WBbt:0004017 vs WBls:0000023

While goondicones 1-8 exhibit little to no in vitro inhibitory activity against Gram-positive, Gram-negative, and/or fungal pathogens, human carcinoma cells, or the livestock gastrointestinal parasite Haemonchus contortus L1-L3 larvae, 5 and 6 (and, to a lesser extent, 1) inhibit the motility of heartworm Dirofilaria immitis microfilaria (IC50 10-11 μM).

However, this H-2-controlled difference was not apparent in cells from mice receiving 400-600 L1 larvae.

We found no significant changes in the transcript level of most extracellular ligands in both bone morphogenic protein (BMP) and activin branches of the TGF-β signaling pathway between nematode-infected larvae and uninfected controls.

Eosinophils were not produced in cultures of bone marrow cells from either IL-5+/+ or IL-5-/- mice which were stimulated with excretory secretory antigen of T. canis larvae.

We investigated the effects of albendazole (ABZ), HLE, and their combination in Mesocestoides vogae infected mice, focusing on lymphoid cells in the peritoneal cavity, the site of larval proliferation and parasite-induced immunosuppression.

In this study, we attempted to determine whether pentylenetetrazol (a GABAergic receptor antagonist, PTZ)-induced seizures influence cell proliferation in zebrafish larvae (5 and 15 days of post-fertilization), using bromodeoxyuridine (BrdU) to label dividing cells.

We report that (i) the O. volvulus antigen, Ov58GPCR is a G-protein coupled receptor (GPCR) conserved in related nematodes, (ii) synthetic peptides predicted to be in the extracellular domain (ECD) of Ov58GPCR are indeed immunogenic epitopes in actively-infected individuals, (iii) synthetic peptide cocktails discriminate between actively-infected individuals, treated individuals and healthy African controls, (iv) polyclonal antibodies against one of the peptides or against the bacterially-expressed ECD reacted specifically with the native antigen of O. volvulus total and surface extracts, (v) Ov58GPCR is transcribed in both larvae and adult parasite stages, (vi) IgG and IgE responses to the recombinant ECD decline with ivermectin treatment.

Cells isolated from bladder wall of racemose larvae were established in primary cell culture and insulin stimulated their proliferation in a dose-dependent manner.

We demonstrated that mice immunized with MAP containing CD4+ T cell and B cell epitopes (MAP-TB) induced significantly higher protection against the challenge of T. spiralis larvae (35.5% muscle larva reduction) compared to the MAP containing B cell epitope alone (MAP-B) with a 12.4% muscle larva reduction.

Compared with untreated ML, four genes were up-regulated in both bile-activated and cell-cultured larvae, including calcium-dependent secretion activator (Csa; 2.55- and 16.04-fold, respectively), multi cystatin-like domain protein precursor (Mcd; 4.36 and 52), serine protease (Sp; 2.03 and 20.02), and intermediate filament protein ifa-1 (Ifa 1; 2 and 3.31).

ATP synthase F1, beta subunit (ATPase; 0.58 and 0.51) and serine protease precursor (Spp; 0.42 and 0.65) were down-regulated in both bile-activated and cell-cultured larvae.

The expression of two genes, enolase (Eno; 1.51) and ribosomal protein S6 kinase beta-1 (Rsk; 1.49), was up-regulated only in cell-cultured larvae, not in bile-activated larvae.

This study provide some differentially expressed genes among the untreated (normal), bile-activated and cell-cultured larvae of T. spiralis.

In addition, the inhibitory effects of these compounds on IL-6 levels in THP-1 cells stimulated with larval eggs have been examined.

The present data describe the presence in Con A- and antigen-stimulated T cell supernatants (of man or rat) of a factor able to inhibit, in a dose-dependent manner, the platelet cytotoxicity toward the young larvae of Schistosoma mansoni.

Nylon wool non-adherent, T cell enriched fractions of lymphocytes from both mice and horses were stimulated by the S. vulgaris larval mitogen while no proliferation was observed in cultures containing nylon wool adherent, B cell enriched fractions.

In addition, the cultured eosinophils generated approximately 2.5-fold more LTC4 than freshly isolated cells when stimulated with the calcium ionophore A23187 and manifested sevenfold greater antibody-dependent killing of S. mansoni larvae than the freshly isolated, normodense cells from the same donor.

However, IC-21 cells were activated by lymphokine (LK) to kill intracellular (Leishmania donovani amastigotes) and extracellular (Schistosoma mansoni larvae) parasites, as well as tumor cells.

Cellular immune responses against larval and adult schistosome antigens were studied in attenuated cercariae-vaccinated P and C57BL/6 mice to define differences correlating with the inability of P mice to develop vaccine-induced resistance to challenge Schistosoma mansoni infection.

A controlled test method was used to evaluate the efficacy of injectable micelle and oral paste formulations of ivermectin (22,23-dihydroavermectin B1) against 8-week-old Strongylus vulgaris larvae in experimentally infected pony foals.

Cytokine-treated endothelial cells showed increased expression of mRNA for the inducible form of the NO synthase, and both NO production and larval killing were suppressed by treatment with competitive inhibitors.

Moreover, IgE could modulate the SP-dependent functions of platelets since the pre-incubation with myeloma human IgE or with AP2 monoclonal antibodies--known to inhibit the IgE-dependent killing of these cells-leads to a dramatic decrease of the SP dependent cytotoxic activity of platelets towards the larvae.

Indeed the rTNF-beta and, to a lesser extent, rTNF-alpha, induce normal platelets into killer cells for the young larvae of schistosome.

These results confirm the role of cellular immunity in controlling the first stages of the larval development of E. multilocularis and indicate the necessity for a careful follow-up of any recurrence of alveolar echinococcosis in patients treated with CsA after liver transplantation.

On the other hand, a lower dose of TCDD was required in aged rats to suppress the combined humoral and cellular responses that limit the burden of encysted larvae, compared to young rats.

Immunohistocytochemistry revealed that Bm-MIF was localized to cells of the hypodermis/lateral chord, the uterine wall, and larvae developing in utero.

Mast cells and lymphocyte aggregates were present in the tissue of glands chronically stimulated with parasite larvae while eosinophils were only present if the gland had been recently stimulated.

Finally, oral treatment of rats with Vimang or mangiferin, daily for 50 days, inhibited mast cell degranulation as evaluated by the passive cutaneous anaphylaxis test (sensitization with infected mouse serum with a high IgE titre, then stimulation with the cytosolic fraction of T. spiralis muscle larvae).

In search for novel drug targets, we concentrate on factors of the cellular signaling machinery and report herein the characterization of a novel gene, Emmpk2, which is expressed in the parasite's larval stage and which codes for a member of the mitogen-activated protein kinase (MAPK) family.

The results of qPCR and Western blot revealed that rTsSPc significantly up-regulated the expression of Caco-2 cell apoptosis-related proteins (Caspase 3, Caspase 9 and Caspase 8, Bax and Cytochrome c), activated the apoptosis pathway, and thereby induced Caco-2 apoptosis. rTsSPc bound and interacted with PGAM5 receptor in Caco-2 cells and induced apoptosis, reduced the tight junctions (TJs) expression levels and damaged the Caco-2 monolayer integrity and barrier function, and promoted larval invasion.

We evaluated six alternative in vitro assays, namely the feeding inhibition assay, the colourimetric AlamarBlue®, MTT formazan and acid phosphatase activity assays, as well as isothermal calorimetry and the xCELLigence System using Ancylostoma ceylanicum third-stage larvae, stimulated third-stage larvae and adults.

The recombinant Cry1Ia12 protein, corresponding to the cry1Ia12 gene expressed in Escherichia coli cells, showed moderate toxicity towards first instar larvae of both cotton boll weevil and fall armyworm.

By producing IL-10 at the initiation of infection, eosinophils expand IL-10(+) myeloid dendritic cells and CD4(+) IL-10(+) T lymphocytes that inhibit inducible NO synthase (iNOS) expression and protect intracellular larvae.

During very early gastrulation, Brn1/2/4 is first expressed in cells associated with the prospective oral/foregut side of the blastopore, and during larval development in 4d blastomere descendants.

Vaccine administration by either route induced both humoral and cellular immune response against TspE1, which provided the partial protection against challenge infection with T. spiralis, as shown by significant reduction of larval burden in muscles.

Previous in vitro studies have demonstrated that mast cells (MC) can be directly activated by Trichinella spiralis larvae 1 (TSL-1) antigens.

The results indicate that during experimental A. costaricensis infection a parasite-specific immune response, directed via MHC-II molecules and CD4+ T cells, is not essential for the survival of C57BL/6 mice during the acute phase of infection, whereas the elimination of first-stage larvae seems to be regulated by a MHC-II- and CD4+ T-cell-dependent mechanism.

Cells obtained from larvae stimulated at any of the studied hormone concentrations showed greater mean fluorescence intensity when compared to non-stimulated cells.

The probiotic stimulated immune cell recruitment to the intestinal mucosa, which can be involved in the diminished capacity of larval penetration in the mucosa, resulting in the reduced infection intensity observed during acute infection.

It primarily downregulates the expression of LIN28, thereby promoting cell differentiation and larval phase transitions in nematodes, mammals and insects.

Nematode extracellular vesicles regulate larval development, animal communication, and ageing via conserved extracellular vesicles proteins.

HasPOU-IV is first expressed in sets of ventral epidermal cells in the newly hatched trochophore larvae.

Both genes are expressed in some ventral neuroectodermal cells; however the expression of Gva-Cdx fades in later larval stages while the expression of Gva-Xolx in these cells persists.

Additionally, Pax2/5/8 is expressed in epidermal spicule-secreting or associated cells of the larval trunk and in the region of the developing protonephridia.

More importantly, adiponectin pretreatment of Caco2 cells prevented T. spiralis larval invasion in vitro and its administration during infection enhanced intestinal IL-13 secretion and worm expulsion in vivo.

Knocking down CK8 in Caco-2 cells and ROCK1 pathway inhibitor Y27632 obviously inhibited the activation of RhoA/ROCK1 pathway, abolished rTsSPc-decreased TJs expression, rTsSPc-increased paracellular permeability, and inhibited larval invasion of Caco-2 monolayers in vitro.

Treatment with the dual cyclooxygenase (COX-1/-2) inhibitors indomethacin and ibuprofen, and the COX-2-selective inhibitor celecoxib partially blocked these cellular responses and was associated with enhanced numbers of infective larvae in the lung and adult worms in the duodenum.

The fusion product has been expressed in recombinant form in Escherichia coli cells, purified, and its neurotoxic activity has been assayed on the larvae of the moth Galleria mellonella, a simple experimental model to test the toxicity of compounds in insects.

The cells were transferred intravenously to genetically identical worm-free sheep which, together with controls, were challenged with 50,000 larvae and killed nine days later.

In agreement with previous results demonstrating an IFN-gamma-dependent cell-mediated protective mechanism in this vaccination model, Ag-elicited peritoneal macrophages from syngeneic recipients of this clone were activated to kill schistosome larvae (schistosomula) in vitro.

The rTsTPX2-activated macrophages (MrTsTPX2) were tested for polarization, their ability to evoke naïve CD4+ T cells, and resistance to the larval infection after adoptive transfer in BALB/c mice.

HeFoxA1 is apparently expressed in ectomesoderm cells involved in forming the larva-specific protonephridium (the so-called head kidney).

Moreover, rTsCatL2 disrupted the intestinal epithelial barrier by inducing cellular autophagy. rTsCatL2 disrupts the intestinal epithelial barrier and facilitates T. spiralis larval invasion.

The mean percentage of PRL-R+ cells in non-stimulated larvae, measured by flow cytometry was 7.3±0.3%.

URF13 was expressed in Spodoptera frugiperda (fall army-worm) cells (Sf9) in culture and in Trichoplusia ni (cabbage looper) larvae with a baculovirus vector.

Whole-mount in situ hybridization identified two selected ciliary genes, Tctex1d2 and Cfap45, were specially expressed in circumoral ciliary cells of the early-segmentation larvae.

We observed that MDSC-like cells are induced both by larvae and adult stages of H polygyrus bakeri.

During the early cleavage stages beta-catenin was destabilized/degraded in animal hemisphere blastomeres and became localized to the nuclei of the four vegetal-most cells at the 64-cell stage, which give rise to definitive larval and adult endoderm.

The non-feeding, intracellular first-stage larvae elicited few differences, with 4 transcripts showing an increased and 9 a decreased abundance relative to controls.

A cell stressors assay showed that H(2)O(2) effectively induced larval metamorphosis of H. elegans, but the inductivity of H(2)O(2) was also inhibited by both SB inhibitors.

The native antigen is localized in the intestinal cells of third-stage larvae and in the hypodermis and cuticle of fourth-stage larvae and adult parasites.

The Drosophila imaginal disc growth factors (IDGFs) induce the proliferation of imaginal disc cells and terminate cell proliferation at the end of larval development.

Our results show how pheromone or endocrine signaling pathways can coordinately regulate both developmental progression and cell-fate transitions in C. elegans larvae under stress so that the developmental schedule of cell fates remains unaffected by changes in developmental trajectory.

How these cells promote larval development, however, remains a mystery.

Actin polymerization was implicated in the Caenorhabditiselegans fusogen EFF-1 engagement in a reconstituted Drosophila cell culture system, and the actin-binding protein spectraplakin links EFF-1 to the actin cytoskeleton and promotes cell-cell fusions in C. elegans larvae.

Thus, the actin cytoskeleton differently promotes cell-cell fusion by regulating fusogen localization to the fusing plasma membrane in larvae or to intracellular vesicles in embryos.

Here we describe live animal fluorescence-activated cell sorting (laFACS), a protocol for automatic selection of live first larval stage (L1) animals using a standard FACS system.

For instance, in Caenorhabditis elegans all cell divisions required for the larval body plan are completed within six hours after fertilization, with seven mitotic cycles(1); the sixteen or more mitoses of Drosophila embryogenesis occur in less than 24 hr(2).

Using immunofluorescence assays targeting proteins from each of the viruses, and in situ hybridization, we demonstrate viral proteins and RNAs localize to intestinal cells in larval stage Caenorhabditis nematodes.

Surprisingly, drpr knockdown cell-autonomously prevents autophagy induction in dying salivary gland cells, but not in larval fat body cells following starvation.

Therefore, our results indicate that Wnt signaling globally regulates the asymmetric, stem cell-like division of most or all somatic seam cells during C. elegans larval development, and that Wnt pathway regulation of stem cell-like behavior is conserved in nematodes.

The stereotyped pattern of DTC migration is carefully controlled by extracellular and cell surface molecules during larval development.

Germ cells undergoing mitosis during larval stages are especially sensitive to DGLA, but exposure to DGLA during adulthood also reduces germ cells and brood size, in part by inducing inappropriate apoptosis of meiotic germ cells.

We have used C. elegans as a model system to investigate the mechanism of resistance to 5-FU, which induces germ cell death and inhibits larval development in C. elegans.

Loss of both p170 and p130 suppressed germ cell proliferation and arrested larval development.

Ci-POU-IV is expressed in the precursor cells of the neural system during development and in the neural system of the larva.

First, an interaction between the distal-most pair of sheath cells and the proliferation zone of the germ line is required for larval germline amplification.

TORC1 activity promotes both stem cell fate and proliferation in the Caenorhabditis elegans hermaphrodite germline stem cell system to facilitate expansion of the larval germline Progenitor Zone (PZ) pool in response to nutrients.

A 4-6-week antibiotic therapy with doxycycline, for example, resulted in the loss of Wolbachia that subsequently led to extensive apoptosis of somatic cells, germline, embryos, and microfilariae, as well as inhibition of fourth-stage larval development.

The Gram-negative bacterium Photorhabdus luminescens is an excellent organism to study phenotypic heterogeneity since their life cycle involves a symbiotic interaction with soil nematodes as well as a pathogenic association with insect larvae.

Redistribution of glucose transporter 4 (GLUT4) and phosphorylation of Akt were observed in nurse cells, consistent with enhancement of glucose uptake and glycogen storage by larvae that is known to occur.

The AVM-CRF biological activity survey shows excellent toxicological properties against Plutella xylostella larvae, which confirms that α-CD caps could be uncapped enzymatically in vivo and release AVM, inducing P. xylostella larval death.

In contrast, blocking mast cell degranulation reduced the worm burden in IL-6-/- mice partially, suggesting that release of mast cell-derived mediators improves larval migration to some degree.

Its cell source and physical characteristics suggest that it is similar to a monokine, eosinophil-cytotoxicity-enhancing factor (M-ECEF), that activates human eosinophil toxicity to Schistosoma mansoni larvae.

These cells might be T helper cells since B cells were stimulated to proliferate in the presence of both T cells and S. vulgaris larval mitogen.

Under appropriate conditions of activation and surface membrane stimulation, IC-21 cells could be induced to release soluble cytotoxic factors retaining larvacidal activity.

As previously shown for mammalian cell targets, the effects of NO in susceptible larval stages may involve enzymes required for aerobic energy metabolism, since similar cytotoxicity was demonstrated by chemical inhibitors of the citric acid cycle or mitochondrial respiration.

T. spiralis infection induced a significant increase in density of CD105+ve/CD45-ve cells that could represent MSCs in both intestinal and muscle sections, similarly the intramuscular injected larval crude antigen caused more infiltration of such cells in muscles compared to muscle sections from healthy control mice.

The plasminogen-binding property of O. volvulus alpha-enolase may support plasmin-mediated proteolysis including degradation of host's extracellular matrix thereby promoting the migration of larval stages through tissues.

HeOtx is also expressed in a group of cells in the dorsal midline of the early trochophore larva in putative posterior sensory organ precursors.

An immunocytochemical study showed that p53 was expressed in the nucleoplasm of basophilic cell in the cyst and Trichinella larvae, which suggested involvement of these apoptosis genes in the nurse cell formation.

Critically, VHA-19 is expressed in the excretory cell in both larvae and adults, suggesting that it may have a role in osmoregulation in C. elegans more generally, probably in trafficking or secretion pathways.

Studies employing these methods recently bolstered the hypothesis that S. stercoralis uses cellular signaling pathways homologous to three that regulate dauer larval development in Caenorhabditis elegans to regulate morphogenesis and development of its infective third-stage larva.

Interestingly, characteristics of necrotic cell death were observed in the hypodermis and intestine of the arrested larvae suggesting that pH homeostasis via the E subunit of V-ATPase is required for the cell survival in C. elegans.

The down-regulation of hox gene expression in most somatic cells at the end of larval development may be one cause for the absence of cell proliferation in adult C. elegans.