scholarly journals The Many Facets of Sphingolipids in the Specific Phases of Acute Inflammatory Response

2018 ◽  
Vol 2018 ◽  
pp. 1-12 ◽  
Author(s):  
Sabine Grösch ◽  
Alice V. Alessenko ◽  
Elisabetta Albi
Keyword(s):  
Biological Activity ◽  
Inflammatory Response ◽  
Immune Cells ◽  
Inflammatory Process ◽  
Acute Inflammatory Response ◽  
Exogenous Agents ◽  
The Many

This review provides an overview on components of the sphingolipid superfamily, on their localization and metabolism. Information about the sphingolipid biological activity in cell physiopathology is given. Recent studies highlight the role of sphingolipids in inflammatory process. We summarize the emerging data that support the different roles of the sphingolipid members in specific phases of inflammation: (1) migration of immune cells, (2) recognition of exogenous agents, and (3) activation/differentiation of immune cells.

scholarly journals Inflammasomes inMycobacterium tuberculosis-Driven Immunity

2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Sebastian Wawrocki ◽  
Magdalena Druszczynska
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Inflammatory Response ◽  
Immune Responses ◽  
Proinflammatory Cytokines ◽  
Immune Cells ◽  
Protein Complexes ◽  
Inflammasome Activation ◽  
Host Immune Responses ◽  
Multimeric Protein

The development of effective innate and subsequent adaptive host immune responses is highly dependent on the production of proinflammatory cytokines that increase the activity of immune cells. The key role in this process is played by inflammasomes, multimeric protein complexes serving as a platform for caspase-1, an enzyme responsible for proteolytic cleavage of IL-1βand IL-18 precursors. Inflammasome activation, which triggers the multifaceted activity of these two proinflammatory cytokines, is a prerequisite for developing an efficient inflammatory response against pathogenicMycobacterium tuberculosis(M.tb). This review focuses on the role of NLRP3 and AIM2 inflammasomes inM.tb-driven immunity.

scholarly journals Disruption of γ-Glutamyl Leukotrienase Results in Disruption of Leukotriene D4 Synthesis In Vivo and Attenuation of the Acute Inflammatory Response

2001 ◽  
Vol 21 (16) ◽  
pp. 5389-5395 ◽  
Author(s):  
Zheng-Zheng Shi ◽  
Bing Han ◽  
Geetha M. Habib ◽  
Martin M. Matzuk ◽  
Michael W. Lieberman
Keyword(s):  
Inflammatory Response ◽  
Double Mutant ◽  
Inflammatory Process ◽  
Embryonic Stem ◽  
Acute Inflammatory Response ◽  
Leukotriene D4 ◽  
Glutamyl Transpeptidase ◽  
Targeting Strategy ◽  
Deficient Mice

ABSTRACT To study the function of γ-glutamyl leukotrienase (GGL), a newly identified member of the γ-glutamyl transpeptidase (GGT) family, we generated null mutations in GGL (GGLtm1) and in both GGL and GGT (GGLtm1-GGTtm1) by a serial targeting strategy using embryonic stem cells. Mice homozygous for GGLtm1 show no obvious phenotypic changes. Mice deficient in both GGT and GGL have a phenotype similar to the GGT-deficient mice, but ∼70% of these mice die before 4 weeks of age, at least 2 months earlier than mice deficient only in GGT. These double-mutant mice are unable to cleave leukotriene C4 (LTC4) to LTD4, indicating that this conversion is completely dependent on the two enzymes, and in some organs (spleen and uterus) deletion of GGL alone abolished more than 90% of this activity. In an experimental model of peritonitis, GGL alone is responsible for the generation of peritoneal LTD4. Further, during the development of peritonitis, GGL-deficient mice show an attenuation in neutrophil recruitment but not of plasma protein influx. These findings demonstrate an important role for GGL in the inflammatory response and suggest that LTC4 and LTD4 have distinctly different functions in the inflammatory process.

Role of miR-146a in regulation of the acute inflammatory response to monosodium urate crystals

2015 ◽  
Vol 74 (4) ◽  
pp. 786-790 ◽  
Author(s):  
Nicola Dalbeth ◽  
Bregina Pool ◽  
Odette M Shaw ◽  
Jacquie L Harper ◽  
Paul Tan ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Acute Inflammatory Response ◽  
Monosodium Urate ◽  
Monosodium Urate Crystals ◽  
Urate Crystals

scholarly journals "Platinum on the road": Interactions of antitumoral cisplatin with proteins

2008 ◽  
Vol 80 (12) ◽  
pp. 2715-2725 ◽  
Author(s):  
Fabio Arnesano ◽  
Giovanni Natile
Keyword(s):  
Biological Activity ◽  
Antitumor Activity ◽  
Cell Membrane ◽  
The Road ◽  
Specific Proteins ◽  
On The Road ◽  
The Many

When the antitumor activity of cisplatin was discovered, no one would have thought of the existence of specific proteins able to transport Pt across the cell membrane or to specifically recognize DNA modified by this drug. However, such proteins do exist and, furthermore, are specific for the Pt substrate considered. It follows that proteins are deeply involved in managing the biological activity of cisplatin. It is expected that, after the first 20 years in which most of the efforts were devoted to understanding its mode of interaction with DNA and consequent structural and functional alterations, the role of proteins will be more deeply scavenged. How cisplatin can survive the attack of the many platinophiles present in the extracellular and intracellular media is the issue addressed in this article. Significantly, differences are observed between cisplatin, carboplatin, and oxaliplatin.

scholarly journals Depletion of Neutrophils Exacerbates the Early Inflammatory Immune Response in Lungs of Mice Infected withParacoccidioides brasiliensis

2016 ◽  
Vol 2016 ◽  
pp. 1-17 ◽  
Author(s):  
Paula Andrea Pino-Tamayo ◽  
Juan David Puerta-Arias ◽  
Damaris Lopera ◽  
Martha Eugenia Urán-Jiménez ◽  
Ángel González
Keyword(s):  
Monoclonal Antibody ◽  
Immune Response ◽  
Inflammatory Response ◽  
Paracoccidioides Brasiliensis ◽  
Yeast Cells ◽  
Histopathological Analysis ◽  
Acute Inflammatory Response ◽  
Fungal Load ◽  
Inflammatory Immune Response

Neutrophils predominate during the acute phase of theParacoccidioides brasiliensisinfection. Herein, we determined the role of the neutrophil during the early stages of experimental pulmonary paracoccidioidomycosis using a monoclonal antibody (mAb) specific for neutrophils. Male BALB/c mice were inoculated intranasally with1.5×106or2×106P. brasiliensisyeast cells. The mAb was administered 24 h before infection, followed by doses every 48 h until mice were sacrificed. Survival time was evaluated and mice were sacrificed at 48 h and 96 h after inoculation to assess cellularity, fungal load, cytokine/chemokine levels, and histopathological analysis. Neutrophils from mAb-treated mice were efficiently depleted (99.04%). Eighty percent of the mice treated with the mAb and infected with1.5×106yeast cells died during the first two weeks after infection. When mice were treated and infected with2×106yeast cells, 100% of them succumbed by the first week after infection. During the acute inflammatory response significant increases in numbers of eosinophils, fungal load and levels of proinflammatory cytokines/chemokines were observed in the mAb-treated mice. We also confirmed that neutrophils are an important source of IFN-γand IL-17. These results indicate that neutrophils are essential for protection as well as being important for regulating the early inflammatory immune response in experimental pulmonary paracoccidioidomycosis.

The role of TLR2 in the acute inflammatory response induced by Bothrops atrox snake venom

Toxicon ◽  
2016 ◽  
Vol 118 ◽  
pp. 121-128 ◽  
Author(s):  
Vanessa Moreira ◽  
Catarina Teixeira ◽  
Henrique Borges da Silva ◽  
Maria Regina D'Império Lima ◽  
Maria Cristina Dos-Santos
Keyword(s):  
Inflammatory Response ◽  
Snake Venom ◽  
Acute Inflammatory Response ◽  
Bothrops Atrox

scholarly journals Infiltration of circulating myeloid cells through CD95L contributes to neurodegeneration in mice

2015 ◽  
Vol 212 (4) ◽  
pp. 469-480 ◽  
Author(s):  
Liang Gao ◽  
David Brenner ◽  
Enric Llorens-Bobadilla ◽  
Gonzalo Saiz-Castro ◽  
Tobias Frank ◽  
...  
Keyword(s):  
Immune Cells ◽  
Dopaminergic Neurons ◽  
Inflammatory Process ◽  
Myeloid Cells ◽  
Innate Immune ◽  
Innate Response ◽  
Apoptosis Inducer ◽  
Induced Apoptosis ◽  
Specific Deletion

Neuroinflammation is increasingly recognized as a hallmark of neurodegeneration. Activated central nervous system–resident microglia and infiltrating immune cells contribute to the degeneration of dopaminergic neurons (DNs). However, how the inflammatory process leads to neuron loss and whether blocking this response would be beneficial to disease progression remains largely unknown. CD95 is a mediator of inflammation that has also been proposed as an apoptosis inducer in DNs, but previous studies using ubiquitous deletion of CD95 or CD95L in mouse models of neurodegeneration have generated conflicting results. Here we examine the role of CD95 in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridin (MPTP)–induced neurodegeneration using tissue-specific deletion of CD95 or CD95L. We show that DN death is not mediated by CD95-induced apoptosis because deletion of CD95 in DNs does not influence MPTP-induced neurodegeneration. In contrast, deletion of CD95L in peripheral myeloid cells significantly protects against MPTP neurotoxicity and preserves striatal dopamine levels. Systemic pharmacological inhibition of CD95L dampens the peripheral innate response, reduces the accumulation of infiltrating myeloid cells, and efficiently prevents MPTP-induced DN death. Altogether, this study emphasizes the role of the peripheral innate immune response in neurodegeneration and identifies CD95 as potential pharmacological target for neurodegenerative disease.

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