scholarly journals Lysophosphatidylcholine: A Novel Modulator ofTrypanosoma cruziTransmission

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Mário A. C. Silva-Neto ◽  
Alan B. Carneiro ◽  
Livia Silva-Cardoso ◽  
Georgia C. Atella
Keyword(s):  
Immune System ◽  
Chagas Disease ◽  
Inflammatory Cells ◽  
Parasite Infection ◽  
Atheromatous Plaque ◽  
No Production ◽  
Parasite Transmission ◽  
Parasite Invasion ◽  
Cellular Processes ◽  
Signaling Mechanisms

Lysophosphatidylcholine is a bioactive lipid that regulates a large number of cellular processes and is especially present during the deposition and infiltration of inflammatory cells and deposition of atheromatous plaque. Such molecule is also present in saliva and feces of the hematophagous organismRhodnius prolixus, a triatominae bug vector of Chagas disease. We have recently demonstrated that LPC is a modulator ofTrypanosoma cruzitransmission. It acts as a powerful chemoattractant for inflammatory cells at the site of the insect bite, which will provide a concentrated population of cells available for parasite infection. Also, LPC increases macrophage intracellular calcium concentrations that ultimately enhance parasite invasion. Finally, LPC inhibits NO production by macrophages stimulated by liveT. cruzi, and thus interferes with the immune system of the vertebrate host. In the present paper, we discuss the main signaling mechanisms that are likely used by such molecule and their eventual use as targets to block parasite transmission and the pathogenesis of Chagas disease.

scholarly journals Absence of Bim sensitizes mice to experimental Trypanosoma cruzi infection

2021 ◽  
Vol 12 (7) ◽  
Author(s):  
Marcela Hernández-Torres ◽  
Rogério Silva do Nascimento ◽  
Monica Cardozo Rebouças ◽  
Alexandra Cassado ◽  
Kely Catarine Matteucci ◽  
...  
Keyword(s):  
T Cells ◽  
Trypanosoma Cruzi ◽  
Chagas Disease ◽  
Parasite Load ◽  
Peritoneal Macrophages ◽  
T Cell Response ◽  
No Production ◽  
Similar Reduction ◽  
Ifn Γ

AbstractChagas disease is a life-threatening disorder caused by the protozoan parasite Trypanosoma cruzi. Parasite-specific antibodies, CD8+ T cells, as well as IFN-γ and nitric oxide (NO) are key elements of the adaptive and innate immunity against the extracellular and intracellular forms of the parasite. Bim is a potent pro-apoptotic member of the Bcl-2 family implicated in different aspects of the immune regulation, such as negative selection of self-reactive thymocytes and elimination of antigen-specific T cells at the end of an immune response. Interestingly, the role of Bim during infections remains largely unidentified. To explore the role of Bim in Chagas disease, we infected WT, Bim+/−, Bim−/− mice with trypomastigotes forms of the Y strain of T. cruzi. Strikingly, our data revealed that Bim−/− mice exhibit a delay in the development of parasitemia followed by a deficiency in the control of parasite load in the bloodstream and a decreased survival compared to WT and Bim+/− mice. At the peak of parasitemia, peritoneal macrophages of Bim−/− mice exhibit decreased NO production, which correlated with a decrease in the pro-inflammatory Small Peritoneal Macrophage (SPM) subset. A similar reduction in NO secretion, as well as in the pro-inflammatory cytokines IFN-γ and IL-6, was also observed in Bim−/− splenocytes. Moreover, an impaired anti-T. cruzi CD8+ T-cell response was found in Bim−/− mice at this time point. Taken together, our results suggest that these alterations may contribute to the establishment of a delayed yet enlarged parasitic load observed at day 9 after infection of Bim−/− mice and place Bim as an important protein in the control of T. cruzi infections.

scholarly journals MicroRNA expression profile in bovine mammary gland parenchyma infected by coagulase-positive or coagulase-negative staphylococci

2021 ◽  
Vol 52 (1) ◽  
Author(s):  
Emilia Bagnicka ◽  
Ewelina Kawecka-Grochocka ◽  
Klaudia Pawlina-Tyszko ◽  
Magdalena Zalewska ◽  
Aleksandra Kapusta ◽  
...  
Keyword(s):  
Mammary Gland ◽  
Immune System ◽  
Differentially Expressed ◽  
Bacterial Invasion ◽  
Coagulase Negative Staphylococci ◽  
Cellular Processes ◽  
Differentially Expressed Mirnas ◽  
Non Coding Rnas ◽  
Coagulase Positive Staphylococci ◽  
Generation Sequencing

AbstractMicroRNAs (miRNAs) are short, non-coding RNAs, 21–23 nucleotides in length which are known to regulate biological processes that greatly impact immune system activity. The aim of the study was to compare the miRNA expression in non-infected (H) mammary gland parenchyma samples with that of glands infected with coagulase-positive staphylococci (CoPS) or coagulase-negative staphylococci (CoNS) using next-generation sequencing. The miRNA profile of the parenchyma was found to change during mastitis, with its profile depending on the type of pathogen. Comparing the CoPS and H groups, 256 known and 260 potentially new miRNAs were identified, including 32 that were differentially expressed (p ≤ 0.05), of which 27 were upregulated and 5 downregulated. Comparing the CoNS and H groups, 242 known and 171 new unique miRNAs were identified: 10 were upregulated (p ≤ 0.05), and 2 downregulated (p ≤ 0.05). In addition, comparing CoPS with H and CoNS with H, 5 Kyoto Encyclopedia of Genes and Genomes pathways were identified; in both comparisons, differentially-expressed miRNAs were associated with the bacterial invasion of epithelial cells and focal adhesion pathways. Four gene ontology terms were identified in each comparison, with 2 being common to both immune system processes and signal transduction. Our results indicate that miRNAs, especially miR-99 and miR-182, play an essential role in the epigenetic regulation of a range of cellular processes, including immunological systems bacterial growth in dendritic cells and disease pathogenesis (miR-99), DNA repair and tumor progression (miR-182).

Immunohistochemical Study of Presence of T Cells, B Cells, and Macrophages in Periradicular Lesions of Primary Teeth

2008 ◽  
Vol 32 (4) ◽  
pp. 287-293 ◽  
Author(s):  
Michele Bolan ◽  
Daniele de Almeida Lima ◽  
Cláudia Pinto Figueiredo ◽  
Gabriella Di Giunta ◽  
Maria José de Carvalho Rocha
Keyword(s):  
T Cells ◽  
Immune System ◽  
B Cells ◽  
Primary Teeth ◽  
Microscopic Analysis ◽  
Inflammatory Cells ◽  
Periapical Lesions ◽  
Inflammatory Processes ◽  
Local Inflammatory Reaction

BACKGROUND: The periapical lesion is the result of a local inflammatory reaction caused by bacteria and its products present on the root canal. The interaction between inflammatory cells and bacteria elicit both specific and non-specific immune responses. OBJETIVE: Due to the lack of studies evaluating the role of the immune system in periapical lesions of primary teeth and considering the potentially systemic effects that these infections can cause in children, especially because of the immaturity of their immune system, we sought to evaluate the presence of T cells, B cells and macrophages on periradicular lesions in primary teeth. STUDY DESIGN: 14 periradicular lesions were analyzed. The immunohistochemistry technique was performed using CD45RO, CD20, CD68 monoclonal antibodies aiming to identify T cells, B cells and macrophages, respectively. Cells were quantified by microscopic analysis of histological sections. RESULTS: Mean percentage of positive cells CD45RO was 11.76; CD20 was 5.25; CD68 was 10.92. Our results showed that T and B cells and macrophages comprise the majority of the inflammatory infiltrate. CONCLUSION: We concluded that both humoral and cell mediated immune reactions take place in periradicular lesions of primary teeth. The immune system plays an important role on the periradicular inflammatory processes in primary teeth.

scholarly journals Cytokine Patterns in Brain Tumour Progression

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Radu Albulescu ◽  
Elena Codrici ◽  
Ionela Daniela Popescu ◽  
Simona Mihai ◽  
Laura Georgiana Necula ◽  
...  
Keyword(s):  
Immune System ◽  
Inflammatory Cytokines ◽  
Tumour Growth ◽  
Tumour Progression ◽  
Inflammatory Cells ◽  
Serum Levels ◽  
Angiogenic Factors ◽  
System Response ◽  
Gm Csf ◽  
Immune System Response

Inflammation represents the immune system response to external or internal aggressors such as injury or infection in certain tissues. The body’s response to cancer has many parallels with inflammation and repair; the inflammatory cells and cytokines present in tumours are more likely to contribute to tumour growth, progression, and immunosuppression, rather than in building an effective antitumour defence. Using new proteomic technology, we have investigated serum profile of pro- (IL-1β, IL-6, IL-8, IL-12, GM-CSF, and TNF-α) and anti-inflammatory cytokines (IL-4, IL-10), along with angiogenic factors (VEGF, bFGF) in order to assess tumoural aggressiveness. Our results indicate significant dysregulation in serum levels of cytokines and angiogenic factors, with over threefold upregulation of IL-6, IL-1β, TNF-α, and IL-10 and up to twofold upregulation of VEGF, FGF-2, IL-8, IL-2, and GM-CSF. These molecules are involved in tumour progression and aggressiveness, and are also involved in a generation of disease associated pain.

scholarly journals U-Bang-Haequi Tang: A Herbal Prescription that Prevents Acute Inflammation through Inhibition of NF-κB-Mediated Inducible Nitric Oxide Synthase

2014 ◽  
Vol 2014 ◽  
pp. 1-12 ◽  
Author(s):  
Min Hwangbo ◽  
Ji Yun Jung ◽  
Sung Hwan Ki ◽  
Sang Mi Park ◽  
Kyung Hwan Jegal ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Acute Inflammation ◽  
Nuclear Translocation ◽  
Inflammatory Cells ◽  
Raw264.7 Cells ◽  
No Production ◽  
Traditional Korean Medicine ◽  
Korean Medicine ◽  
Forsythia Suspensa ◽  
Herbal Prescription

Since antiquity, medical herbs have been prescribed for both treatment and preventative purposes. Herbal formulas are used to reduce toxicity as well as increase efficacy in traditional Korean medicine.U-bang-haequi tang(UBT) is a herbal prescription containingArctii fructusandForsythia suspensaas its main components and has treated many human diseases in traditional Korean medicine. This research investigated the effects of UBT against an acute phase of inflammation. For this, we measured induction of nitric oxide (NO) and related proteins in macrophage cell line stimulated by lipopolysaccharide (LPS). Further, paw swelling was measured in carrageenan-treated rats. Carrageenan significantly induced activation of inflammatory cells and increases in paw volume, whereas oral administration of 0.3 or 1 g/kg/day of UBT inhibited the acute inflammatory response. In RAW264.7 cells, UBT inhibited mRNA and protein expression levels of iNOS. UBT treatment also blocked elevation of NO production, nuclear translocation of NF-κB, phosphorylation of Iκ-Bαinduced by LPS. Moreover, UBT treatment significantly blocked the phosphorylation of p38 and c-Jun NH2-terminal kinases by LPS. In conclusion, UBT prevented both acute inflammation in rats as well as LPS-induced NO and iNOS gene expression through inhibition of NF-κB in RAW264.7 cells.

Biology and pathology of atherosclerosis

2010 ◽  
pp. 2873-2881
Author(s):  
Robin P. Choudhury ◽  
Edward A. Fisher
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Vessel Wall ◽  
Inflammatory Process ◽  
Inflammatory Cells ◽  
Vascular Wall ◽  
Atheromatous Plaque ◽  
Apo B ◽  
Initial Stage ◽  
Intimal Layer

Formation of an atheromatous plaque—this is an inflammatory process that involves the contribution of endothelial cells, monocytes, and smooth muscle cells in conjunction with the deposition of atherogenic lipoproteins in the intimal layer of the vascular wall. The initial stage involves activation of the endothelium at regions of nonlaminar flow in vessels resulting in increased permeability to Apo B-containing lipoproteins (LDL). Inflammatory cells, in particular monocytes, are recruited into the intimal layer of the vessel wall via the action of chemokines and adhesion molecules mobilized by activated endothelium....

scholarly journals Suppression of arthritis by an inhibitor of nitric oxide synthase.

1993 ◽  
Vol 178 (2) ◽  
pp. 749-754 ◽  
Author(s):  
N McCartney-Francis ◽  
J B Allen ◽  
D E Mizel ◽  
J E Albina ◽  
Q W Xie ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Inflammatory Responses ◽  
Inflammatory Cells ◽  
No Production ◽  
Streptococcal Cell Wall ◽  
Cell Mediated Immune Response ◽  
A Cell ◽  
Nos Inhibitor ◽  
Oxide Synthase ◽  
Articular Index

Nitric oxide (NO), a toxic radical gas produced during the metabolism of L-arginine by NO synthase (NOS), has been implicated as a mediator of immune and inflammatory responses. A single injection of streptococcal cell wall fragments (SCW) induces the accumulation of inflammatory cells within the synovial tissue and a cell-mediated immune response that leads destructive lesions. We show here that NO production is elevated in the inflamed joints of SCW-treated rats. Administration of NG-monomethyl-L-arginine, an inhibitor of NOS, profoundly reduced the synovial inflammation and tissue damage as measured by an articular index and reflected in the histopathology. These studies implicate the NO pathway in the pathogenesis of an inflammatory arthritis and demonstrate the ability of a NOS inhibitor to modulate the disease.

scholarly journals Increased heart fibrosis and acute infection in a murine Chagas disease model associated with organophosphorus pesticide metabolite exposure

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Dunia Margarita Medina-Buelvas ◽  
Elizabet Estrada-Muñiz ◽  
Miriam Rodríguez-Sosa ◽  
Mineko Shibayama ◽  
Libia Vega
Keyword(s):  
Chagas Disease ◽  
Cardiac Fibrosis ◽  
Acute Infection ◽  
Disease Model ◽  
Parasitic Infection ◽  
Organophosphorus Pesticide ◽  
Parasite Burden ◽  
Myocardial Damage ◽  
Inflammatory Cells ◽  
Inflammatory Macrophages

AbstractSome reports suggest that exposure to organophosphorus (OP) pesticides increases the incidence of infections. Ethylated dialkylphosphates (EtDAPs) are metabolites of OP pesticides widely distributed with immunomodulatory potential. Chagas disease is produced by Trypanosoma cruzi parasites, and resolution of this infection requires the activation of inflammatory macrophages (MΦ), which results in cardiac fibrosis. Some reports indicate that EtDAPs increase the amount of the anti-inflammatory alternatively activated MΦ (M2; CD206+F4/80+). Therefore, we analyzed the course of T. cruzi infection, MΦ profiles from peritoneal exudate cells (PECs), inflammatory cell infiltration and fibrosis in the heart of BALB/c mice exposed to diethyldithiophosphate (DEDTP), diethylthiophosphate (DETP) or diethylphosphate (DEP, 0.01 g/kg), common DAPs produced by OP pesticides, 24 h before infection with T. cruzi. We found that DEDTP increased the parasite burden in blood by 99% at the peak of the infection and enhanced the myocardial damage due to an increase in infiltrated inflammatory cells (induced by DEDTP or DETP) and fibrosis (induced by EtDAPs). In the PECs, exposure to EtDAPs increased the proportion of the MΦ subpopulations of M2a, M2b and M2d, which are associated with tissue repair. These results indicate that exposure to EtDAPs can exacerbate the acute phase of a parasitic infection and increase the long-term damage to the heart.

scholarly journals Enhancement of immune response against Bordetella spp. by disrupting immunomodulation

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Monica C. Gestal ◽  
Laura K. Howard ◽  
Kalyan Dewan ◽  
Hannah M. Johnson ◽  
Mariette Barbier ◽  
...  
Keyword(s):  
Immune Response ◽  
Immune System ◽  
Immune Cells ◽  
Lymphoid Tissue ◽  
Protective Immunity ◽  
Inflammatory Cells ◽  
Host Immune System ◽  
Initial Growth ◽  
Wild Type ◽  
Sterilizing Immunity

AbstractWell-adapted pathogens must evade clearance by the host immune system and the study of how they do this has revealed myriad complex strategies and mechanisms. Classical bordetellae are very closely related subspecies that are known to modulate adaptive immunity in a variety of ways, permitting them to either persist for life or repeatedly infect the same host. Exploring the hypothesis that exposure to immune cells would cause bordetellae to induce expression of important immunomodulatory mechanisms, we identified a putative regulator of an immunomodulatory pathway. The deletion of btrS in B. bronchiseptica did not affect colonization or initial growth in the respiratory tract of mice, its natural host, but did increase activation of the inflammasome pathway, and recruitment of inflammatory cells. The mutant lacking btrS recruited many more B and T cells into the lungs, where they rapidly formed highly organized and distinctive Bronchial Associated Lymphoid Tissue (BALT) not induced by any wild type Bordetella species, and a much more rapid and strong antibody response than observed with any of these species. Immunity induced by the mutant was measurably more robust in all respiratory organs, providing completely sterilizing immunity that protected against challenge infections for many months. Moreover, the mutant induced sterilizing immunity against infection with other classical bordetellae, including B. pertussis and B. parapertussis, something the current vaccines do not provide. These findings reveal profound immunomodulation by bordetellae and demonstrate that by disrupting it much more robust protective immunity can be generated, providing a pathway to greatly improve vaccines and preventive treatments against these important pathogens.

scholarly journals Signaling regulation of fetoplacental angiogenesis

2011 ◽  
Vol 212 (3) ◽  
pp. 243-255 ◽  
Author(s):  
Kai Wang ◽  
Jing Zheng
Keyword(s):  
Cell Proliferation ◽  
Blood Flow ◽  
Growth Factor ◽  
Normal Pregnancy ◽  
Endothelial Cell Proliferation ◽  
No Production ◽  
Growth And Survival ◽  
Signaling Mechanisms ◽  
Placental Blood ◽  
And Migration

During normal pregnancy, dramatically increased placental blood flow is critical for fetal growth and survival as well as neonatal birth weights and survivability. This increased blood flow results from angiogenesis, vasodilatation, and vascular remodeling. Locally produced growth factors including fibroblast growth factor 2 (FGF2) and vascular endothelial growth factor A (VEGFA) are key regulators of placental endothelial functions including cell proliferation, migration, and vasodilatation. However, the precise signaling mechanisms underlying such regulation in fetoplacental endothelium are less well defined, specifically with regard to the interactions amongst protein kinases (PKs), protein phosphatase, and nitric oxide (NO). Recently, we and other researchers have obtained solid evidence showing that different signaling mechanisms participate in FGF2- and VEGFA-regulated fetoplacental endothelial cell proliferation and migration as well as NO production. This review will briefly summarize currently available data on signaling mediating fetoplacental angiogenesis with a specific emphasis on PKs, ERK1/2, AKT1, and p38 MAPK and protein phosphatases, PPP2 and PPP3.

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