scholarly journals Live and Heat-KilledLactobacillus rhamnosusATCC 7469 May Induce Modulatory Cytokines Profiles on Macrophages RAW 264.7

2015 ◽  
Vol 2015 ◽  
pp. 1-6 ◽  
Author(s):  
Adeline Lacerda Jorjão ◽  
Felipe Eduardo de Oliveira ◽  
Mariella Vieira Pereira Leão ◽  
Cláudio Antonio Talge Carvalho ◽  
Antonio Olavo Cardoso Jorge ◽  
...  
Keyword(s):  
Immune Responses ◽  
Lactobacillus Rhamnosus ◽  
Raw 264.7 ◽  
Tukey Test ◽  
Mouse Macrophages ◽  
Stimulation Of

This study aimed to evaluate the capacity ofLactobacillus rhamnosusand/or its products to induce the synthesis of cytokines (TNF-α, IL-1β, IL-4, IL-6, IL-10, and IL-12) by mouse macrophages (RAW 264.7). Three microorganism preparations were used: liveL.rhamnosus(LLR) suspension, heat-killedL.rhamnosus(HKLR) suspension, and the supernatant of a heat-killedL.rhamnosus(SHKLR) suspension, which were cultured with macrophages (37°C, 5% CO2) for 2 h and 30 min. After that, cells were cultured for 16 h. The supernatants were used for the quantitation of cytokines, by ELISA. The results were compared with the synthesis induced by lipopolysaccharide (LPS) and analysed, using ANOVA and Tukey test, 5%. LLR and HKLR groups were able to significantly increase the production of TNF-α, IL-6, and IL-10 (P<0.05). SHKLR also significantly increased the production of TNF-αand IL-10 (P<0.05) but not IL-6 (P>0.05). All theL.rhamnosussuspensions were not able to produce detectable levels of IL-1βor significant levels of IL-4 and IL-12 (P>0.05). In conclusion, live and heat-killedL.rhamnosussuspensions were able to induce the synthesis of different cytokines with proinflammatory (TNF-αand IL-6) or regulatory (IL-10) functions, suggesting the role of strainL.rhamnosusATCC 7469 in the modulation or in the stimulation of immune responses.

scholarly journals myo-Inositol is an osmolyte in rat liver macrophages (Kupffer cells) but not in RAW 264.7 mouse macrophages

1997 ◽  
Vol 326 (1) ◽  
pp. 289-295 ◽  
Author(s):  
Ulrich WARSKULAT ◽  
Christian WEIK ◽  
Dieter HÄUSSINGER
Keyword(s):  
Rat Liver ◽  
Kupffer Cells ◽  
Mrna Level ◽  
Raw 264.7 ◽  
Mrna Levels ◽  
Mouse Macrophages ◽  
Taurine Uptake ◽  
Inositol Uptake ◽  
Stimulation Of

The role of myo-inositol as an osmolyte was studied in cultured rat liver macrophages (Kupffer cells). Hyperosmotic exposure of Kupffer cells stimulated myo-inositol uptake and led to an increase in the mRNA levels for the sodium/myo-inositol co-transporter (SMIT). Conversely, hypo-osmotic (205 m-osM) exposure diminished myo-inositol uptake when compared with normo-osmotic (305 m-osM) control incubations. The hyperosmolarity-induced SMIT mRNA increase was counteracted by added myo-inositol or betaine. In contrast with Kupffer cells, there was only a slight hyperosmotic stimulation of myo-inositol uptake in RAW 264.7 mouse macrophages, and the myo-inositol transporter (SMIT) mRNA was not detectable. Further, a slight stimulation of taurine uptake and an increase in taurine transporter (TAUT) mRNA level by hyperosmolarity was observed in RAW 264.7 cells, whereas hypo-osmolarity led to a decrease in taurine uptake and TAUT mRNA level. When Kupffer cells were preloaded with myo-inositol, hypo-osmotic exposure led to a rapid efflux of myo-inositol from the cells. Myo-inositol efflux was also stimulated by phagocytosis of latex particles; however, latex was without effect on the hyperosmolarity-induced increase of SMIT mRNA levels. The results suggest a role of myo-inositol as an osmolyte in rat Kupffer cells but not in RAW 264.7 mouse macrophages. The functional relevance of this osmolyte strategy might lie in the maintenance of cell volume homeostasis during phagocytosis in Kupffer cells; however, the interplay with the other osmolytes betaine and taurine remains to be established.

scholarly journals Vpr Enhances Tumor Necrosis Factor Production by HIV-1-Infected T Cells

2015 ◽  
Vol 89 (23) ◽  
pp. 12118-12130 ◽  
Author(s):  
Ferdinand Roesch ◽  
Léa Richard ◽  
Réjane Rua ◽  
Françoise Porrot ◽  
Nicoletta Casartelli ◽  
...  
Keyword(s):  
Immune Responses ◽  
Proinflammatory Cytokine ◽  
Tumor Necrosis ◽  
Cellular Proteins ◽  
Accessory Protein ◽  
Infected Cells ◽  
Hiv 1 ◽  
Necrosis Factor ◽  
Stimulation Of

ABSTRACTThe HIV-1 accessory protein Vpr displays different activities potentially impacting viral replication, including the arrest of the cell cycle in the G2phase and the stimulation of apoptosis and DNA damage response pathways. Vpr also modulates cytokine production by infected cells, but this property remains partly characterized. Here, we investigated the effect of Vpr on the production of the proinflammatory cytokine tumor necrosis factor (TNF). We report that Vpr significantly increases TNF secretion by infected lymphocytes.De novoproduction of Vpr is required for this effect. Vpr mutants known to be defective for G2cell cycle arrest induce lower levels of TNF secretion, suggesting a link between these two functions. Silencing experiments and the use of chemical inhibitors further implicated the cellular proteins DDB1 and TAK1 in this activity of Vpr. TNF secreted by HIV-1-infected cells triggers NF-κB activity in bystander cells and allows viral reactivation in a model of latently infected cells. Thus, the stimulation of the proinflammatory pathway by Vpr may impact HIV-1 replicationin vivo.IMPORTANCEThe role of the HIV-1 accessory protein Vpr remains only partially characterized. This protein is important for viral pathogenesis in infected individuals but is dispensable for viral replication in most cell culture systems. Some of the functions described for Vpr remain controversial. In particular, it remains unclear whether Vpr promotes or instead prevents proinflammatory and antiviral immune responses. In this report, we show that Vpr promotes the release of TNF, a proinflammatory cytokine associated with rapid disease progression. Using Vpr mutants or inhibiting selected cellular genes, we show that the cellular proteins DDB1 and TAK1 are involved in the release of TNF by HIV-infected cells. This report provides novel insights into how Vpr manipulates TNF production and helps clarify the role of Vpr in innate immune responses and inflammation.

scholarly journals Bcl2 negatively regulates Protective Immune Responses During Mycobacterial Infection

2021 ◽  
Vol 12 (1) ◽  
pp. 94-109
Author(s):  
Aayushi Singh ◽  
Vandana Anang ◽  
Chaitenya Verma ◽  
Shakuntala Surender Kumar Saraswati ◽  
Ankush Kumar Rana ◽  
...  
Keyword(s):  
Immune Responses ◽  
Inflammatory Cytokine ◽  
Critical Role ◽  
Mycobacterial Infection ◽  
Defense Responses ◽  
Inhibitor Of Apoptosis ◽  
Human Pbmcs ◽  
Bacterial Burden ◽  
Stimulation Of

Abstract We previously reported that M. tb on its own as well as together with HIV inhibits macrophage apoptosis by upregulating the expression of Bcl2 and Inhibitor of Apoptosis (IAP). In addition, recent reports from our lab showed that stimulation of either macrophages or BMDCs results in the significant upregulation of Bcl2. In this report, we delineate the role of Bcl2 in mediating defense responses from dendritic cells (BMDCs) during mycobacterial infection. Inhibiting Bcl2 led to a significant decrease in intracellular bacterial burden in BMDCs. To further characterize the role of Bcl2 in modulating defense responses, we inhibited Bcl2 in BMDCs as well as human PBMCs to monitor their activation and functional status in response to mycobacterial infection and stimulation with M. tb antigen Rv3416. Inhibiting Bcl2 generated protective responses including increased expression of co-stimulatory molecules, oxidative burst, pro-inflammatory cytokine expression and autophagy. Finally, co-culturing human PBMCs and BMDCs with antigen-primed T cells increased their proliferation, activation and effector function. These results point towards a critical role for Bcl2 in regulating BMDCs defense responses to mycobacterial infection.

scholarly journals Neolymphogenesis and Immunogistogochemical Study of Lymph Nodes in Breast Cancer

2020 ◽  
Vol 9 (4) ◽  
pp. 266-272
Author(s):  
Sh. Kh. Gantsev ◽  
R. A. Rustamkhanov ◽  
Sh. R. Kzyrgalin ◽  
D. S. Tursumetov
Keyword(s):  
Breast Cancer ◽  
Lymph Node ◽  
Immune Responses ◽  
Lymph Nodes ◽  
Immunohistochemical Expression ◽  
Functional Zones ◽  
High Level ◽  
Fixed Panel ◽  
Stimulation Of

Background. Our previous studies have shown that postnatally formed lymph nodes (PNFLN) can serve as a source of biological signals activating antitumour immune reactions and suppressing the spread of metastatic malignant cells.Aim. To determine the expression of CD3, CD20, CD68 in native, sentinel and postnatally induced lymph nodes of the axillary zone in breast cancer.Materials and methods. The study involved an analysis of digitalized images of the immunohistochemical expression of a fixed panel of antibodies CD3, CD20, CD68. The expression levels were assessed quantitatively by counting the expressed cells in each studied node for four main structural and functional zones.Results and Discussion. The results of a comparative immunohistochemical study of native, sentinel and postnatally induced lymph nodes showed that the content of CD3, CD20, CD68 demonstrates fundamental differences in different lymph node structures.Сonclusions 1. In postnatally induced lymph nodes, compared to native and sentinel lymph nodes, the distinct expression of antibodies to the main immunocompetent cells, which realize key immune responses in the lymph node, can indicate an increased functional status of the newly formed lymph nodes. 2. The study demonstrated a high level of antigenic stimulation of T and B lymphocytes in postnatally induced lymph nodes, as well as indicated a possible role of macrophage cells in the stimulation of neolymphogenesis and the formation of new lymph nodes. 3. The study provides the basis for further research into postnatal induced lymph nodes in cancer patients.

Stimulation of Ca(2+)-dependent exocytosis of the sperm acrosome by cAMP acting downstream of phospholipase A2

Reproduction ◽  
2000 ◽  
pp. 57-68 ◽  
Author(s):  
J Garde ◽  
ER Roldan
Keyword(s):  
Arachidonic Acid ◽  
Phospholipase A2 ◽  
Phospholipase C ◽  
Phosphodiesterase Inhibitors ◽  
Dibutyryl Camp ◽  
Camp Phosphodiesterase ◽  
Ram Sperm ◽  
Camp Formation ◽  
Stimulation Of

Spermatozoa undergo exocytosis in response to agonists that induce Ca2+ influx and, in turn, activation of phosphoinositidase C, phospholipase C, phospholipase A2, and cAMP formation. Since the role of cAMP downstream of Ca2+ influx is unknown, this study investigated whether cAMP modulates phospholipase C or phospholipase A2 using a ram sperm model stimulated with A23187 and Ca2+. Exposure to dibutyryl-cAMP, phosphodiesterase inhibitors or forskolin resulted in enhancement of exocytosis. However, the effect was not due to stimulation of phospholipase C or phospholipase A2: in spermatozoa prelabelled with [3H]palmitic acid or [14C]arachidonic acid, these reagents did not enhance [3H]diacylglycerol formation or [14C]arachidonic acid release. Spermatozoa were treated with the phospholipase A2 inhibitor aristolochic acid, and dibutyryl-cAMP to test whether cAMP acts downstream of phospholipase A2. Under these conditions, exocytosis did not occur in response to A23187 and Ca2+. However, inclusion of dibutyryl-cAMP and the phospholipase A2 metabolite lysophosphatidylcholine did result in exocytosis (at an extent similar to that seen when cells were treated with A23187/Ca2+ and without the inhibitor). Inclusion of lysophosphatidylcholine alone, without dibutyryl-cAMP, enhanced exocytosis to a lesser extent, demonstrating that cAMP requires a phospholipase A2 metabolite to stimulate the final stages of exocytosis. These results indicate that cAMP may act downstream of phospholipase A2, exerting a regulatory role in the exocytosis triggered by physiological agonists.

Role of convalescent plasma therapy in new Coronavirus disease (nCOVID-19): A review

2020 ◽  
Vol 11 (SPL1) ◽  
pp. 546-549
Author(s):  
Shweta Dadarao Parwe ◽  
Milind Abhimanyu Nisargandha ◽  
Rishikesh Thakre
Keyword(s):  
Clinical Trial ◽  
Immune Responses ◽  
Indian Population ◽  
Preventive Treatment ◽  
The Body ◽  
Therapeutic Antibodies ◽  
Plasma Therapy ◽  
Host Immune Responses ◽  
Transparent Liquid

Hitherto, there is no proper line of treatment for the new (nCOVID19). The development of unique antiviral drugs has taken precedence. Therapeutic antibodies () will be a significantly beneficial agent against nCOVID-19. Here the host immune responses to new discussed in this review provide strategy and further treatment and understanding of clinical interventions against nCOVID-19. Plasma therapy uses the antibodies found in the blood of people recovering (or convalesced) from an infection to treat infected patients. When an infection occurs, the body begins producing proteins specially made to kill the germ, called antibodies. Those antibodies coat specifically plasma in the blood of survivors, the yellow transparent liquid blood portion for months or even years. research assesses plasma use from Convalescent patients of infected with nCOVID-19 as a possible preventive treatment. But it is not yet recommended as a line of treatment, and it is used as a clinical trial in the new in Indian population.

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