scholarly journals Temporal variation in an immune response gene (MHC I) in anadromous Salmo trutta in an Irish river before and during aquaculture activities

2006 ◽  
Vol 63 (7) ◽  
pp. 1248-1255 ◽  
Author(s):  
James Coughlan ◽  
Philip McGinnity ◽  
Brian O'Farrell ◽  
Eileen Dillane ◽  
Ola Diserud ◽  
...  

Abstract Several studies have documented the genetic effects of intraspecific hybridization of cultured and wild Atlantic salmon (Salmo salar L.). However, the effect of salmon aquaculture on wild congeners is not so well understood. Diseases, introduced or increased in incidence by salmon aquaculture activities, may have an impact on co-occurring wild sea trout (Salmo trutta L.), as implied by the steep decline in sea trout numbers in many Irish, Scottish, and Norwegian rivers since the late 1980s, which may be linked to sea lice infestations associated with marine salmonid farming. Our data suggest that salmon farming and ocean ranching can indirectly affect, most likely mediated by disease, the genetics of cohabiting sea trout by reducing variability at major histocompatibility class I genes. We studied samples of DNA extracted from scales of sea trout in the Burrishoole River, in the west of Ireland, before and at intervals during aquaculture activities. In these samples, allelic variation at a microsatellite marker, tightly linked to a locus critical to immune response (Satr-UBA), was compared with variation at six neutral microsatellite loci. A significant decline in allelic richness and gene diversity at the Satr-UBA marker locus, observed since aquaculture started and which may indicate a selective response, was not reflected by similar reductions at neutral loci. Subsequent recovery of variability at the Satr-UBA marker, seen among later samples, may reflect an increased contribution by resident brown trout to the remaining sea trout stock.

1994 ◽  
Vol 29 (3) ◽  
pp. 37-41 ◽  
Author(s):  
W. G. Cazemier

In the past, the anadromous salmonids, Atlantic salmon (Salmo salar) and sea-trout (Salmo trutta), have formed natural populations in the river Rhine. From the beginning of the nineteenth century onwards, the greater part of the drainage area of the river has been gradually altered from a more or less rural and agricultural area, into a highly industrialised one with subsequent industrialisation, river-engineering and heavy pollution. These developments are considered to be the major cause for the disappearance of the populations of anadromous salmonid fish in the 1950s. The water quality has recovered significantly during the past 25 years. From about 1975 onwards, this process gave rise to a recovery of the anadromous trout population. Results of recent studies of the sea-trout migration pattern are presented. They reveal that nowadays these salmonids can complete their up- and downstream migrations from the North Sea to places, situated at hundreds of kilometres upward the river and vica versa. The numbers of recorded Atlantic salmon and catch locations in inland waters are presented. They show a significant increase since 1989. These phenomena can be understood as promising signs of the recovery of the Rhine aquatic ecosystem.


Nutrients ◽  
2021 ◽  
Vol 13 (2) ◽  
pp. 328 ◽  
Author(s):  
Claudio Salaris ◽  
Melania Scarpa ◽  
Marina Elli ◽  
Alice Bertolini ◽  
Simone Guglielmetti ◽  
...  

SARS-CoV-2 is a newly emerging virus that currently lacks curative treatments. Lactoferrin (LF) is a naturally occurring non-toxic glycoprotein with broad-spectrum antiviral, immunomodulatory and anti-inflammatory effects. In this study, we assessed the potential of LF in the prevention of SARS-CoV-2 infection in vitro. Antiviral immune response gene expression was analyzed by qRT-PCR in uninfected Caco-2 intestinal epithelial cells treated with LF. An infection assay for SARS-CoV-2 was performed in Caco-2 cells treated or not with LF. SARS-CoV-2 titer was determined by qRT-PCR, plaque assay and immunostaining. Inflammatory and anti-inflammatory cytokine production was determined by qRT-PCR. LF significantly induced the expression of IFNA1, IFNB1, TLR3, TLR7, IRF3, IRF7 and MAVS genes. Furthermore, LF partially inhibited SARS-CoV-2 infection and replication in Caco-2 intestinal epithelial cells. Our in vitro data support LF as an immune modulator of the antiviral immune response with moderate effects against SARS-CoV-2 infection.


2021 ◽  
Vol 83 (1) ◽  
Author(s):  
Christian John Hurry ◽  
Alexander Mozeika ◽  
Alessia Annibale

AbstractDescribing the anti-tumour immune response as a series of cellular kinetic reactions from known immunological mechanisms, we create a mathematical model that shows the CD4$$^{+}$$ + /CD8$$^{+}$$ + T-cell ratio, T-cell infiltration and the expression of MHC-I to be interacting factors in tumour elimination. Methods from dynamical systems theory and non-equilibrium statistical mechanics are used to model the T-cell dependent anti-tumour immune response. Our model predicts a critical level of MHC-I expression which determines whether or not the tumour escapes the immune response. This critical level of MHC-I depends on the helper/cytotoxic T-cell ratio. However, our model also suggests that the immune system is robust against small changes in this ratio. We also find that T-cell infiltration and the specificity of the intra-tumour TCR repertoire will affect the critical MHC-I expression. Our work suggests that the functional form of the time evolution of MHC-I expression may explain the qualitative behaviour of tumour growth seen in patients.


2020 ◽  
Vol 8 (Suppl 3) ◽  
pp. A145-A145
Author(s):  
Stefano Pierini ◽  
Rashid Gabbasov ◽  
Linara Gabitova ◽  
Yumi Ohtani ◽  
Michael Klichinsky

BackgroundDespite the remarkable efficacy achieved by CAR-T therapy in hematologic malignancies, application in solid tumors has been challenging. We previously developed human CAR-M and demonstrated that adoptive cell transfer of CAR-M into xenograft models of human cancer controls tumor progression and improves overall survival [1]. Given that CAR-M are professional antigen presenting cells, we developed an immunocompetent animal model to evaluate the potential for induction of a systemic anti-tumor immune response.MethodsMurine bone marrow-derived macrophages were engineered to express an anti-HER2 CAR using the chimeric adenoviral vector Ad5f35. CAR-M were phenotypically and functionally evaluated in vitro and in syngeneic models. To evaluate CAR-M efficacy in an immunocompetent animal model, BALB/c mice were engrafted with CT26-HER2+ tumors (single-tumor model) and were treated with intratumoral CAR-HER2 or untransduced (UTD) macrophages. To evaluate epitope spreading, we simultaneously engrafted BALB/c mice with CT26-HER2+ and CT26-Wt tumors on opposite flanks (dual-tumor model), and treated mice with CAR-M or controls into the CT26-HER2+ tumor only. Peripheral and tumor-infiltrating immune cells were phenotypically and functionally characterized.ResultsIn addition to efficient gene delivery, Ad5f35 transduction promoted a pro-inflammatory (M1) phenotype in murine macrophages. CAR-M, but not control UTD macrophages, phagocytosed HER2+ target cancer cells. Anti-HER2 CAR-M eradicated HER2+ murine CT26 colorectal and human AU-565 breast cancer cells in a dose-dependent manner. CAR-M increased MHC-I and MHC-II expression on tumor cells and promoted tumor-associated antigen presentation and T cell activation. In vivo, CAR-M treatment led to tumor regression and improved overall survival in the CT26-HER2+ single-tumor model. In the dual-tumor model, CAR-M treatment cleared 75% of CT26-HER2+ tumors and inhibited the growth rate of contralateral CT26-WT tumors, demonstrating an abscopal effect. CAR-M treatment led to increased infiltration of intratumoral CD4+ and CD8+ T, NK, and dendritic cells – as well as an increase in T cell responsiveness to the CT26 MHC-I antigen gp70, indicating enhanced epitope spreading. Given the impact CAR-M had on endogenous T-cell immunity, we evaluated the combination of CAR-M and anti-PD1 in the CT26-HER2 model and found that the combination further enhanced tumor control and overall survival.ConclusionsThese results demonstrate that CAR-M therapy induces epitope spreading via activation of endogenous T cells, orchestrating a systemic immune response against solid tumors. Moreover, our findings provide rationale for the combination of CAR-M with immune checkpoint inhibitors. The anti-HER2 CAR-M CT-0508 will be evaluated in an upcoming Phase I clinical trial.ReferenceKlichinsky M, Ruella M, Shestova O, et al. Human chimeric antigen receptor macrophages for cancer immunotherapy. Nat Biotechnol 2020;38(8):947–953.


2003 ◽  
Vol 77 (2) ◽  
pp. 99-109 ◽  
Author(s):  
J.M. Behnke ◽  
F. Iraqi ◽  
D. Menge ◽  
R.L. Baker ◽  
J. Gibson ◽  
...  

AbstractThe host-protective immune response to infection with gastrointestinal (GI) nematodes involves a range of interacting processes that begin with recognition of the parasite's antigens and culminate in an inflammatory reaction in the intestinal mucosa. Precisely which immune effectors are responsible for the loss of specific worms is still not known although many candidate effectors have been proposed. However, it is now clear that many different genes regulate the response and that differences between hosts (fast or strong versus slow or weak responses) can be explained by allelic variation in crucial genes associated with the gene cascade that accompanies the immune response and/or genes encoding constitutively expressed receptor/signalling molecules. Major histocompatibility complex (MHC) genes have been recognized for some time as decisive in controlling immunity, and evidence that non-MHC genes are equally, if not more important in this respect has also been available for two decades. Nevertheless, whilst the former have been mapped in mice, only two candidate loci have been proposed for non-MHC genes and relatively little is known about their roles. Now, with the availability of microsatellite markers, it is possible to exploit linkage mapping techniques to identify quantitative trait loci (QTL) responsible for resistance to GI nematodes. Four QTL for resistance to Heligmosomoides polygyrus, and additional QTL affecting faecal egg production by the worms and the accompanying immune responses, have been identified. Fine mapping and eventually the identification of the genes (and their alleles) underlying QTL for resistance/susceptibility will permit informed searches for homologues in domestic animals, and human beings, through comparative genomic maps. This information in turn will facilitate targeted breeding to improve resistance in domestic animals and, in human beings, focused application of treatment and control strategies for GI nematodes.


Nature ◽  
1982 ◽  
Vol 295 (5847) ◽  
pp. 329-331 ◽  
Author(s):  
Leonore A. Herzenberg ◽  
Takeshi Tokuhisa ◽  
Kyoko Hayakawa ◽  
Leonard A. Herzenberg

2014 ◽  
Vol 54 (7) ◽  
pp. 476-484 ◽  
Author(s):  
D. S. Pavlov ◽  
E. D. Pavlov ◽  
E. V. Ganzha ◽  
V. V. Kostin ◽  
V. Yu. Ponomareva

Sign in / Sign up

Export Citation Format

Share Document