Avian pathogenic
E. coli
(APEC) is the etiologic agent of avian colibacillosis, the most common disease responsible for chicken morbidity in the world. Although multiple virulence-associated factors ...were identified, their prevalence in Algeria is still poorly known. In the present research, 92 avian pathogenic
E. coli
(APEC) isolates were recovered from broilers with clinical signs and lesions of colibacillosis. In addition, 32
E. coli
isolates collected from feces of healthy birds (AFEC) were included for comparison. All isolates were investigated by PCR for the presence of a total of 11 virulence-associated genes described for avian pathogenic (
iroN
,
ompT
,
hlyF
,
iss
,
iutA
, and
fimC
) and diarrheagenic
E. coli
(
eae
,
stx
,
elt
/
est
,
ipaH
, and
aggR
). The sensitivity of 39 APEC isolates to 16 antibiotics was also determined using antimicrobial pretreated microplates. Here, we report that 98% of the examined isolates host at least one of the tested virulence factors. The most prevalent genes in APEC were
iutA
(90.6%),
ompT
(86.9%), and
iss
(85.8%); whereas,
iutA
(78.1%),
fimC
(78.1%), and
iroN
(68.7%) were the highest prevalent genes in AFEC. Our data showed that none of the AFEC isolates harbor any of the tested diarrheagenic genes. Moreover, only
elt
/
est
(5.4%),
stx
(2.1%), and
ipaH
(2.1%) genes were carried by APEC isolates. We further established that ceftazodime, ceftiofur, mequindox, amoxicillin/clavulanic acid, and meropenem were the most efficient antibiotics against the analyzed APEC isolates. Overall, our findings provide more insights about APEC and AFEC virulence potential in Algeria which could participate in the fight against colibacillosis.
Cigarette smoke is one of the main factors in Chronic Obstructive Pulmonary Disease (COPD), a respiratory syndrome marked by persistent respiratory symptoms and increasing airway obstruction. ...Perturbed NAD+/NADH levels may play a role in various diseases, including lung disorders like COPD. In our study, we investigated the preventive effect of NADH supplementation in an experimental model of COPD induced by cigarette smoke extract (CSE). N = 64 mice randomly distributed in eight groups were injected with NADH (two doses of 100 mg/kg or 200 mg/kg) or dexamethasone (2 mg/kg) before being exposed to CSE for up to 9 weeks. Additionally, NADH supplementation preserved lung antioxidant defenses by preventing the functional loss of key enzymes such as superoxide dismutase (SOD), glutathione peroxidase (GPX), catalase, and the expression levels of glutathione (GSH) (
= 4,
< 0.001). It also reduced oxidative damage markers, such as malondialdehyde (MDA) and nitrites (
= 4,
< 0.001). A marked increase in tissue myeloperoxidase activity was assessed (MPO), confirming neutrophils implication in the inflammatory process. The latter was significantly ameliorated in the NADH-treated groups (
< 0.001). Finally, NADH prevented the CSE-induced secretion of cytokines such as Tumor Necrosis Factor alpha (TNF-α), IL-17, and IFN-y (
= 4,
< 0.001). Our study shows, for the first time, the clinical potential of NADH supplementation in preventing key features of COPD via its unique anti-inflammatory and antioxidant properties.
We recently used a murine model of allergic airway inflammation to show that poly(ADP-ribose) polymerase-1 (PARP-1) plays an important role in the pathogenesis of asthma-related lung inflammation. In ...this study, we show that PARP-1 inhibition, by a novel inhibitor (TIQ-A) or by gene deletion, prevented eosinophilic infiltration into the airways of OVA-challenged mice. Such impairment of eosinophil recruitment appeared to take place after IgE production. OVA challenge of wild-type mice resulted in a significant increase in IL-4, IL-5, IL-10, IL-13, and GM-CSF secretions. Although IL-4 production was moderately affected in OVA-challenged PARP-1(-/-) mice, the production of IL-5, IL-10, IL-13, and GM-CSF was completely inhibited in ex vivo OVA-challenged lung cells derived from these animals. A single TIQ-A injection before OVA challenge in wild-type mice mimicked the latter effects. The marked effect PARP-1 inhibition exerted on mucus production corroborated the effects observed on the Th2 response. Although PARP-1 inhibition by gene knockout increased the production of the Th1 cytokines IL-2 and IL-12, the inhibition by TIQ-A exerted no effect on these two cytokines. The failure of lung cells derived from OVA-challenged PARP-1(-/-) mice to synthesize GM-CSF, a key cytokine in eosinophil recruitment, was reestablished by replenishment of IL-5. Furthermore, intranasal administration of IL-5 restored the impairment of eosinophil recruitment and mucus production in OVA-challenged PARP-1(-/-) mice. The replenishment of either IL-4 or IgE, however, did not result in such phenotype reversals. Altogether, these results suggest that PARP-1 plays a critical role in eosinophil recruitment by specifically regulating the cascade leading to IL-5 production.
The aim of this study was to prepare microcapsules based on a natural polymer chitosan solution (high degree of deacetylation (DDA), low molecular weight (
MW
), and low viscosity)/sodium alginate in ...the presence of a crosslinking agent (glutaraldehyde), in order to encapsulate and vectorise the active principle towards the diseased organ (colon), without being diffused into other levels of the digestive tract, to increase the therapeutic effectiveness of treatment by chemotherapy and to reduce undesirable effects. The method of preparation of the microcapsules obtained from the sodium alginate/chitosan solution/active ingredients system was examined by conventional optical microscopy. In addition, an
in vitro
study was carried out on the active ingredients’ release profiles, depending on the pH simulating the gastric and intestinal media for the seven systems proposed. It should be mentioned that, in the basic medium (pH(colon) = 8), the release of the active ingredients is of the utmost importance. Nevertheless, control of this release can be improved by a crosslinking agent and the coating method. The dry sodium alginate / chitosan solution / active ingredients + crosslinking 2 % formulation coated with non-crosslinked chitosan (Formulation 7) is the standard formula that meets all the criteria from our earlier work, with a core release rate of 67 %. The PSD was unimodal, with sizes ranging from 750 µm to 900 µm.
Cilj ove studije bio je pripremiti mikrokapsule na bazi prirodne polimerne otopine kitozana (visokog stupnja deacetiliranja (DDA), niske molekulske mase (
MW
) i niske viskoznosti)/natrijeva alginata u prisutnosti umreženog agensa (glutaraldehida), za inkapsuliranje i vektoriziranje aktivnog sastojka prema bolesnom organu (debelom crijevu), bez difuzije u druge razine probavnog trakta, kako bi se povećala terapijska učinkovitost liječenja kemoterapijom i smanjili neželjeni učinci. Metoda pripreme mikrokapsula dobivenih iz sustava natrijeva alginata/otopine kitozana/aktivnih sastojaka ispitana je uobičajenom optičkom mikroskopijom. Uz to, provedeno je istraživanje
in vitro
na profilima oslobađanja aktivnih sastojaka, ovisno o pH koji simulira želučani i crijevni medij za sedam predloženih sustava. Treba napomenuti da je u osnovnom mediju (pH(debelog crijeva) = 8) oslobađanje aktivnih sastojaka od najveće važnosti. Ipak, kontrola tog ispuštanja može se poboljšati sredstvom za umrežavanje i metodom premazivanja. Suha formulacija otopina natrijeva alginata/kitozana/aktivnih sastojaka + umreženog 2 % presvučena neumreženim kitozanom (formulacija 7) standardna je formula koja udovoljava svim kriterijima iz našeg ranijeg rada s brzinom otpuštanja jezgre od 67 %. PSD je bio unimodalan s veličinama koje su se kretale od 750 µm do 900 µm.
...there is an urgent need for a sound framework for R&D towards developing novel and effective vaccines for human and animal diseases. Furthermore, it will collaborate with experts from the World ...Health Organisation (WHO), the Office International des Epizooties (OIE), the African Union Centre for Disease Control (AU CDC), the African Field Epidemiology Network (AFENET), the Global Alliance for Vaccine and Immunisation (GAVI) and the Global Alliance for Livestock Vaccine and Medicine (GALVmed) to take advantage of the resources available in these regional and international organisations. Membership of AfVANET is free and we can be followed on Twitter @AAfvanet and Facebook. 1 Faculty of Veterinary Science, University of Pretoria, Pretoria, South Africa, 2 National Veterinary Research Institute, Vom, Plateau, Nigeria, 3 Department of Zoology, University of Ibadan, Ibadan, Nigeria, 4 College of Veterinary Medicine and Agriculture, Addis Ababa University, Addis Ababa, Ethiopia, 5 Biotechnology Unit, University of Buea, Buea, Cameroon, 6 Faculty of Veterinary Medicine, Department of Veterinary Medicine, University of Abuja, Abuja, Nigeria, 7 Department of Biomedical Sciences, University of Health and Allied Sciences, Ho, Ghana, 8 ARC-Onderstepoort Veterinary Research, Pretoria, South Africa, 9 School of Medical Laboratory Science, Institute of Health, Jimma University, Jimma, Ethiopia, 10 International Livestock Research Institute, Nairobi, Kenya, 11 University Cheikh Anta Diop and Pasteur Institute, Dakar, Senegal, 12 Faculty of Sciences, University of Médéa, Médéa, Algeria
We previously showed that DNA fragmentation factor, which comprises a caspase-3-activated DNase (CAD) and its inhibitor (ICAD), may influence the rate of cell death by generating PARP-1-activating ...DNA breaks. Here we tested the hypothesis that ICAD-deficient colon epithelial cells exhibiting resistance to death stimuli may accumulate additional genetic modifications, leading to a tumorigenic phenotype. We show that ICAD deficiency may be associated with colon malignancy in humans. Indeed, an examination of ICAD expression using immunohistochemistry in an array of both colon cancer and normal tissues revealed that ICAD expression levels were severely compromised in the cancerous tissues. Upon DNA damage caused by a low dose of irradiation, ICAD cells acquire a tumorigenic phenotype. Colon epithelial cells derived from ICAD mice showed a significant resistance to death induced by the colon carcinogen dimethylhydrazine in vitro and in mice. Such resistance was associated with a decrease in PARP-1 activation. In an animal model of dimethylhydrazine-induced colon tumorigenesis, ICAD(-/-) mice developed significantly higher numbers of tumors with markedly larger sizes than the wild-type counterparts. Interestingly, the phenotype of the ICAD(-/-) mice was not associated with a significant increase in the precancerous aberrant crypt foci suggesting a potential link to tumor progression rather than initiation. More importantly, ICAD deficiency was associated with severe genomic instability as assessed by array comparative genomic hybridization. Such genomic instability consisted most prominently of amplifications but with sizable deletions as compared to the wild-type counterparts affecting several cancer-related genes including RAF-1, GSN, LMO3, and Fzd6 independently of p53. Altogether, our results present a viable case for the involvement of ICAD deficiency in colon carcinogenesis and show that apoptosis and genomic instability may comprise the means by which such deficiency may contribute to the process of increasing susceptibility to carcinogen-induced tumorigenesis.
Seafood rapidly deteriorates; storage by cooling in ice is a common technique for prolonging its freshness and quality. The current study compared the shelf life and quality of ice-preserved European ...sea bass (Dicentrarchus labrax) sourced from two different intensive fish farming systems: terrestrial ponds using heated water from a power plant and floating cages in the open sea. Using sensory analysis, the fish cultured in the heated water ponds were rejected as unacceptable for consumption after 13 days, while the fish reared in the floating cages were rejected after 15 days. Total viable counts of aerobic bacteria, pH, total volatile basic nitrogen and trimethylamine levels were consistently higher in the fish cultured in heated water ponds. Chemical, bacteriological and organoleptic acceptability demonstrated that fish rearing conditions were important for storage and needs to be taken into consideration for fish management and processing.
•Fish quality during preservation depends on the fish farming conditions.•European sea bass reared at high temperatures showed a shorter shelf-life.•Fish reared in sea cages showed longer shelf-life and better quality.
Diabetes mellitus is a chronic metabolic disease characterized by persistent hyperglycemia, revealing a decrease in insulin efficiency. The sustained glucotoxic pancreatic microenvironment increases ...reactive oxygen species generation, resulting in chronic oxidative stress responsible for massive DNA damage. This triggers PARP-1 activation with both NAD
+
and ATP depletion, affecting drastically pancreatic beta cells’ energy storage and leading to their dysfunction and death. The aim of the present study is to highlight the main histological changes observed in pancreatic islets pre-treated with a unique NADH intraperitoneal injection in a streptozotocin-(STZ)-induced diabetes model. In order to adjust NADH doses, a preliminary study with three different doses, 500 mg/kg, 300 mg/kg, and 150 mg/kg, respectively, was conducted. Subsequently, and on the basis of the results of the aforementioned study, Wistar rats were randomly divided into four groups: non-diabetic control group, diabetics (STZ 45 mg/kg), NADH-treated group (150 mg/kg) 15 min before STZ administration, and NADH-treated group (150 mg/kg) 15 min after STZ administration. The effect of NADH was assessed by blood glucose level, TUNEL staining, histo-morphological analysis, and immunohistochemistry. The optimum protective dose of NADH was 150 mg/kg. NADH effectively decreased hyperglycemia and reduced diabetes induced by STZ. Histologically, NADH pre-treatment revealed a decrease in beta cell death favoring apoptosis over necrosis and therefore preventing inflammation with further beta cell destruction. Our data clearly demonstrate that NADH prior or post-treatment could effectively prevent the deleterious loss of beta cell mass in STZ-induced diabetes in rats and preserve the normal pancreatic islet’s function.
Graphical abstract
Middle East Respiratory Syndrome (MERS) is a zoonotic disease. Dromedary camel is responsible of its transmission to humans. Accordingly, several human cases have been reported worldwide with a high ...mortality rate. In Algeria, no data reported on MERS prevalence in camels. This is a first seroprevalence study MERS-CoV in Algerian dromedaries. A total of 87 camel blood samples from EL -MENIAA and Ghardaia, were analyzed by anti-MERS-CoV IgG ELISA camel. The seroprevalence was 64 % and it significantly increases with age. Larger serological and molecular screening is needed to precisely determine the rate of MERS active circulation among Algerian dromedary population.
A functional relationship between the apoptotic endonuclease DNAS1L3 and the chemotherapeutic drug VP-16 was established. The lymphoma cell line, Daudi, exhibited a significant resistance to VP-16 ...treatment in comparison to the lymphoma/leukemia cell line, U-937. While U-937 cells degraded their DNA into internucleosomal fragments, Daudi cells failed to undergo such fragmentation in response to the drug. Activation of both caspase-3 and DNA fragmentation factor was not sufficient to trigger internucleosomal DNA fragmentation in Daudi cells. No correlation was found between expression levels of topoisomerase-II, Pgp, Bcl-2, Bax, or Bad and decreased sensitivity of Daudi cells to VP-16. Daudi cells failed to express DNAS1L3 and ectopic expression of this protein significantly sensitized the cells to VP-16. An enhancement of caspase-3 activity and collapse of mitochondrial membrane potential underlie DNAS1L3-mediated sensitization of Daudi cells to VP-16, which may be a direct result of DNAS1L3-mediated increase in PARP-1-activating DNA breaks after VP-16 treatment. Our results suggest that DNAS1L3 plays an active role in lymphoma cell sensitization to VP-16 and that its deficiency may constitute a novel mechanism of drug resistance in these cells.
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