scholarly journals Acidic chitinase primes the protective immune response to gastrointestinal nematodes

2016 ◽  
Vol 17 (5) ◽  
pp. 538-544 ◽  
Author(s):  
Kevin M Vannella ◽  
Thirumalai R Ramalingam ◽  
Kevin M Hart ◽  
Rafael de Queiroz Prado ◽  
Joshua Sciurba ◽  
...  
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.


2005 ◽  
Vol 195 (1) ◽  
pp. 37-43 ◽  
Author(s):  
Lily P. H. Yang ◽  
Björn K. G. Eriksson ◽  
Zinta Harrington ◽  
Nigel Curtis ◽  
Selwyn Lang ◽  
...  

2015 ◽  
Vol 98 (5) ◽  
pp. 827-836 ◽  
Author(s):  
S. Das ◽  
K. Halder ◽  
A. Goswami ◽  
B. P. Chowdhury ◽  
N. K. Pal ◽  
...  

Author(s):  
Alok Joshi ◽  
R.P. Gupta ◽  
Selvaraj Pavulraj ◽  
Bidhan Chandra Bera ◽  
Taruna Anand ◽  
...  

Background: Equine herpesvirus type 1 (EHV-1) is the most important viral pathogen of equines, causing respiratory illness, abortion, neonatal foal mortality and neurologic disorders. Large numbers of commercial EHV-1 vaccines are available to protect equines from the disease, but they provide only partial protection. Despite immunization with inactivated and modified live virus vaccine, mares show abortions. Present study was aimed to investigate the immunogenicity and protective efficacy of EHV-1 recombinant glycoprotein B (rgB) and gB expressing plasmid DNA against EHV-1 infection in BALB/c mice model.Methods: About 3-4 weeks old 225 female BALB/c mice were selected for the comparative study of immunization followed by challenged with EHV-1/India/Tohana/96-2 strain virus in 5 different groups of 45 animals each.Result: Following immunization, rgB vaccinated mice showed optimal stimulation of EHV-1 gB specific cell mediated and humoral mediated immunity (HMI and CMI). The gB expressing plasmid DNA vaccinated mice developed only CMI while inactivated whole virus vaccinated mice had only HMI. Upon EHV-1 challenge, all infected mice displayed variable levels of clinical signs with changes in body weight, however, vaccinated mice showed very rapid recovery with optimal protection. Positive control group mice showed severe pulmonary lesions along with persistence virus infection till 5 days post challenge (dpc) whereas vaccinated mice had less pulmonary lesion only up to 3dpc. Minimal lung lesions and early virus clearance was observed in the rgB immunized mice in comparison to the gB plasmid DNA and inactivated EHV-1 vaccine immunized mice. It has been concluded that immunization with rgB elicits optimum protective immune response against EHV-1 infection in mice model. The rgB could be a potential vaccine candidate against EHV-1 infection in equine in the future.


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