Plasma Levels Of IgA Research Articles

A241 CORRELATION BETWEEN PLASMA IGA LEVEL AND BIOLOGICAL THERAPY IN PATIENTS WITH INFLAMMATORY BOWEL DISEASE

Abstract Background IgA is the predominant antibody class secreted by intestinal immune cells. However, the level of plasma IgA in Inflammatory Bowel Disease (IBD) patients under medical treatment remains unknown. Therefore, our study aimed to investigate the relationship between plasma IgA concentration in IBD patients under biological therapy. Aims To assess the correlation between plasma IgA level in IBD patients under biological therapy. Methods We collected data from outpatient clinics at our hospital, including 12 IBD patients, comprising 4 patients with Crohn's disease (CD) and 8 patients with Ulcerative Colitis (UC). Data was collected between 2020 and 2023. We measured plasma IgA concentrations both before initiating biologic therapy and at the 14th week of biological treatment (4 under Adalimumab and 8 under Vedolizumab). Additionally, we compared baseline plasma IgA levels between 24 IBD patients (7 CD and 17 UC) and 24 healthy individuals. Student T test was used for statistical analyze. Results The average baseline plasma IgA level was significantly higher in IBD patients (2134±187.2 ug/ml, mean ± standard error) when compared to healthy individuals (1346± 114.8 ug/ml, p=0.0008). In the view of CD and UC, the baseline plasma IgA level was 2179±439.4 ug/ml and 2116±203.1 ug/ml, respectively. Baseline plasma IgA level also showed statistical significantly higher in CD and UC compared to healthy individuals (p=0.0063, p=0.0005, respectively), and without difference between UC and CD patients (p=0.8824) (Figure 1A). Furthermore, we investigated the impact of biological therapy on plasma IgA levels in IBD patients, finding a significant decrease in plasma IgA levels after biological therapy (2182±254.7 ug/ml to 1824±135.5 ug/ml, p=0.0181). Similar trend was noted in UC patients under biological therapy with borderline statistical significant (2141± 307.7ug/ml to1809±173.3ug/ml, p=0.0561), but not found in CD patients (2265±518.3 ug/ml to 1855±247.5 ug/ml, p= 0.1333)(Figure 1B). Conclusions We found that baseline plasma IgA level was higher in IBD patients compared to healthy individuals. Besides, plasma IgA level decreased after biological therapy in IBD patients, especially in UC patients. These findings suggest that plasma IgA level may be a potential biomarker for IBD patients. Funding Agencies None

Impact of RYGB surgery on plasma immunoglobulins: association between blood pressure and glucose levels six months after surgery.

We aimed to study levels of natural antibodies in plasma, and their associations to clinical and fecal biomarkers, before and 6 months after Roux-en-Y gastric bypass (RYGB) surgery. Thirty individuals with obesity [16 type 2 diabetic, 14 non-diabetic (ND)] had RYGB surgery. Total plasma IgA, IgG and IgM antibody levels and specific antibodies to oxidized low-density lipoprotein (oxLDL), malondialdehyde-acetaldehyde adducts, Porphyromonas gingivalis gingipain A hemagglutinin domain (Rgp44), and phosphocholine were measured using chemiluminescence immunoassay. Associations between plasma and fecal antibodies as well as clinical markers were analyzed. RYGB surgery reduced blood pressure, and the glycemic state was improved. A higher level of diastolic blood pressure was associated with lower plasma antibodies to oxLDL after surgery. Also, lower level of glucose markers associated with lower level of plasma antibodies to bacterial virulence factors. Antibodies to oxLDL decreased after surgery, and positive association between active serum lipopolysaccharide and specific oxLDL antibodies was detected. Total IgG levels decreased after surgery, but only in ND individuals. Reduced level of total plasma IgG, improved state of hypertension and hyperglycemia and their associations with decreased levels of specific antibodies in plasma, suggest an improved state of systemic inflammation after RYGB surgery.

Airway and Systemic Immune Responses Following the Third COVID-19 Vaccination in COPD Patients.

Booster vaccinations are required to maintain protection against COVID-19. COPD patients are at higher risk of developing severe illness following SARS-CoV-2 infection. Previous cross-sectional analysis after the second COVID-19 booster showed similar immune responses in COPD patients and controls, but pre-vaccination samples were not available. This longitudinal study evaluated systemic and airway immune responses in COPD patients using samples obtained pre- and post-third COVID-19 vaccination. Twelve COPD patients were recruited, with plasma, nasal and sputum (n = 10) samples collected pre-vaccination and 4- and 14-weeks post vaccination. Samples were analyzed for anti-spike IgA and IgG and cellular immunity. The ability of plasma and nasal samples to block ACE2-spike protein interaction was assessed for Wild type, Delta, and Omicron spike variants. Vaccinations increased anti-spike IgG in plasma (p < 0.001), nasal (IgG p < 0.001) and sputum (p = 0.002) samples, IgA in plasma (p < 0.001) and blood cellular immunity (p = 0.001). Plasma and nasal anti-spike IgA levels correlated (rho: 0.6, p = 0.02), with similar results for IgG (rho: 0.79, p = 0.003). Post-vaccination nasal (p = 0.002) and plasma (p < 0.001) samples were less effective at blocking Omicron spike binding to ACE2 compared to the Wild type spike variant. Airway and systemic immune responses against SARS-CoV-2 increased in COPD patients following a third COVID-19 vaccination. Nasal and systemic responses in COPD patients were less effective against Omicron variant compared to previous variants.

Dietary Betaine Supplementation Enhances Colonic Barrier Function through the Nrf2/Keap1 and TLR4-NF-κB/MAPK Signaling Pathways and Alters Colonic Microbiota in Bama Mini-Pigs.

This study evaluated the effects of betaine supplementation in sows and/or their offspring's diets on the redox status, immune and inflammatory levels, colonic barrier function, and colonic microbial community of offspring piglets. Thirty-six Bama mini-sows on day 3 of gestation and their weaned offspring piglets (28 d of age) were randomly allocated to the following treatments: (1) sows and their weaned offspring fed the basal diet (control group, Con group); (2) sows fed the basal diet with 3.50 kg/t betaine, and their weaned offspring fed the basal diet (sows betaine group, SB group); (3) sows fed the basal diet with 3.50 kg/t betaine, and their weaned offspring fed the basal diet with 2.50 kg/t betaine (sow-offspring betaine group, S-OB group). Six offspring piglets from each group were selected to collect plasma and colon samples on d 30, 60, and 90 after weaning. Compared with the Con group, the plasma levels of IgA, IgM, GSH-Px, and SOD during d 30-90 after weaning, IFN-α, T-AOC, and GSH on d 30 and 60 after weaning were increased, while MDA during d 30-90 after weaning was decreased in the SB and S-OB groups (p < 0.05). In addition, the plasma levels of IFN-γ on d 60 and T-AOC on d 30 after weaning were higher in the S-OB group than those in the Con group (p < 0.05). In the colon, betaine supplementation increased plasma T-AOC, GSH, and SOD levels while decreasing MDA concentration (p < 0.05). Betaine supplementation improved the colonic protein abundances of ZO-1, occludin, and claudin in offspring and activated the Nrf2/Keap1 signaling pathway while inhibiting the TLR4-NF-κB/MAPK signaling pathway on d 90 after weaning. The 16S rRNA sequencing results showed that betaine supplementation altered colonic microbiota composition by increasing the relative abundances of Verrucomicrobia and Actinobacteria in the SB group while decreasing proinflammatory-associated microbiota abundances (Tenericutes, Prevotella, and Parabacteroides) (p < 0.05). Collectively, these findings suggest that dietary betaine supplementation in sows and/or their offspring could improve offspring piglets' redox status and immune and anti-inflammatory levels and enhance the colonic barrier function by activating Nrf2/Keap1 and inhibiting TLR4-NF-κB/MAPK signaling pathways.

Deficiency of germinal center kinase TRAF2 and NCK-interacting kinase (TNIK) in B cells does not affect atherosclerosis.

Atherosclerosis is the underlying cause of many cardiovascular diseases, such as myocardial infarction or stroke. B cells, and their production of pro- and anti-atherogenic antibodies, play an important role in atherosclerosis. In B cells, TRAF2 and NCK-interacting Kinase (TNIK), a germinal center kinase, was shown to bind to TNF-receptor associated factor 6 (TRAF6), and to be involved in JNK and NF-κB signaling in human B cells, a pathway associated with antibody production. We here investigate the role of TNIK-deficient B cells in atherosclerosis. ApoE-/-TNIKfl/fl (TNIKBWT) and ApoE-/-TNIKfl/flCD19-cre (TNIKBKO) mice received a high cholesterol diet for 10 weeks. Atherosclerotic plaque area did not differ between TNIKBKO and TNIKBWT mice, nor was there any difference in plaque necrotic core, macrophage, T cell, α-SMA and collagen content. B1 and B2 cell numbers did not change in TNIKBKO mice, and marginal zone, follicular or germinal center B cells were unaffected. Total IgM and IgG levels, as well as oxidation specific epitope (OSE) IgM and IgG levels, did not change in absence of B cell TNIK. In contrast, plasma IgA levels were decreased in TNIKBKO mice, whereas the number of IgA+ B cells in intestinal Peyer's patches increased. No effects could be detected on T cell or myeloid cell numbers or subsets. We here conclude that in hyperlipidemic ApoE-/- mice, B cell specific TNIK deficiency does not affect atherosclerosis.

Differences in peripheral and central metabolites and gut microbiome of laying hens with different feather-pecking phenotypes.

Feather pecking (FP) is a maladaptive behavior in laying hens that is associated with numerous physiological traits, including those involving the central neurotransmitter system and the immune system, which have been identified in many species as being regulated by the gut microbiota via the "microbiota-gut-brain" (MGB) axis. Yet, it is unknown whether and how gut microbiota influences FP by regulating multiple central neurotransmission systems and immune system. This study was measured the prevalence of severe FP (SFP) in the commercial layer farm. The chicken flock with the highest frequency of SFP were selected for FP phenotype identification. Nontargeted metabolomics was performed to investigated the differences in the peripheral and central metabolites and 16S rDNA sequencing was performed to investigated the differences in gut microbiome of laying hens with different FP phenotypes. Correlation analysis was performed to determine the potential mechanism by which the disturbed gut microbiota may modulate host physiology and behavior. The results showed that pullets (12 weeks of age) showed significantly higher SFP frequencies than chicks (6 weeks of age) and adults (22 weeks of age; p < 0.05). Compared to neutrals (N), peckers (P) exhibited the stress-induced immunosuppression with the increased plasma levels of corticosterone and norepinephrine, and the decreased plasma levels of IgA, IL-1, IL-6 and tumor necrosis factor α (p < 0.05). In the cecum, the relative abundances of Bacteroides and Gemmiger were higher in the P group, while Roseburia, Ruminococcus2, Anaerostipes, Lachnospiracea_incertae_sedis and Methanobrevibacter were more enriched in the N group. Moreover, increased plasma levels of L-tryptophan, beta-tyrosine and L-histidine were found in the P group (p < 0.05). Notably, in the P group, hippocampal levels of L-tryptophan, xanthurenic acid, L-histidine and histamine were improved and showed a positive association with L-glutamic acid levels. Plasma levels of L-tryptophan, beta-tyrosine and L-histidine were both positively correlated with Bacteroides abundance but negatively correlated with Methanobrevibacter abundance. Overall, these findings suggest that the development of FP may be affected by the gut microbiota, which regulates the central glutamatergic nerve system by altering the metabolism of tryptophan, histidine and tyrosine.

Clostridium butyricum alleviates LPS-induced acute immune stress in goats by regulating bacterial communities and blood metabolites.

The mitigation and prevention of acute immune stress are essential for livestock production. Clostridium butyricum (C. butyricum) has shown positive effects in stabilizing intestinal microbiota disorders, improving immune function and inhibiting disease development, but its effects on ruminants are unclear. Therefore, the current trial hypothesized that C. butyricum could improve goats' immune function and antioxidant capacity by regulating bacterial communities and blood metabolism and effectively alleviating the acute immune stress induced by Lipopolysaccharides (LPS). Sixteen healthy goats were fed C. butyricum for 70 days, and the goats were challenged with LPS on day 71. Blood and feces were collected at 0h and 6h after the challenge to evaluate the effects of C. butyricum on their intestinal microbiota, immune function, antioxidant function, and plasma metabolites. The results showed that C. butyricum had no significant effect on plasma biochemical parameters at the beginning of the LPS challenge. However, supplementation with C. butyricum increased plasma levels of IgA, IgG, T-SOD, and T-AOC (P < 0.05), but TNF-α, IL-6, and MDA were decreased (P < 0.05). In contrast, IL-10 showed an increasing trend (P < 0.10). Rectal microbiota analysis showed that C. butyricum significantly increased the relative abundance of Epsilonbacteraeota at the phylum level of goats; at the genus level, the relative abundances of Campylobacter and Anaerorhabdus]_furcosa_group were also significantly increased (P < 0.05). Christensenellaceae_R-7_group as the dominant microbiota also showed a significant increase in their abundance values, while Clostridium and Lachnospiraceae_UCG-001 were significantly lower (P < 0.05). When the LPS challenge continued up to 6h, dietary supplementation with C. butyricum still resulted in significantly higher plasma concentrations of IgA, IL-10, and T-SOD in goats than in the control group, reducing TNF-α levels (P < 0.05). In addition, plasma levels of T-CHOL and LDL were significantly reduced, and the expression of d-proline was significantly upregulated according to metabolomic analysis (P < 0.05). In conclusion, dietary supplementation with C. butyricum helped optimize the expression of bacterial communities and plasma metabolites to enhance the ability of goats to alleviate acute immune stress.

IgA-Based Secretory Response in Tears of COVID-19 Patients: A Potential Biomarker of Pro-Inflammatory State in Course of SARS-CoV-2 Infection.

Mucosal immunity, including secretory IgA (sIgA), plays an important role in the early defence against SARS-CoV-2 infection. However, a comprehensive evaluation of the local immune response in tears in relation to blood antibody reservoirs has not yet been conducted. A total of 179 symptomatic laboratory-confirmed COVID-19 patients were included in this single-centre study. Conjunctival swabs were analysed by a reverse transcription polymerase chain reaction for the detection of SARS-CoV-2 RNA. In parallel, tear samples collected by Schirmer test strips and plasma samples were analysed by ELISA to detect anti-S1 IgA levels. The concentrations of selected inflammatory cytokines in tears were determined by a magnetic bead assay. Anti-SARS-CoV-2 sIgA was present in the tears of 81 (45.25%) confirmed COVID-19 patients, and the tear IgA levels were correlated with the plasma IgA levels (Rs = +0.29, p = 0.0003). SARS-CoV-2 RNA in the conjunctival sac was identified in 18 COVID-19 patients (10%). Positive correlations between the tear IgA level and the concentrations of several cytokines TNF-α (Rs = +0.23, p = 0.002), IL-1β (Rs = +0.25, p < 0.001), IL-2 (Rs = +0.20, p = 0.007), IL-4 (Rs = +0.16, p = 0.04), IL-5 (Rs = +0.36, p < 0.001), IL-6 (Rs = +0.32, p < 0.001), IL-8 (Rs = +0.31, p < 0.001), VEGF (Rs = +0.25, p < 0.001) and GM-CSF (Rs = +0.27, p < 0.001) were also found. Quantitative tear film-based sIgA could potentially serve as a rapid and easily accessible biomarker of external mucosal immunity to SARS-CoV-2. The concentration of sIgA is directly related to individual host immune responses to SARS-CoV-2 infection.

Features of humoral immunity after COVID-19

At the present time, studying humoral immunity to the new coronavirus infection is among the most important tasks. The COVID-19 infection induces a protective pool of specific antibodies determining severity and duration of such immune protection after convalescence. The antibody testing is also necessary for assessing efficiency of anti-COVID vaccines in order to defeat the SARS-CoV-2 pandemic. Despite enormous interest of scientific community in this problem seen in the literature, there is still a lack for longitudinal observations of immunological status (more than 6 months) in the patients who have undergone COVID-19. The aim of this study is a long-term monitoring (9-14 months) of development and extinction of immune response to SARS-CoV-2 infection using quantitative assessment of IgA and IgG levels in peripheral blood of the patients who had COVID-19 in anamnesis. Monitoring of anti-SARS-CoV-2 levels over time has demonstrated significant individual variability, and made it possible to divide the study participants into three groups, according to characteristic features of humoral immunity after documented COVID-19. The study describes characteristic features of humoral immune response for each of these groups. The first group (30% of the study group) exhibited classical pattern of antibody response to viral infection. The second group (40% of study participants) presented with high plasma IgA levels, and their significant excess (about 2 times) over IgG levels throughout the observation period. The third group (30% of study participants), apparently comprised the subjects with increased humoral immunity to SARS-CoV-2 infection. Their plasma antibodies remain at high levels for at least 9-10 months after the onset of infection. The data obtained confirm the pattern of plasma IgA which is not quite typical to viral infections in dynamics after a sufficiently long time period after the disease in most study participants (2nd and 3rd groups; 70% of all volunteers who have recovered from COVID-19) and suggests an important role of this immunoglobulin against SARS-CoV-2 infection. The specific responses of anti-SARS-CoV-2 IgG are very similar to behavior of such antibodies in other viral infections including contacts with coronaviruses from earlier generations. Humoral immunity against SARS-CoV-2 may persist for more than 6 months, thus supporting an assumption that the naturally infected patients are able to resist re-infection for a long time.

Usefulness of Immunoglobulin A in Patients With Decompensated Heart Failure: Is It a Future Marker of Congestion? Preliminary Experience

The purpose of this study was to analyze whether the level of IgA is related to right ventricular function and systemic congestion in patients with decompensated heart failure (HF) and reduced ejection fraction (EF). This was a consecutive prospective and observational study of hospitalized patients diagnosed with decompensated HF with reduced EF. The recruitment period lasted 2 months. In the first 24 hours after admission, clinical assessment, general laboratory tests, determination of HF biomarkers, IgA and echocardiographic study were performed. Patients were classified into 2 groups according to whether the plasma IgA level was lower (n=11) or higher than 300 mg/dL (n=12). Significant differences in IgA levels were found in the peripheral congestion variables (no congestion: 232, interquartile range [IQR], 125-310 mg/dL vs congestion: 429, IQR, 308-520 mg/dL; P=.03). There were also differences in echocardiographic parameters of right ventricular function, with a greater deterioration of right ventricular function in the group with higher IgA levels (P < .05). There was a highly significant correlation between tricuspid annulus systolic excursion values and IgA levels (P=.004). In decompensated HF, patients with greater clinical congestion and echocardiographic parameters of right ventricular dysfunction have higher plasma IgA levels. This study is a preliminary experience that will help to establish the basis of the cardiointestinal syndrome as a clinical picture of systemic congestion in HF.

Renal deposition and clearance of recombinant poly-IgA complexes in a model of IgA nephropathy.

IgA nephropathy (IgAN) is the most common type of glomerulonephritis worldwide, which follows a chronic but nonetheless highly variable course of progression. IgA immune complexes are the primary source of renal deposits in IgAN. Apart from the presence of granular IgA1 deposits in the glomerular mesangium and mesangial hypercellularity as common features, the detailed process of IgA1 deposition and clearance in the kidney remains unclear. We sought to examine the dynamics of IgA deposition and tissue plasticity in response to deposits including their intrarenal clearance. We followed a synthetic approach to produce a recombinant fusion between IgA Fc (rIgA) and a biotin tag, which was subsequently induced with streptavidin (SA) to form an oligomeric poly-IgA mimic. Both uninduced rIgA (mono-rIgA) and polymeric SA-rIgA (poly-rIgA) were injected intravenously into Wistar rats. Plasma IgA levels and renal and liver histology were examined in a time series. In contrast to mono-rIgA, this synthetic poly-rIgA analog formed renal deposits exclusively in the glomerulus and were mostly cleared in 3h. However, repeated daily injections for 12 days caused long-lasting and stronger glomerular IgA deposition together with IgG and complement C3, in association with mesangial cell proliferation, matrix expansion, and variable degrees of albuminuria and hematuria that phenocopied IgAN. Ex vivo, poly-rIgA bound cultured mesangial cells and elicited cytokine production, in addition to activating plasma C3 that was consistent with the actions of IgA immune complexes in IgAN pathogenesis. Remarkably, the kidneys were able to reverse all pathologic manifestations and restore normal glomerular histology 2 weeks after injections were halted. The synthetic model showed the kinetics between the intricate balance of renal deposition and clearance, as well as glomerular plasticity towards healing. Together, the results revealed a priming effect of existing deposits in promoting stronger and longer-lasting IgA deposition to cause renal damage. © 2021 The Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.

Serological Surveillance of COVID-19 Hospitalized Patients in Réunion Island (France) Revealed that Specific Immunoglobulin G Are Rapidly Vanishing in Severe Cases.

Humoral immunity is critically important to control COVID-19. Long-term antibody responses remain to be fully characterized in hospitalized patients who have a high risk of death. We compared specific Immunoglobulin responses against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) between two groups, intensive care unit (ICU) and non-ICU hospitalized patients over several weeks. Plasma specific IgG, IgM, and IgA levels were assessed using a commercial ELISA and compared to an in-house cell-based ELISA. Among the patients analyzed (mean (SD) of age, 64.4 (15.9) years, 19.2% female), 12 (46.2%) were hospitalized in ICU. IgG levels increased in non-ICU cases from the second to the eighth week after symptom onset. By contrast, IgG response was blunted in ICU patients over the same period. ICU patients with hematological malignancies had very weak or even undetectable IgG levels. While both groups had comparable levels of specific IgM antibodies, we found much lower levels of specific IgA in ICU versus non-ICU patients. In conclusion, COVID-19 ICU patients may be at risk of reinfection as their specific IgG response is declining in a matter of weeks. Antibody neutralizing assays and studies on specific cellular immunity will have to be performed.

HIV vaccine delayed boosting increases Env variable region 2-specific antibody effector functions.

In the RV144 HIV-1 phase III trial, vaccine efficacy directly correlated with the magnitude of the variable region 2-specific (V2-specific) IgG antibody response, and in the presence of low plasma IgA levels, with the magnitude of plasma antibody-dependent cellular cytotoxicity. Reenrollment of RV144 vaccinees in the RV305 trial offered the opportunity to define the function, maturation, and persistence of vaccine-induced V2-specific and other mAb responses after boosting. We show that the RV144 vaccine regimen induced persistent V2 and other HIV-1 envelope-specific memory B cell clonal lineages that could be identified throughout the approximately 11-year vaccination period. Subsequent boosts increased somatic hypermutation, a critical requirement for antibody affinity maturation. Characterization of 22 vaccine-induced V2-specific mAbs with epitope specificities distinct from previously characterized RV144 V2-specific mAbs CH58 and CH59 found increased in vitro antibody-mediated effector functions. Thus, when inducing non-neutralizing antibodies, one method by which to improve HIV-1 vaccine efficacy may be through late boosting to diversify the V2-specific response to increase the breadth of antibody-mediated anti-HIV-1 effector functions.

Specific IgA and CLA+ T-Cell IL-17 Response to Streptococcus pyogenes in Psoriasis

Streptococcus pyogenes tonsillar infection is well known to trigger and exacerbate psoriasis lesions in both guttate and plaque forms of the disease. Although mucosal and cutaneous tissues are closely involved in psoriasis pathology, the interaction between their specific immune responses has not been deeply explored. This work aims to address and characterize the presence of humoral responses against S.pyogenes in patients with psoriasis and its putative association with cytokine responses detected invitro in our psoriasis exvivo model, based on the coculture of cutaneous lymphocyte-associated antigen+/- T cells with autologous epidermal cells. Patients with psoriasis presented increased IgA response to S.pyogenes when compared with control subjects. In patients with plaque psoriasis, despite being negative for anti-streptolysin O antibody titer, IgA plasma levels against S.pyogenes correlated with cutaneous lymphocyte-associated antigen+ T-cell-dependent IL-17F response invitro. No association is observed for IgG levels in plaque psoriasis. Similar association is observed for IgA anti-S.pyogenes extract and IL-17A in patients with guttate psoriasis. We propose S.pyogenes-specific IgA as a potential new perspective for better understanding the role of S.pyogenes in psoriasis development.

Comparative evaluation of Lactobacillus strains with different adhesion ability on growth performance and immunomodulatory activity in broiler chickens

The study was designed to assess the effect of 2 Lactobacillus strains (Lactobacillus kefiri 1.3207 and Lactobacillus plantarum 1.2567) with different adherence ability on growth performance and immunomodulatory activity in broiler. The BW and FCR were higher in L. kefiri 1.3207 and L. plantarum 1.2567 groups compared to control group at 42 days of age, and BW of broilers in L. kefiri 1.3207 group was significantly higher than that in L. plantarum 1.2567 group. IgA and IgG contents and the spleen and bursa of Fabricius indices in significantly increased in the L. kefiri 1.3207 group, but not in the L. plantarum 1.2567-treated group. L. kefiri 1.3207 had more significant effect on growth performance, plasma IgA and IgG levels and immune organs indices because it had better adhesion ability.

027 IgA plasma levels, but not IgG, against Streptococcus pyogenes identifies Anti-Streptolysin O negative chronic plaque psoriasis patients with increased specific CLA+ T cells IL17A and IL17F producers

027 IgA plasma levels, but not IgG, against Streptococcus pyogenes identifies Anti-Streptolysin O negative chronic plaque psoriasis patients with increased specific CLA+ T cells IL17A and IL17F producers

Alleviation of mycotoxin biodegradation agent on zearalenone and deoxynivalenol toxicosis in immature gilts

BackgroundThe current study was carried out to evaluate the effects of mycotoxin biodegradation agent (MBA, composed of Bacillus subtilis ANSB01G and Devosia sp. ANSB714) on relieving zearalenone (ZEA) and deoxynivalenol (DON) toxicosis in immature gilts.MethodsA total of forty pre-pubertal female gilts (61.42 ± 1.18 kg) were randomly allocated to four diet treatments: CO (positive control); MO (negative control, ZEA 596.86 μg/kg feed and DON 796 μg/kg feed); COA (CO + 2 g MBA/kg feed); MOA (MO + 2 g MBA/kg feed). Each treatment contained 10 replicates with 1 gilt per replicate. Gilts were housed in an environmentally controlled room with the partially slatted floor.ResultsDuring the entire experimental period of 28 d, average daily gain (ADG) and average daily feed intake (ADFI) of gilts in MO group was significantly reduced compared with those in CO group. The vulva size of gilts was significantly higher in MO group than CO group. In addition, significant increases in the plasma levels of IgA, IgG, IL-8, IL-10 and PRL were determined in MO group compared with that in CO group. ZEA and DON in the diet up-regulated apoptotic caspase-3 in ovaries and uteri, along with down-regulated the anti-apoptotic protein Bcl-2 in ovaries. The supplementation of MBA into diets co-contaminated with ZEA and DON significantly increased ADG, decreased the vulva sizes, reduced the levels of IgG, IL-8 and PRL in plasma, and regulated apoptosis in ovaries and uteri of gilts.ConclusionsThe present results indicated that feeding diet contaminated with ZEA and DON simultaneously (596.86 μg/kg + 796 μg/kg) had detrimental effects on growth performance, plasma immune function and reproductive status of gilts. And MBA could reduce the negative impacts of these two toxins, believed as a promising feed additive for mitigating toxicosis of ZEA and DON at low levels in gilts.

Immunization with gingipain A hemagglutinin domain of Porphyromonas gingivalis induces IgM antibodies binding to malondialdehyde-acetaldehyde modified low-density lipoprotein.

Treatment of periodontitis has beneficial effects on systemic inflammation markers that relate to progression of atherosclerosis. We aimed to investigate whether immunization with A hemagglutinin domain (Rgp44) of Porphyromonas gingivalis (Pg), a major etiologic agent of periodontitis, would lead to an antibody response cross-reacting with oxidized low-density lipoprotein (OxLDL) and how it would affect the progression of atherosclerosis in low-density lipoprotein receptor-deficient (LDLR-/-) mice. The data revealed a prominent IgM but not IgG response to malondialdehyde-acetaldehyde modified LDL (MAA-LDL) after Rgp44 and Pg immunizations, implying that Rgp44/Pg and MAA adducts may share cross-reactive epitopes that prompt IgM antibody production and consequently confer atheroprotection. A significant negative association was observed between atherosclerotic lesion and plasma IgA to Rgp44 in Rgp44 immunized mice, supporting further the anti-atherogenic effect of Rgp44 immunization. Plasma IgA levels to Rgp44 and to Pg in both Rgp44- and Pg-immunized mice were significantly higher than those in saline control, suggesting that IgA to Rgp44 could be a surrogate marker of immunization in Pg-immunized mice. Distinct antibody responses in plasma IgA levels to MAA-LDL, to Pg lipopolysaccharides (Pg-LPS), and to phosphocholine (PCho) were observed after Rgp44 and Pg immunizations, indicating that different immunogenic components between Rpg44 and Pg may behave differently in regard of their roles in the development of atherosclerosis. Immunization with Rgp44 also displayed atheroprotective features in modulation of plaque size through association with plasma levels of IL-1α whereas whole Pg bacteria achieved through regulation of anti-inflammatory cytokine levels of IL-5 and IL-10. The present study may contribute to refining therapeutic approaches aiming to modulate immune responses and inflammatory/anti-inflammatory processes in atherosclerosis.

Aberrant expression of interleukin-10 and activation-induced cytidine deaminase in B cells from patients with Behçet's disease.

Despite extensive studies, the pathogenesis of Behçet's disease (BD) remains unclear. In particular, the roles of B cells in patients with BD have not been elucidated. Activation-induced cytidine deaminase (AID) is a critical enzyme for immunoglobulin (Ig) heavy chain class switching and somatic hypermutation in B cells and the abnormal expression of AID in various immune conditions has previously been studied. B10 cells, an interleukin (IL)-10-secreting subset of regulatory B cells, function to downregulate inflammation and autoimmunity. Thus, in the present study, the relevance of B cells in patients with BD was investigated. The plasma levels of IL-10 and IgA and the proportions of cluster of differentiation (CD)43+ B cells, excluding naïve B cells, were measured in 16 patients with BD and 16 age- and sex-matched healthy controls (HCs). Additionally, the mRNA levels of IL-10 and AID were assessed in B cells from fresh peripheral blood samples of the BD patients and HCs. The plasma level of IL-10 in patients with BD did not differ significantly from that in HCs. Similarly, there was no significant difference in the plasma level of IgA, although a slight increase was observed in patients with BD compared with that in HCs. There were no differences in CD43+CD19+ B cell numbers between patients with BD and HCs. However, IL-10 mRNA levels were significantly reduced (P<0.05), while AID mRNA levels were significantly increased (P<0.01) in the B cells of patients with BD compared with those in HCs. These results provide insight into the role of B cells in patients with BD.

Potential Predictive Role of Lipid Peroxidation Markers for Type 2 Diabetes in the Adult Tunisian Population

We evaluated the potential clinical relevance of malondialdehyde (MDA) and autoantibodies to copper oxidized low-density lipoprotein (CuOx-LDL) in type 2 diabetes occurrence. This cross-sectional study enrolled 69 normoglycemic subjects, 18 prediabetic patients and 108 type 2 diabetes patients. MDA concentration was assessed spectrophotometrically. Plasma IgG, IgA and IgM levels to CuOx-LDL were determined by ELISA. Plasma MDA levels were considerably higher in obese, prediabetic and type 2 diabetes subjects compared to controls. In multiple linear regression analysis, both MDA and IgA to CuOx-LDL were significantly associated with glucose metabolism markers (p<0.05). Multiple logistic regression analyses showed that high plasma MDA and IgA to CuOx-LDL were independent risk factors for type 2 diabetes (OR 1.196, 95% CI: 1.058 to 1.353; p=0.004; OR 1.626, 95% CI: 1.066 to 2.481; p=0.024; respectively). Importantly, elevated IgA to CuOx-LDL predicted incident diabetes in patients with prediabetes (OR 2.321, 95% CI:1.063 to 5.066; p=0.035). From stratified analyses by body mass index (BMI), both MDA and IgA to CuOx-LDL remained independent predictors of type 2 diabetes occurrence in non-obese subjects (p<0.05). More interesting, elevated IgA to CuOx-LDL levels could be predictors of type 2 diabetes in obese prediabetic subjects (p=0.044). Conversely, neither IgG nor IgM to CuOx-LDL was associated with glucose metabolism markers, obesity or type 2 diabetes. Plasma MDA and IgA to CuOx-LDL were significantly associated with blood markers of glucose metabolism. High levels of MDA and IgA to CuOx-LDL could independently predict type 2 diabetes development in normoglycemia and prediabetic subjects.