WBls:0000023 vs WBbt:0004017

Animals lacking CGT do not synthesize GSLs, arrest growth at the first larval stage, and display defects in a subset of cells in their digestive tract; these defects impair larval feeding, resulting in a starvation-induced growth arrest.

That AVM induced the activation of PKC was found not only in the Drosophila larvae but also in Drosophila S2 cells.

In the brains of 5 dpf larvae, PTZ treatment significantly reduced the number of BrdU-labeled cells in the telencephalic area (pallium and subpallium), diencephalic area (thalamus and preoptic area), medial tectal proliferation zone, and medial cerebellar proliferation zone to 52.4%, 62.9%, 47.2%, and 54.0% of the controls, respectively.

Neurocysticercosis is a parasitic brain disease caused by the larval form (Cysticercus cellulosae) of Taenia solium and is the leading cause of preventable epilepsy worldwide.

Trichinella spiralis, as well as its muscle larvae excretory-secretory products (ES L1), given either alone or via dendritic cells (DCs), induce a tolerogenic immune microenvironment in inbred rodents and successfully ameliorate experimental autoimmune encephalomyelitis.

Muscle larvae excretory-secretory products (MLES) typically induce parasite-specific immune responses such as the Th2 response and regulatory T cells (Tregs) by modulating dendritic cell (DC) phenotype via the recognition of pattern recognition receptors (PRRs), such as Nod-like receptors (NLRs).

We asked whether the OMVs of C. lytica induce larval settlement due to cell membrane components or through delivery of specific cargo.

The recombinant C-type lectin protein (r-CTL) derived from Toxocara canis larvae is thought to play a role in promoting regulatory T cell-dominant immune responses in toxocariasis.

Peripheral lymphocytes from 16 patients with chronic uncomplicated strongyloidiasis and 15 non-infected controls were stimulated in vitro with Strongyloides stercoralis larval antigens, other non-parasite antigens and the T cell mitogen phytohemagglutinin (PHA).

Larvae of the helminth parasite Schistosoma mansoni are efficiently killed in vitro by lymphokine-activated macrophages, leading to the hypothesis that these cells may participate in the effector mechanism of protective immunity against schistosomiasis.

These results indicate that amastigotes and schistosome larvae are susceptible to killing by nonoxidative cytotoxic mechanism induced by lymphokine activation but, on the other hand, support the concept that the killing of log-growth phase promastigotes by nonactivated cells is dependent upon the respiratory burst.

The larvacidal activity of macrophage supernatant fluids was abrogated by addition of either anti-TNF antisera or Zn+2, which has been shown to inhibit TNF-induced damage of tumour cells.

Preincubation of T. spiralis L1 larvae with nitrite also caused an increase in the number of CD4(+) and CD8(+) cells as well as IL-2, IL-5, and INF-gamma levels.

We have compared the susceptibilities of different stages of larvae to killing by nitric oxide (NO), which was previously shown to be involved in the larvicidal function of cytokine-activated cytotoxic effector cells.

Lung-stage larvae obtained 1 week after infection were not killed in vitro by NO generated either by a chemical NO donor or by activated cells.

Excretory/secretory products from larvae early in the infection were found to suppress T cell proliferative responses in vitro as well as the production of IFN-gamma and IL-4.

Following to the results of Microculture Tetrazolium Test (MTT), five concentrations of the extraction of the second stage larvae were chosen to induce the apoptosis of A549 cells.

It was determined that eosinophils killed the S. stercoralis larvae in naïve mice, whereas these cells were not required for the accelerated killing of larvae in immunized mice.

Here, in mice exposed to vaccinating radiation-attenuated schistosome larvae, which induce high levels of protective immunity to challenge infection, we describe the parasite-induced migration of Langerhans cells (LCs) from the epidermal site of immunisation to the sdLN using a specific monoclonal antibody that recognises langerin (CD207).

While none of the larvae induced the secretion of pro-inflammatory IL-12p70, the production of immunosuppressive IL-10 was elevated in response to primary cell E/S-products.

Excretory-secretory antigens of Trichinella spiralis muscle larvae can induce the semi-matured status of rat dendritic cells.

In conclusion, T. spiralis larva intestinal invasion induced the production of Th2 and Th17 cell-related cytokines, and the cytokines decreased with T(reg) cell-related cytokine.

Recently, it was shown that TSL-1 antigens from T. spiralis muscle larvae induce IL-4 and TNF release by unsensitized, normal mast cells (MC) involving an Ig-independent mechanism.

Larvae were not killed in immunized mice if contact between host cells and the parasites was prevented.

AIP (apoptosis-inducing protein) is a protein purified and cloned from Chub mackerel infected with the larval nematode, Anisakis simplex, which induces apoptosis in various mammalian cells including human tumor cell lines.

To investigate the potential antifouling mechanism of 12-MTA in the larval settlement of Hydroides elegans, the expression level of four marker genes, namely, Ran GTPase activating protein (GAP), ATP synthase (AS), NADH dehydrogenase (ND), and cell division cycle protein (CDC), was compared among the untreated larvae (the control), isobutylmethylxanthine (an effective settlement inducer), and 12-MTA-treated larvae.

BSF larvae deploy rapid cellular defenses, such as phagocytosis and encapsulation, supported by a broad and dynamic humoral arsenal-including dozens of antimicrobial peptides (AMPs), lysozyme, and melanization factors-that are often strongly induced following microbial challenge.

Larvae did not invade IEC-6 cells, but did cause the cells to take up parasite glycoproteins.

Furthermore, we evaluated the in vitro effects of T. spiralis excretory/secretory (ES) products from muscle larvae on specific functions (viability, proliferative response, apoptosis) in two cell lines (HeLa and U937), as well as its ability to induce GSTO1, p-AkT, p-ERK1/2 and p-JNK1.

The involvement of second messengers in the control of activation-induced changes to the surface of Trichinella spiralis infective larvae was investigated using membrane-permeant photo-activatable 'caged' compounds to alter intracellular levels of inositol trisphosphate (IP3), calcium ions (Ca2+) and cyclic AMP (cAMP).

We explored the properties of soluble extracts from Leishmania infantum promastigotes, Toxoplasma gondii tachyzoites, Trichinella spiralis muscle larvae to expand the pool of T-regulatory cells in a population of polyclonally activated T cells in the absence of accessory cells, and compared their effects to those induced by Plasmodium falciparum extracts.

Carefully controlled experiments in defined inbred strains of mice – with enhanced recovery of larvae in tandem with measurements of cellular, histopathological and molecular processes – have greatly enhanced our knowledge of the early phase of infection, a phase crucial to the success or failure of adult worm establishment.

An in vitro invasion assay showed that, when anti-TspSP-1.2 serum, serum of infected mice and normal mouse serum were added to the medium, the invasion rate of the infective larvae in an HCT-8 cell monolayer was 33.0%, 89.4%, and 96.2%, respectively (P<0.05), indicating that the anti-TspSP-1.2 serum partially prevented the larval invasion of intestinal epithelial cells.

The present study demonstrates how an experimental infection with endoparasitic nematode larvae (Anisakis simplex) induces cellular and humoral immune responses in rainbow trout Oncorhynchus mykiss.

The results showed that rTs-serpin can induce partial protection against Trichinella larvae challenge in mice, when compared to the FCA-/FIA-formulated vaccination, the IMS1313 plus rTs-serpin mixture showed higher humoral immunity and similar levels of cellular immunity and worm reduction rate.

Finally, living L3 larvae were able to promote in both wt and mutant mice, an oxidative burst response and the release of neutrophil extracellular traps (NET).

Compounds 10, 17, 20, and 22 were identified as the most potent compounds, inhibiting the development of the fourth larval (L4) stage of H. contortus at sub-nanomolar potencies while displaying strong selectivity toward the parasite when tested in vitro against the human MCF10A cell line.

Secreted proteins from T. spiralis infective larvae inhibit nucleotide-induced mast cell activation, and that induced by ADP and UDP is specifically blocked by parasite secretory 5'-nucleotidase.

Resistant animals control larval colonization by the production of a protective antibody response regulated by Th2 T cells.

In general, the larvae induced a limited cellular response apart from the occurrence of focal melanin macrophage aggregates and individual eosinophilic granular cells in the connective tissue capsule.

In C. elegans, IIS also regulates development into the diapause state known as dauer, a quiescent larval form that enables C. elegans to endure harsh environments through morphological adaptation, improved cellular repair, and slowed metabolism.

Because little is known about targets of the Wnt signaling pathways acting during larval VPC and seam cell differentiation, we sought to identify genes regulated by Wnt signaling in these two hypodermal cell types.

In the third larval stage, the anchor cell in the somatic gonad first induces and then invades the adjacent epidermal vulval precursor cells.

Dauer larva formation in Caenorhabditis elegans is controlled by chemosensory cells that respond to environmental cues.

Mutations in genes of the C. elegans heterochronic pathway cause altered temporal patterns of larval development, in which cells at certain larval stages execute cell division patterns or differentiation programs normally specific for other stages.

In a third instar larva the mRNA was localized to a single layer of epidermal cells immediately underlying the procuticle region of the integument. cDNA or genomic sequences that are highly related to fragments of LcCS-1 were demonstrated in three insect orders, one arachnid and Caenorhabditis elegans, thereby attesting to the importance of this enzyme in these chitin-producing organisms.

MYRF loss-of-function or acute depletion suppresses and flattens this network, causing developmental arrest during the late intermolt phase of each larval cycle and stalling molting, seam cell division, and vulval morphogenesis.

In this study, using CD154-/- mice exposed to radiation-attenuated S. mansoni larvae, we demonstrate roles for CD154/CD40 in the activation of skin-derived APCs and the development of Th1 cells in the skin-draining lymph nodes (sdLN).

The present results suggest that in vitro product secreted by larvae in hepatic cysts causes subversion of the cellular immune response in the host.

Therefore, it is possible that the S. vulgaris mitogen released by both viable parasites and degenerating larvae might induce T cell dependent production of immunoglobulin in vivo and account for the beta-globulinaemia, of which IgG(T) is a major component, in S vulgaris infected horses.

We conclude that whereas the priming of Th1 responses soon after exposure to schistosome larvae is completely CD40/CD154 dependent, IL-4, IL-5, and IL-13 are independent of CD154, suggesting a dichotomy in the specific mechanisms that induce these cytokines by CD4+ cells in the sdLN.

It has been advanced that larva-induced host muscle fibre changes may be regulated at muscle gene transcription level whilst host regulatory pathways governed by cell cycle phase may also contribute to larval development.

However, in postmitotic larval cells, none of these factors individually were required for telomere anchoring, which suggests that additional mechanisms anchor in late development.

These data are consistent with the hypothesis that the inability to control L3 larval colonization, adult worm infection and egg production is due to the activation of the inflammatory Th17 T cell subset.