ovalbumin and Immune-System-Diseases

Probiotics regulate host immune balance, which may reduce immune-related diseases. The effects and mechanisms of Lactobacillus rhamnosus 2016SWU.05.0601 (Lr-0601) on the immune response in ovalbumin (OVA)-sensitized mice were explored.. Lr-0601 reduced serum immunoglobulin (Ig)E and OVA-IgE and attenuated the alteration in lung pathology in OVA-sensitized mice. Lr-0601 blocked OVA-induced up-regulation in serum T helper (Th) 2 and Th17 cytokines but increased the serum levels of Th1 and regulatory T (Treg) cytokines in OVA-sensitized mice. OVA also markedly reduced the protein levels of spleen T-box transcription factor and forkhead/winged helix transcription factor p3, leading to the reduced mRNA expression of interferon-γ and interleukin (IL)-10. By contrast, OVA markedly increased the protein expression of spleen GATA-binding protein 3 and retinoid-related orphan receptor γt, as well as the mRNA expression of spleen IL-4 and IL-17. These changes induced by OVA were reversed by Lr-0601. Moreover, Lr-0601 helped alleviate OVA-induced intestinal microbiota dysbiosis. A correlation was found between specific genera and immune-associated cytokines.. The combined results indicate that Lr-0601 modulated the balance of Th1/Th2 and Treg/Th17 in OVA-sensitized mice, which was associated with the regulation of immune-related transcription factors and gut microbiota. Lr-0601 can potentially be used as a probiotic for preventing immune-related diseases. © 2020 Society of Chemical Industry.

Topics: Animals; Female; Gastrointestinal Microbiome; Humans; Immune System Diseases; Immunoglobulin E; Interleukin-10; Lacticaseibacillus rhamnosus; Male; Mice; Ovalbumin; Probiotics; Spleen; T-Lymphocytes, Regulatory; Th1 Cells; Th2 Cells; Transcription Factors

Clinical study showed that smoking during pregnancy deceased the thymus size in newborns. However, the long-term effect remains unclear. This study was aimed to observe the effects of prenatal nicotine exposure (PNE) on the development of thymus and the T-lymphocyte subpopulation in mice offspring from the neonatal to adulthood. Both the thymus weight and cytometry data indicated that PNE caused persistent thymic hypoplasia in male offspring from neonatal to adult period and transient changes in female offspring from neonatal to prepuberal period. Flow cytometry analysis disclosed a permanent decreased proportion and number of mature CD4 single-positive (SP) T cells in thymus of both sex. In addition, the PNE male offspring showed a more serious thymus atrophy in the ovalbumin (OVA)-sensitized model. Moreover, increased autophagic vacuole and elevated mRNA expression of Beclin 1 were noted in PNE fetal thymus. In conclusion, PNE offspring showed thymus atrophy and CD 4 SP T cell reduction at different life stages. Mechanically, PNE induced excessive autophagy in fetal thymocytes might be involved in these changes. All the results provided evidence for elucidating the PNE-induced programmed immune diseases.

Topics: Age Factors; Animals; Animals, Newborn; Autophagy; Beclin-1; CD4-Positive T-Lymphocytes; Female; Immune System Diseases; Male; Maternal Exposure; Mice, Inbred BALB C; Nicotine; Nicotinic Agonists; Ovalbumin; Phenotype; Pregnancy; Prenatal Exposure Delayed Effects; Thymocytes; Thymus Gland

Autonomic dysreflexia (AD), a potentially dangerous complication of high-level spinal cord injury (SCI) characterized by exaggerated activation of spinal autonomic (sympathetic) reflexes, can cause pulmonary embolism, stroke, and, in severe cases, death. People with high-level SCI also are immune compromised, rendering them more susceptible to infectious morbidity and mortality. The mechanisms underlying postinjury immune suppression are not known. Data presented herein indicate that AD causes immune suppression. Using in vivo telemetry, we show that AD develops spontaneously in SCI mice with the frequency of dysreflexic episodes increasing as a function of time postinjury. As the frequency of AD increases, there is a corresponding increase in splenic leucopenia and immune suppression. Experimental activation of spinal sympathetic reflexes in SCI mice (e.g., via colorectal distension) elicits AD and exacerbates immune suppression via a mechanism that involves aberrant accumulation of norepinephrine and glucocorticoids. Reversal of postinjury immune suppression in SCI mice can be achieved by pharmacological inhibition of receptors for norepinephrine and glucocorticoids during the onset and progression of AD. In a human subject with C5 SCI, stimulating the micturition reflex caused AD with exaggerated catecholamine release and impaired immune function, thus confirming the relevance of the mouse data. These data implicate AD as a cause of secondary immune deficiency after SCI and reveal novel therapeutic targets for overcoming infectious complications that arise due to deficits in immune function.

Topics: Adrenergic beta-2 Receptor Antagonists; Animals; Antigens, CD; Autonomic Dysreflexia; Blood Pressure; Butoxamine; Colon; Corticosterone; Disease Models, Animal; Epinephrine; Female; Hormone Antagonists; Humans; Immune System Diseases; Immunosuppression Therapy; Mice; Mifepristone; Norepinephrine; Ovalbumin; Physical Stimulation; Spinal Cord Injuries; T-Lymphocytes; Telemetry

Toll-like receptors (TLRs) as pattern recognition receptors, participate in both innate and adaptive immune responses, and seem to play an important role in the pathogenesis of asthma. This study aimed to identify key TLRs involved in antigen induced pulmonary inflammation (AIPI), a rat model for asthma, and to explore the role of TLRs in the disease development.. E3 rats were sensitized with ovalbumin (OVA)/alum intraperitoneally and intranasally challenged with OVA to induce AIPI model. TLR1-9 and cytokine mRNA expression in spleen, lung and mediastinal lymph node (mLN) tissues were screened by quantitative real-time polymerase chain reaction. TLR7 expression was found to be significantly down-regulated in spleen while TLR3 and TLR8 expression was up-regulated in mLN of AIPI rats. Furthermore, imiquimod (a ligand of TLR7) and TLR3 specific short-hairpin RNA plasmid for RNA interference were administrated, respectively, in vivo to AIPI rats to observe their effects on the disease by assessing various asthmatic parameters. The numbers of total cells, eosinophils, macrophages and lymphocytes were counted according to differential morphology in bronchoalveolar lavage fluid. Serum IgE and OVA specific IgG(1) concentration was detected by enzyme-linked immunosorbent assay. The results showed that both TLR7 ligand treatment and TLR3 RNAi in vivo decreased serum IgE level and interleukin-4 mRNA expression.. TLR3 in mLN and TLR7 in spleen both systemically modulate disease development in AIPI rats via altering serum IgE concentration relevant to Th2 responses. And these findings may provide an important clue for further research in the asthma pathogenesis and suggest a new remedy for asthma treatment.

Topics: Animals; Antibody Formation; Antigens; Disease Models, Animal; Gene Expression Regulation; Immune System; Immune System Diseases; Immunoglobulin E; Interleukin-4; Lymph Nodes; Organ Specificity; Ovalbumin; Pneumonia; Rats; RNA, Messenger; Spleen; Th2 Cells; Toll-Like Receptor 3; Toll-Like Receptor 7

There is concern about the growing environmental levels of brominated dioxins. Brominated dioxins are known to bind and activate the transcription factor aryl hydrocarbon receptor (AhR), as their chlorinated congeners do. However, data on the potency of brominated dioxins for immunotoxicity in vivo is largely lacking, even though the immune system is a vulnerable target for dioxins. In this study, we investigated the immunotoxic effects on mice of the brominated dioxins, 2,3,7,8-tetrabromodibenzo-p-dioxin (TBDD) and 1,2,3,7,8-pentabromodibenzo-p-dioxin (PeBDD), in comparison with those of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and 1,2,3,7,8-pentachlorodibenzo-p-dioxin (PeCDD), the two most toxic chlorinated dioxins, to gain insight into the potency of brominated dioxins for immunotoxicity. C57BL/6 mice were dosed with the dioxins and immunized with ovalbumin (OVA), and several endpoints that sensitively detect immunotoxicity were investigated, including IL-5 production by the splenocytes. The results of the present study demonstrated that TCDD and TBDD show identical effects on a per weight basis at 1.0-10mug/kg for all the endpoints examined. PeCDD also showed effects similar to those of TCDD. On the other hand, PeBDD showed somewhat dose-independent effects and was more potent at a lower dose and less potent at a higher dose than PeCDD. Dose-dependent linearity of PeBDD-induced induction of CYP1A1, an AhR target gene, was also less clear in the spleen than in the liver. These results have provided valuable data for estimating the potency of brominated dioxins for immunotoxicity.

Topics: Animals; Cytochrome P-450 CYP1A1; Dioxins; Female; Immune System Diseases; Immunoglobulin M; Interleukin-5; Liver; Mice; Mice, Inbred C57BL; Ovalbumin; Receptors, Aryl Hydrocarbon; Reverse Transcriptase Polymerase Chain Reaction; Spleen; T-Lymphocytes

To identify the means by which in-vitro-generated regulatory T cells, similar to those in anterior chamber-associated immune deviation (ACAID), suppress antigen-specific T-cell responses.. T regulators (T regs), generated by stimulating ovalbumin (OVA)-specific Tcr transgenic DO11.10 T cells with OVA-pulsed, TGF-beta2-treated peritoneal exudates cells (PEC), or their supernatants were added to OVA-pulsed PEC that were used to activate DO11.10 T cells in vitro or to suppress OVA-specific delayed hypersensitivity (DH) induction in vivo.. OVA-pulsed PECs exposed in vitro to TGF-beta-producing T regs or their supernatants failed to activate DO11.10 T cells in vitro, and suppressed DH in mice immunized with OVA plus adjuvant.. T cells exposed to TGF-beta2-pretreated, antigen-pulsed PECs secrete soluble factors, including active TGF-beta that regulate OVA-specific responses by forcing antigen-presenting cells to promote deviant T-cell activation in vitro and in vivo.

Topics: Animals; Anterior Chamber; Antibody Formation; Antigen-Presenting Cells; Cells, Cultured; Exudates and Transudates; Female; Hypersensitivity, Delayed; Immune System Diseases; Mice; Mice, Inbred BALB C; Mice, Transgenic; Ovalbumin; Peritoneum; T-Lymphocytes; Transforming Growth Factor beta; Transforming Growth Factor beta2

Topics: Anaphylaxis; Dextrans; Genetics; Hypersensitivity; Immune System Diseases; Ovalbumin; Rats; Research; Toxicology

Topics: Animals; Egg White; Guinea Pigs; Hypersensitivity; Immune System Diseases; Ovalbumin

Topics: Animals; Egg White; Guinea Pigs; Hypersensitivity; Immune System Diseases; Iodine; Iodine Radioisotopes; Ovalbumin

Topics: Dextrans; Edema; Hypersensitivity; Immune System Diseases; Ovalbumin; Ovomucin; Proteins; Serotonin

Topics: Animals; Chloroquine; Dextrans; Edema; Hypersensitivity; Immune System Diseases; Ovalbumin; Rats

Topics: Animals; Cardiovascular System; Egg White; Hypersensitivity; Immune System Diseases; Mesentery; Ovalbumin; Rabbits

Topics: Antibodies; Hypersensitivity; Immune System Diseases; In Vitro Techniques; Ovalbumin

Topics: Animals; Guinea Pigs; Hypersensitivity; Immune System Diseases; Ovalbumin; Skin