scholarly journals In Ovo and Oral Administration of Probiotic Lactobacilli Modulate Cell- and Antibody-Mediated Immune Responses in Newly Hatched Chicks

2021 ◽  
Vol 12 ◽  
Author(s):  
Mohammadali Alizadeh ◽  
Jegarubee Bavananthasivam ◽  
Bahram Shojadoost ◽  
Jake Astill ◽  
Khaled Taha-Abdelaziz ◽  
...  

There is some evidence that lactobacilli can strengthen the immune system of chickens. This study evaluated the effects of in ovo and oral administration of a lactobacilli cocktail on cytokine gene expression, antibody-mediated immune responses, and spleen cellularity in chickens. Lactobacilli were administered either in ovo at embryonic day 18, orally at days 1, 7, 14, 21, and 28 post-hatches, or a combination of both in ovo and post-hatch inoculation. On day 5 and 10 post-hatch, spleen and bursa of Fabricius were collected for gene expression and cell composition analysis. On days 14 and 21 post-hatch, birds were immunized with sheep red blood cells (SRBC) and keyhole limpet hemocyanin (KLH), and sera were collected on days 7, 14, and 21 post-primary immunization. Birds that received lactobacilli (107 CFU) via in ovo followed by weekly oral administration showed a greater immune response by enhancing antibody responses, increasing the percentage of CD4+ and CD4+CD25+ T cells in the spleen and upregulating the expression of interferon (IFN)-α, IFN-β, interleukin (IL)-8, IL-13, and IL-18 in the spleen and expression of IFN-γ, IL-2, IL-6, IL-8, IL-12, and IL-18 in the bursa. These findings suggest that pre-and post-hatch administration of lactobacilli can modulate the immune response in newly hatched chickens.

2020 ◽  
Author(s):  
Mohammadali Alizadeh ◽  
Jegarubee Bavananthasivam ◽  
Bahram Shojadoost ◽  
Jake Astill ◽  
Khaled Abdelaziz ◽  
...  

Abstract There is some evidence that lactobacilli can strengthen immune system of chickens. This study evaluated the effects of in ovo and oral administration of a lactobacilli cocktail on cytokine gene expression, antibody-mediated immune response, and spleen cellularity in chickens. Lactobacilli were administered either in ovo at embryonic day 18, orally to hatched chicks at days 1, 7, 14, 21, and 28 post-hatches, or by both treatments combined. On days 5 and 10 post-hatch, spleen and bursa of Fabricius were collected for gene expression and cell composition analysis. On days 14 and 21 post-hatch, birds were injected with sheep red blood cells (SRBC) and keyhole limpet hemocyanin (KLH), and sera were collected on days 7, 14, and 21 post-primary immunization. Birds that received lactobacilli (107 CFU) via in ovo followed by weekly oral administration showed a greater immune response by enhancing antibody response, increasing the percentage of CD4+ and CD4+CD25+ T cells in the spleen, and upregulating the expression of the expression of interferon (IFN)-α, IFN-β, interleukin (IL)-12, and IL-13 in the spleen and expression of IFN-γ, IL-2, IL-6, IL-8, IL-12, and IL-18 in bursa. These findings suggest that pre-and post-hatch administration of lactobacilli modulate immune response in newly hatched chickens.


Author(s):  
Mohammadali Alizadeh ◽  
Bahram Shojadoost ◽  
Jake Astill ◽  
Khaled Taha-Abdelaziz ◽  
Seyed Hossein Karimi ◽  
...  

2020 ◽  
Vol 14 (Supplement_1) ◽  
pp. S137-S137
Author(s):  
H M Baer ◽  
E MacDonald ◽  
A Ferguson ◽  
A M Scott ◽  
M I Khan ◽  
...  

Abstract Background Crohn’s disease (CD) is a chronic inflammatory gastrointestinal condition, with globally increasing incidence. Patients with CD suffer from a loss of tolerance towards their commensal microbiota causing an aberrant immune response, occurring in a protracted relapse and remission cycle. Although a variety of frontline therapies is currently available, including targeted therapies such as biologic drugs, 30–40% of CD patients still require surgery to manage the disease. At present, the immunobiology of CD is not fully understood. However, differences in immune responses between patients might play an important role in diverse treatment responses. The aim of this study was to identify differences in peripheral and local immune responses of CD to understand differences in disease behaviour and treatment outcome. Methods Peripheral blood mononuclear cells and plasma were isolated from whole blood of a cross-sectional CD patient cohort (nCD = 12) and normal controls (NC, nNC = 28). Flow cytometry analysis and multiplex assays were used to quantify immune cell populations and cytokine levels, respectively. The local immune response was analysed by bulk RNA sequencing of mucosal colonic biopsies either from inflamed CD or normal tissue. Gene signatures were then followed up by validation in publicly deposited gene expression datasets (nCD = 36, nNC = 24), and by measurement of specific proteins using our archived samples. Results Peripheral immunophenotyping of the initial cross-sectional study displayed three different types of CD patients, characterised by either a decrease in leukocyte populations, an increase of cytokines, or a change in both. Analysis of the RNAseq data derived from colonic biopsies revealed four distinct clusters in genes associated with the immune response in CD patients. Further pathway analysis showed one cluster with an enriched B cell signature and another cluster with an elevated macrophage and neutrophil response. We utilised publicly available gene expression datasets to validate these signatures in a larger cohort and identified a selection of patients with an up-regulated pro-inflammatory macrophage response. Using correlation analysis, we suggest an immunopathotype with increased macrophage activation which is potentially associated with a more severe form of the disease. Conclusion We have identified distinct immunopathotypes in both the peripheral and local immune response of CD patients. Further investigation will correlate these distinct immune responses in CD with clinical parameters, to understand associations between diverse treatment responses and disease behaviours.


2021 ◽  
Vol 99 (Supplement_3) ◽  
pp. 360-361
Author(s):  
Sharon A Norton ◽  
Amanda A Adams

Abstract Senior horses often exhibit chronic inflammation and decreased immune responses. Dietary Saccharomyces cerevisiae fermentation product (SCFP; Diamond V, Cedar Rapids, IA) has been shown to affect immune responses in several species. This study aimed to evaluate SCFP-mediated immune function in senior horses. Sixteen horses (24.8 ± 3.0 y; BW = 545.8 ± 61.9 kg) were allotted to two treatments: CON (n = 8; no SCFP supplementation) and SCFP top dressed onto a common concentrate for 56 d (21 g/d; n = 8). Body condition score (BCS), BW, whole blood cytokine (INF-ɣ, TNF-α, IL-1β, IL-6, IL-10, IL-4, IL-8, IL-13, IL-17) and COX-1 and COX-2 gene expression were measured at d 0, 42, 49 and 56. Horses were challenged with a monovalent influenza vaccine at d 42 (MIV; Fluvacc Innovator; Zoetis Animal Health, Parsippany, NJ). Pre-MIV (d 0–42) and post-MIV (d 42–56) responses were analyzed using general mixed model procedures. Pre-MIV, BW tended to increase (P = 0.09) over time. Expression of IL-10 tended to be lower for SCFP than CON (P = 0.09) and IL-13 expression decreased over time (P < 0.05). Post-MIV, BCS linearly increased over time (P = 0.006) while TNF-α tended to increase at d 49 and return to d 42 levels by d 56 (P = 0.06). Both INF-ɣ and IL-10 expression were lower for SCFP vs CON (P < 0.05). Gene expression of COX-2 tended to decrease (P = 0.06) at d 49 and return to the d 42 baseline by d 56. Gene expression of IL-13 tended to decrease with SCFP but increased with CON at d 49 with both returning to d 42 levels by d 56 (P = 0.08). Influenza H1 titers increased over time post-vaccination (P < 0.001) with no difference between treatments. Dietary SCFP may modulate pro-inflammatory and anti-inflammatory cytokine gene expression in senior horses.


2012 ◽  
Vol 20 (2) ◽  
pp. 146-155 ◽  
Author(s):  
Feng Qian ◽  
Christopher R. Bolen ◽  
Chunxia Jing ◽  
Xiaomei Wang ◽  
Wei Zheng ◽  
...  

ABSTRACTHepatitis C virus (HCV) is the most common chronic blood-borne infection in the United States, with the majority of patients becoming chronically infected and a subset (20%) progressing to cirrhosis and hepatocellular carcinoma. Individual variations in immune responses may help define successful resistance to infection with HCV. We have compared the immune response in primary macrophages from patients who have spontaneously cleared HCV (viral load negative [VL−],n= 37) to that of primary macrophages from HCV genotype 1 chronically infected (VL+) subjects (n= 32) and found that macrophages from VL− subjects have an elevated baseline expression of Toll-like receptor 3 (TLR3). Macrophages from HCV patients were stimulatedex vivothrough the TLR3 pathway and assessed using gene expression arrays and pathway analysis. We found elevated TLR3 response genes and pathway activity from VL− subjects. Furthermore, macrophages from VL− subjects showed higher production of beta interferon (IFN-β) and related IFN response genes by quantitative PCR (Q-PCR) and increased phosphorylation of STAT-1 by immunoblotting. Analysis of polymorphisms in TLR3 revealed a significant association of intronic TLR3 polymorphism (rs13126816) with the clearance of HCV and the expression of TLR3. Of note, peripheral blood mononuclear cells (PBMCs) from the same donors showed opposite changes in gene expression, suggesting ongoing inflammatory responses in PBMCs from VL+ HCV patients. Our results suggest that an elevated innate immune response enhances HCV clearance mechanisms and may offer a potential therapeutic approach to increase viral clearance.


1977 ◽  
Vol 145 (5) ◽  
pp. 1228-1236 ◽  
Author(s):  
T H Hünig ◽  
A Schimpl ◽  
E Wecker

Spleen cells of dinitrophenyl keyhole limpet hemocyanin (DNPKLH) primed and boosted mice produced a nonantigen-specific helper factor upon in vitro challenge with DNPKLH. This helper factor displays all of the biological characteristics so far described for TRF produced by allogeneic or Concanavalin A stimulation of mouse spleen cells. It restores the primary anti-SRBC response in nude spleen cultures following the same kinetics of action as T-cell-replacing factor (TRF). Conversely, TRF restores the primary in vitro immune response of nude spleen cultures to DNPKLH. TRF also restores the secondary anti-hapten IgG response of T-cell-deprived spleen cell cultures derived from DNPKLH primed and boosted mice. Here the need for carrier specificity is fully overcome. The data therefore suggest that TRF, as a nonantigen-specific maturation signal, is involved in the primary and secondary immune responses to both particulate and soluble antigens.


2017 ◽  
Vol 91 (15) ◽  
Author(s):  
Ariana G. Bravo Cruz ◽  
Aiguo Han ◽  
Edward J. Roy ◽  
Arielle B. Guzmán ◽  
Rita J. Miller ◽  
...  

ABSTRACT All viruses strategically alter the antiviral immune response to their benefit. The vaccinia virus (VACV) K1 protein has multiple immunomodulatory effects in tissue culture models of infection, including NF-κB antagonism. However, the effect of K1 during animal infection is poorly understood. We determined that a K1L-less vaccinia virus (vΔK1L) was less pathogenic than wild-type VACV in intranasal and intradermal models of infection. Decreased pathogenicity was correlated with diminished virus replication in intranasally infected mice. However, in intradermally inoculated ears, vΔK1L replicated to levels nearly identical to those of VACV, implying that the decreased immune response to vΔK1L infection, not virus replication, dictated lesion size. Several lines of evidence support this theory. First, vΔK1L induced slightly less edema than vK1L, as revealed by histopathology and noninvasive quantitative ultrasound technology (QUS). Second, infiltrating immune cell populations were decreased in vΔK1L-infected ears. Third, cytokine and chemokine gene expression was decreased in vΔK1L-infected ears. While these results identified the biological basis for smaller lesions, they remained puzzling; because K1 antagonizes NF-κB in vitro, antiviral gene expression was expected to be higher during vΔK1L infection. Despite these diminished innate immune responses, vΔK1L vaccination induced a protective VACV-specific CD8+ T cell response and protected against a lethal VACV challenge. Thus, vΔK1L is the first vaccinia virus construct reported that caused a muted innate immune gene expression profile and decreased immune cell infiltration in an intradermal model of infection yet still elicited protective immunity. IMPORTANCE The vaccinia virus (VACV) K1 protein inhibits NF-κB activation among its other antagonistic functions. A virus lacking K1 (vΔK1L) was predicted to be less pathogenic because it would trigger a more robust antiviral immune response than VACV. Indeed, vΔK1L was less pathogenic in intradermally infected mouse ear pinnae. However, vΔK1L infection unexpectedly elicited dramatically reduced infiltration of innate immune cells into ears. This was likely due to decreased expression of cytokine and chemokine genes in vΔK1L-infected ears. As such, our finding contradicted observations from cell culture systems. Interestingly, vΔK1L conferred protective immunity against lethal VACV challenge. This suggests that the muted immune response triggered during vΔK1L infection remained sufficient to mount an effective protective response. Our results highlight the complexity and unpredictable nature of virus-host interactions, a relationship that must be understood to better comprehend virus pathogenesis or to manipulate viruses for use as vaccines.


1994 ◽  
Vol 180 (2) ◽  
pp. 693-698 ◽  
Author(s):  
P Lu ◽  
X Zhou ◽  
S J Chen ◽  
M Moorman ◽  
S C Morris ◽  
...  

The costimulatory signal provided to T cells through CTLA-4-ligand interactions is required for T cell activation resulting in increased interleukin 2 (IL-2) production in vitro, but its role in the production of IL-4 and other cytokines is unclear and few in vivo studies have been performed to confirm results of in vitro experiments. We have examined the in vivo effects of blocking CTLA-4 ligands on the T helper cell 2 (Th2)-associated mucosal immune response that follows oral infection of mice with the nematode parasite, Heligmosomoides polygyrus. CTLA-4Ig administration inhibited H. polygyrus-induced increases in mesenteric lymph node (MLN) B cell major histocompatibility complex class II expression and size and T cell-derived IL-4 gene expression. In addition, CTLA-4 immunoglobulin (Ig) partially blocked increased IL-3, IL-5, and IL-9 cytokine gene expression in Peyer's patch (PP) and MLN 8 d after primary inoculation of mice with the parasite. Increases in the number of IL-4- but not IL-5-secreting cells were also inhibited by CTLA-4Ig. H. polygyrus-induced elevations in serum IgE levels but not blood eosinophils, were markedly inhibited by CTLA-4Ig. These results suggest that stimulation of CD28 and/or CTLA-4 is required for T cell priming leading to IL-4 cytokine production, B cell activation, and IgE secretion during a Th2-like, mucosal immune response to a nematode parasite.


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