1α-treated PBMCs. In conclusion, naturally occurring antibodies against SAA and anti-SAA1α could play a physiological role in down-regulating their antigen and proinflammatory cytokines leading to the resolution of the acute phase and could be an important therapeutic option in patients with chronic inflammatory diseases.</p></div

Positive correlation between levels of anti-SAA and anti-SAA1α antibodies.

Correlation between levels of anti-SAA and anti-SAA1α antibodies in sera of 300 HBDs is shown. Spearman coefficient (r), 95% confidence interval (CI) and p value are indicated. Ab, antibody; HBDs, healthy blood donors; SAA, serum amyloid A.</p

Anti-SAA and anti-SAA1α levels in IVIg.

<p>Octagam IVIg was serially diluted in sample dilution buffer (dilution range of 1.56–50 μg/ml) and analyzed for the presence of anti-SAA and anti-SAA1α antibodies using <i>in-house</i> ELISA. IVIg, intravenous immunoglobulin; SAA, serum amyloid A.</p

Naturally occurring antibodies against serum amyloid A reduce IL-6 release from peripheral blood mononuclear cells - Fig 3

<p><b>Immunoglobulin avidity of anti-SAA (A) and anti-SAA1α (B) antibodies.</b> Avidity of IgG antibodies against SAA and SAA1α was determined in 6 HBDs samples (3 male, 3 female; as indicated in brackets) using increasing concentration of NaCl in sample dilution buffer. As control, 1% BSA in PBS+0.1% Tween-20 with the same NaCl concentrations, was used. BSA, bovine serum albumin; HBDs, healthy blood donors; PBS; phosphate buffered saline; SAA, serum amyloid A.</p

Demographics of healthy blood donors.

<p>Demographics of healthy blood donors.</p

Levels of anti-SAA and anti-SAA1α antibodies.

<p><b>(A)</b> Boxplots show the median OD (A₄₅₀) and IQR for anti-SAA and anti-SAA1α levels in the sera of 300 HBDs (220 male and 80 female). The number of samples in each group is indicated in brackets. Whiskers represent 5^th and 95^th percentile. Medians between groups were compared using Man Whitney U-test. *p <0.05, ** p <0.01 and *** p <0.001. <b>(B)</b> Shown are medians for anti-SAA and anti-SAA1α levels in HBDs sera based on age distribution (4 groups). The number of samples in each group is indicated in brackets. HBDs, healthy blood donors; SAA, serum amyloid A.</p

Amino acid alignments of hrSAA and hrSAA1α.

<p>Amino acid alignments of hrSAA and hrSAA1α.</p