Capsulated cells of Aeromonas salmonicida grown in vitro have different functional properties than capsulated cells grown in vivo

1995 ◽  
Vol 41 (10) ◽  
pp. 941-945 ◽  
Author(s):  
Rafael A. Garduño ◽  
William W. Kay

When grown in vivo in the peritoneal cavity of rainbow trout, Aeromonas salmonicida produces a clearly defined capsule with virulence-related functions. Aeromonas salmonicida grown in vitro in a glucose-rich medium (GRM) has also been reported to produce capsular material. Because in vitro mimicry of in vivo induced traits is highly desirable in vaccine design, the extent to which growth in GRM mimicked in vivo growth was examined. Antibodies specific to in vivo grown cells partially labeled the surface of GRM-grown cells, as well as two distinct proteins (81 700 and 41 000 Mr) in immunoblots of mutants with S-layer or lipopolysaccharide defects. GRM-grown strains showed an increased sensitivity to trout serum in contradistinction to the complete serum resistance of in vivo grown cells; as well, GRM-grown cells were more adherent to trout macrophages. Thus in spite of possessing some surface antigens normally expressed in vivo, cells grown on solid GRM did not possess all functional properties of in vivo grown cells.Key words: Aeromonas salmonicida, bacterial capsules, mimicry of in vivo conditions, furunculosis vaccines.

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Siamak Salehi ◽  
Oliver D. Tavabie ◽  
Augusto Villanueva ◽  
Julie Watson ◽  
David Darling ◽  
...  

AbstractRegulated cell proliferation is an effector mechanism of regeneration, whilst dysregulated cell proliferation is a feature of cancer. We have previously identified microRNA (miRNA) that regulate successful and failed human liver regeneration. We hypothesized that these regulators may directly modify tumor behavior. Here we show that inhibition of miRNAs -503 and -23a, alone or in combination, enhances tumor proliferation in hepatocyte and non-hepatocyte derived cancers in vitro, driving more aggressive tumor behavior in vivo. Inhibition of miRNA-152 caused induction of DNMT1, site-specific methylation with associated changes in gene expression and in vitro and in vivo growth inhibition. Enforced changes in expression of two miRNA recapitulating changes observed in failed regeneration led to complete growth inhibition of multi-lineage cancers in vivo. Our results indicate that regulation of regeneration and tumor aggressiveness are concordant and that miRNA-based inhibitors of regeneration may constitute a novel treatment strategy for human cancers.


2010 ◽  
Vol 111 (4) ◽  
pp. 899-910 ◽  
Author(s):  
Vincent Kam Wai Wong ◽  
Simon Shiu Fai Cheung ◽  
Ting Li ◽  
Zhi-Hong Jiang ◽  
Jing-Rong Wang ◽  
...  

1979 ◽  
Vol 149 (3) ◽  
pp. 745-757 ◽  
Author(s):  
K J Weinhold ◽  
D A Miller ◽  
E F Wheelock

The tumor dormant state established in L5178Y immunized and challenged mice is characterized by a prolonged period of clinical normalcy followed by rapid tumor outgrowth. The tumor cells which emerged after termination of the tumor dormant state had abnormal marker chromosomes identical to those in the L5178Y cells used in the original challenge inoculum, indicating that the emergent tumor cells were progeny of the challenge inoculum. Original and emergent L5178Y cells had equivalent in vivo growth rates, when inoculated into normal DBA/2 mice. The emergent L5178Y cells were less susceptible than original cells to in vitro lysis by tumor dormant PC. Original and emergent L5178Y cells expressed common tumor-associated target antigens for cytolytic effector cells. Both modulation and masking of these target antigens were ruled out as mechanisms for decreased susceptibility to cell-mediated cytolysis. Immunofluorescence revealed heterogeneity in tumor-associated antigen expression within both original and emergent cell populations, with a decreased intensity of staining in the emergent population. Both populations were equally susceptible to lysis by alloimmune cells, alloantiserum, and anti-Thy 1.2 serum, but emergent cells were less susceptible to lysis by serum directed against L5178Y TAA. Quantitative absorption revealed that the emergent L5178Y cells expressed eightfold less serologically detectable TAA than the original cells. These findings indicate that the host immune response developing during establishment of the tumor dormant state selects a stable tumor cell subpopulation which expresses decreased amounts of surface tumor-associated target antigens.


2006 ◽  
Vol 80 (23) ◽  
pp. 11651-11657 ◽  
Author(s):  
Xiaodong Zhao ◽  
Enmei Liu ◽  
Fu-Ping Chen ◽  
Wayne M. Sullender

ABSTRACT Respiratory syncytial virus (RSV) is the only infectious disease for which a monoclonal antibody (MAb) is used in humans. Palivizumab (PZ) is a humanized murine MAb to the F protein of RSV. PZ-resistant viruses appear after in vitro and in vivo growth of RSV in the presence of PZ. Fitness for replication could be a determinant of the likelihood of dissemination of resistant viruses. We assessed the fitness of two PZ-resistant viruses (F212 and MP4). F212 grew less well in cell culture than the parent A2 virus and was predicted to be less fit than A2. Equal amounts of F212 and A2 were mixed and passaged in cell culture. F212 disappeared from the viral population, indicating it was less fit than the A2 virus. The MP4 virus grew as well as A2 in culture and in cotton rats. A2/MP4 virus input ratios of 1:1, 10:1, 100:1, and 1,000:1 were compared in competitive replication. For all input ratios except 1,000:1, the MP4 virus became dominant, supplanting the A2 virus. The MP4 virus also dominated the A2 virus during growth in cotton rats. Thus, the mutant MP4 virus was more fit than A2 virus in both in vitro and in vivo competitive replication. Whether this fitness difference was due to the identified nucleotide substitutions in the F gene or to mutations elsewhere in the genome is unknown. Understanding the mechanisms by which mutant virus fitness increased or decreased could prove useful for consideration in attenuated vaccine design efforts.


2002 ◽  
Vol 13 (5) ◽  
pp. 533-543 ◽  
Author(s):  
Jane-Jen Wang ◽  
Yaw-Terng Chern ◽  
Yuh-Fang Chang ◽  
Tsung-Yun Liu ◽  
Chin-Wen Chi

Nutrients ◽  
2018 ◽  
Vol 10 (12) ◽  
pp. 1973 ◽  
Author(s):  
Bhagavathi Sivamaruthi ◽  
Periyanaina Kesika ◽  
Mani Prasanth ◽  
Chaiyavat Chaiyasut

In general, fermented foods (FFs) are considered as functional foods. Since the awareness about the health benefits of FFs has increased, the consumption of FF also improved significantly in recent decades. Diabetes is one of the leading threats of the health span of an individual. The present manuscript details the general methods of the production of FFs, and the results of various studies (in vitro, in vivo, and clinical studies) on the antidiabetic properties of FFs. The fermentation method and the active microbes involved in the process play a crucial role in the functional properties of FFs. Several in vitro and in vivo studies have been reported on the health-promoting properties of FFs, such as anti-inflammation, anticancer, antioxidant properties, improved cognitive function and gastrointestinal health, and the reduced presence of metabolic disorders. The studies on the functional properties of FFs by randomized controlled clinical trials using human volunteers are very limited for several reasons, including ethical reasons, safety concerns, approval from the government, etc. Several scientific teams are working on the development of complementary and alternative medicines to improve the treatment strategies for hyperglycemia.


Blood ◽  
2020 ◽  
Author(s):  
Ahmed Aburima ◽  
Martin Berger ◽  
Benjamin EJ Spurgeon ◽  
Beth A Webb ◽  
Katie S Wraith ◽  
...  

Thrombospondin-1 (TSP-1) is released by platelets upon activation and can promote platelet activation, but its role in haemostasis in vivo is unclear. We show that TSP-1 is a critical mediator of haemostasis that promotes platelet activation by modulating inhibitory cAMP signaling. Genetic deletion of TSP-1 did not affect platelet activation in vitro, but in vivo models of haemostasis and thrombosis demonstrated that TSP-1 deficient mice had prolonged bleeding, defective thrombosis and increased sensitivity to the prostacyclin mimetic iloprost. Adoptive transfer of wild type (WT), but not TSP-1-/- platelets, ameliorated the thrombotic phenotype, suggesting a key role for platelet-derived TSP-1. In functional assays, TSP-1-deficient platelets showed an increased sensitivity to cAMP signaling, inhibition of platelet aggregation and arrest under flow by PGI2. Plasma swap experiments showed that plasma TSP-1 did not correct PGI2 hypersensitivity in TSP-1-/- platelets. By contrast, incubation of TSP-1-/- platelets with releasates from WT platelets or purified TSP-1, but not releasates from TSP-1-/- platelets, reduced the inhibitory effects of PGI2. Activation of WT platelets resulted in diminished cAMP accumulation and downstream signaling, which was associated with increased activity of the cAMP hydrolyzing enzyme phosphodiesterase 3A (PDE3A). PDE3A activity and cAMP accumulation were unaffected in platelets from TSP-1-/- mice. Platelets deficient in CD36, a TSP-1 receptor, showed increased sensitivity to PGI2/cAMP signaling and diminished PDE3A activity, which was unaffected by platelet-derived or purified TSP-1. This suggests that the release of TSP-1 regulates haemostasis in vivo through modulation of platelet cAMP signaling at sites of vascular injury.


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