In addition, morpholino antisense inhibition of NAIP5 activity
in mouse macrophages from resistant mice resulted in an increase in permissiveness of Legionella replication (J: 129300).
Amastigotes with such compromised mitochondrial function were unable to multiply
in mouse macrophages (i.e. mammalian Leishmania target cells), suggesting that inhibition of LMIT1 can abolish parasite virulence.
In the first, principal investigator Glass and colleagues investigated a pair of related transcriptional repressors called Rev - Erb - alpha and Rev - Erb - beta (proteins with important roles in regulating the circadian rhythm in many cell types)
in mouse macrophages.
Not exact matches
We also discovered that when we depleted neutrophils, nerve debris clearance was significantly halted
in both normal
mice and
mice lacking a major population of
macrophages.»
Jerrold Olefsky and colleagues at the University of California, San Diego, killed the bone marrow cells
in mice that make immune cells called
macrophages.
Researchers also found a type of immune cell (multinucleated
macrophage giant cells)
in the ovaries of reproductively «old»
mice only.
But unlike the normal
mice, those with altered
macrophages showed no signs of inflammation, such as changes
in insulin production, high levels of immune chemicals, and
macrophages in their belly fat.
IT»S ELECTRIFYING
Macrophages (green) «plug
in» to heart cells (light purple and pink), providing an electrical boost that helps the heart cells contract and pump blood, a study
in mice finds.
For the research, the scientists used the platform to target colon
macrophages in order to reduce inflammatory symptoms caused by Inflammatory Bowel Disease (IBD)
in mouse models.
In this study, Cherqui's team transplanted wildtype HSPCs into an FA mouse model, reporting that the HSPCs engrafted and soon differentiated into macrophages in key regions of the mice's brain and spinal cord where they appeared to transfer wildtype FXN into deficient neurons and muscle cell
In this study, Cherqui's team transplanted wildtype HSPCs into an FA
mouse model, reporting that the HSPCs engrafted and soon differentiated into
macrophages in key regions of the mice's brain and spinal cord where they appeared to transfer wildtype FXN into deficient neurons and muscle cell
in key regions of the
mice's brain and spinal cord where they appeared to transfer wildtype FXN into deficient neurons and muscle cells.
The research team, Heller says, has already begun experiments to further explore the implications of these results, which include looking at differences
in this pathway between cells taken from allergic and healthy individuals, and testing the efficacy of an inhalable drug that mimics the function of GRB1 and p70S6K to shut off the development of M2
macrophages in the lungs of
mice.
The study compared intestinal wound healing
in two groups of
mice: 1) typical
mice (wild type) found
in nature and 2)
mice genetically deficient
in the healing factor IL - 10, specifically
in macrophages, which impairs their ability to have normal wound repair.
In mice with pancreatic tumors, Kalbasi and other members of the team found relatively high levels of inflammatory compounds including CCL2, the signaling molecule that activates CCR2 on monocytes and
macrophages to make these cells migrate to tumors.
In mice, we found that these drugs can sometimes increase the spread of cancer because they hinder glycolysis in macrophage
In mice, we found that these drugs can sometimes increase the spread of cancer because they hinder glycolysis
in macrophage
in macrophages.
In 2001 Jeffrey W. Pollard and his co-workers at the Albert Einstein College of Medicine described
mice that were genetically engineered to be susceptible to breast cancer tumors but that produced precancerous tissue that did not turn fully malignant unless it enlisted the assistance of
macrophages.
Results showed that naturally healthy
macrophages and gene - corrected
macrophages worked equally well
in correcting the disease
in the
mice.
Antibody formation against sheep erythrocytes by
mouse spleen cells
in vitro requires interactions among antigen - treated
macrophages and lymphoid cells
in cell culsters for only a finite time.
Deletion of the GM - CSF gene
in the
mouse led to reduction and impaired regulatory function of gut tissue
macrophages and dendritic cells which compromised induction of tolerance to food antigens and increased
mice susceptibility to IBD.
In mice engineered so their macrophage cells would mimic those of people, expressing the human SIRPα protein, nanoparticles tagged with the CD47 peptide passports stuck around in the circulation rather than being gobbled u
In mice engineered so their
macrophage cells would mimic those of people, expressing the human SIRPα protein, nanoparticles tagged with the CD47 peptide passports stuck around
in the circulation rather than being gobbled u
in the circulation rather than being gobbled up.
Macrophages may live longer
in humans than
in mice, and the persistence of those cells might be responsible for preserving tattoos
in human skin, he says.
Immunologist Sandrine Henri of the Immunology Center of Marseille - Luminy,
in France, and colleagues tattooed
mice tails with green ink to see how waste - disposing
macrophages in the skin would respond.
Using
mice deficient
in Del - 1, they found that the protein promotes proliferation and differentiation of hematopoetic stem cells, sending more of these progenitor cells down a path toward becoming myeloid cells, such as
macrophages and neutrophils, rather than lymphocytes, such as T cells and B cells.
In this study, the researchers found that macrophages from mice lacking Smurf1 were unable to attach the death - tagging protein ubiquitin to intracellular bacteria, resulting in a failure of the autophagy pathway and runaway growth of the bacteria inside the cell
In this study, the researchers found that
macrophages from
mice lacking Smurf1 were unable to attach the death - tagging protein ubiquitin to intracellular bacteria, resulting
in a failure of the autophagy pathway and runaway growth of the bacteria inside the cell
in a failure of the autophagy pathway and runaway growth of the bacteria inside the cells.
Through studies conducted
in mice, Oliver M. Steinmetz, MD (University Hospital Hamburg Eppendorf,
in Germany) and his colleagues have shown that the messenger protein IL - 6, which is rapidly produced at high levels during an acute inflammatory form of kidney disease, potently dampens activation of tissue - destructive immune cells called
macrophages.
«The protein Smurf1 functions
in specialized white blood cells called
macrophages in both
mice and humans, thereby suggesting a conserved evolutionary pathway,» said Dr. Shiloh, co-senior author of the study along with Dr. Beth Levine, Director of the University's Center for Autophagy Research.
With this goal
in mind, Dr. Divangahi's team vaccinated
mice with BCG and
in a series of experiments observed that
in the bone marrow BCG was able to reprogram or «educate» the stem cells to proliferate and generate TB slaying
macrophages.
«
In the past we have also shown that in mice, certain regulatory mechanisms protect against urinary calcium oxalate stone formation, and that these mechanisms may be mediated by anti-inflammatory Type 2 macrophages (M2s
In the past we have also shown that
in mice, certain regulatory mechanisms protect against urinary calcium oxalate stone formation, and that these mechanisms may be mediated by anti-inflammatory Type 2 macrophages (M2s
in mice, certain regulatory mechanisms protect against urinary calcium oxalate stone formation, and that these mechanisms may be mediated by anti-inflammatory Type 2
macrophages (M2s).
By means of their
mouse model, the hormone researchers from Ulm could prove that dexamethasone — mediated through the dimer function of GR — leads to the release of sphingosine -1-phosphate
in the
macrophages, a tissue hormone that fosters growth, migration and division of cells and has a stabilization effect on inner vessel walls.
Using
mice that had been manipulated to develop MS, the researchers discovered that chronic MS leads to significantly increased levels of succinate, a small metabolite that sends signals to
macrophages and microglia, tricking them into causing inflammation, but only
in cerebrospinal fluid, not
in the peripheral blood.
They show that highly purified NS1 acts as a pathogen - associated molecular pattern (PAMP) that activates
mouse macrophages and human peripheral blood mononuclear cells (PBMCs)
in culture via TLR4, resulting
in release of inflammatory cytokines — an effect that was blocked by either a TLR4 antagonist or an anti-TLR4 antibody.
Our data
in humans and
mice show that adipocyte size is a strong predictor of the percentage of
macrophages in adipose tissue (Figure 3e).
Our results indicate that the percentage of
macrophages in the adipose tissue that surrounds and infiltrates the extensor digitalis longus muscle is increased
in obese
mice compared with lean
mice.
We estimate that the percentage of
macrophages in adipose tissue ranges from under 10 %
in lean
mice and humans to over 50 %
in extremely obese, leptin - deficient
mice and nearly 40 %
in obese humans.
The correlation of adipose tissue
macrophage content with adiposity may affect the interpretation of results obtained from
mice in which transgene expression is driven by the aP2 promoter.
Adipose tissue within muscle contained significant numbers of F4 / 80 +
macrophages, and the percentage of F4 / 80 + cells within this adipose tissue was markedly increased
in obese
mice compared with lean
mice (41 % ± 4 % of
macrophages vs. 12 % ± 2 % of
macrophages, respectively; P < 0.005, mean ± SD)(Figure 4).
In response to infection, mice lock up iron (purple) in their macrophages (middle, right
In response to infection,
mice lock up iron (purple)
in their macrophages (middle, right
in their
macrophages (middle, right).
«We have shown that an endogenous peptide, catestatin, can directly suppress glucose production from hepatocytes and can indirectly suppress lipid accumulation
in liver as well as
macrophage - mediated inflammation
in obese
mice,» said Sushil K. Mahata, PhD, professor of medicine at UC San Diego School of Medicine.
Although the slopes corresponding to adipocyte cross-sectional area for the subcutaneous depot were smaller than (and fell outside the 95 % confidence intervals of) the slopes for the mesenteric and perigonadal depots, this difference was entirely attributable to the fact that the data from three B6.V Lepob / ob
mice fell below the line relating adipocyte area to
macrophage content
in the other animals (Table 1).
Macrophages in the liver and muscle of lean and obese
mice.
Average adipocyte cross-sectional area and the percentage of F4 / 80 + cells (
macrophages)
in adipose tissue depots were determined for each
mouse in this study.
Immunohistochemical detection of cells expressing the
macrophage - specific antigen F4 / 80 (arrows)
in extensor digitalis longus muscles from C57BL / 6J (a and c) Lepob / ob female and (b and d) lean female
mice.
Stimulation of TLR2 / TLR6 triggers profound decreases
in ferroportin mRNA and protein expression
in bone marrow - derived
macrophages, liver and spleen of
mice without changing hepcidin expression.
Mice that carry a homozygous missense mutation
in the Csf1 gene (Csf1op / op) are relatively
macrophage deficient (43, 54, 55).
Macrophages in the adipose tissue of lean
mice were uniformly small, isolated, and widely dispersed among the adipocytes.
Our results indicate that adipose tissue
macrophage accumulation is directly proportional to measures of adiposity
in mice and humans.
The study showed that
mice lacking the SNRK gene had a significantly higher concentration of
macrophages in white fat tissue compared with normal
mice.
In mice, both body mass and adipocyte size were strong predictors of the percentage of F4 / 80 + macrophages in the perigonadal, perirenal, mesenteric, and subcutaneous adipose tissue depot
In mice, both body mass and adipocyte size were strong predictors of the percentage of F4 / 80 +
macrophages in the perigonadal, perirenal, mesenteric, and subcutaneous adipose tissue depot
in the perigonadal, perirenal, mesenteric, and subcutaneous adipose tissue depots.
To determine whether adipose tissue
macrophages express any molecules implicated
in obesity - associated complications, we isolated three cell populations from the parametrial adipose tissue of three obese B6.V Lepob / ob
mice: (a) an adipocyte - enriched population, (b) a stromal vascular
macrophage F4 / 80 + population, and (c) an F4 / 80 — stromal vascular population.
Adipose tissue
macrophages in mice with varying degrees of adiposity.
Flow cytometry of SVCs isolated from two perigondadal adipose tissue depot illustrates that tissue from
macrophage - deficient
mice (b) contains 34 % the number of F4 / 80 + cells found
in adipose tissue from control
mice (a).