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Algiers, Algeria

Lafri I.,Blida University | Lafri I.,National Veterinary School of Algiers | Bitam I.,University of Boumerdes | Beneldjouzi A.,Pasteur Institute of Algeria | Ben Mahdi M.H.,National Veterinary School of Algiers
Bulletin de la Societe Zoologique de France | Year: 2014

A survey of immature and adult mosquitoes was conducted in 15 departments with the aims of inventorying the Culicidae and documenting inter-species relationships in different habitats. In total, 3 families, 7 genera and 17 species were collected, including the first report of Culex territans larvae captured at an altitude of 1750 m and the confirmation of the presence of Aedes albopictus (Dengue, Chikungunya and other arboviruses vector) in Algeria and the Maghreb, based on a second capture in this country. Source

Conti F.,French Institute of Health and Medical Research | Conti F.,University of Paris Descartes | Conti F.,University of Rome Tor Vergata | Lugo-Reyes S.O.,French Institute of Health and Medical Research | And 91 more authors.
Journal of Allergy and Clinical Immunology | Year: 2016

Background: Chronic granulomatous disease (CGD) is a rare primary immunodeficiency caused by inborn errors of the phagocyte nicotinamide adenine dinucleotide phosphate oxidase complex. From the first year of life onward, most affected patients display multiple, severe, and recurrent infections caused by bacteria and fungi. Mycobacterial infections have also been reported in some patients. Objective: Our objective was to assess the effect of mycobacterial disease in patients with CGD. Methods: We analyzed retrospectively the clinical features of mycobacterial disease in 71 patients with CGD. Tuberculosis and BCG disease were diagnosed on the basis of microbiological, pathological, and/or clinical criteria. Results: Thirty-one (44%) patients had tuberculosis, and 53 (75%) presented with adverse effects of BCG vaccination; 13 (18%) had both tuberculosis and BCG infections. None of these patients displayed clinical disease caused by environmental mycobacteria, Mycobacterium leprae, or Mycobacterium ulcerans. Most patients (76%) also had other pyogenic and fungal infections, but 24% presented solely with mycobacterial disease. Most patients presented a single localized episode of mycobacterial disease (37%), but recurrence (18%), disseminated disease (27%), and even death (18%) were also observed. One common feature in these patients was an early age at presentation for BCG disease. Mycobacterial disease was the first clinical manifestation of CGD in 60% of these patients. Conclusion: Mycobacterial disease is relatively common in patients with CGD living in countries in which tuberculosis is endemic, BCG vaccine is mandatory, or both. Adverse reactions to BCG and severe forms of tuberculosis should lead to a suspicion of CGD. BCG vaccine is contraindicated in patients with CGD. © 2016 American Academy of Allergy, Asthma & Immunology. Source

Ladjel-Mendil A.,University of Science and Technology Houari Boumediene | Ladjel-Mendil A.,Pasteur Institute of Algeria | Martin-Eauclaire M.-F.,Aix - Marseille University | Laraba-Djebari F.,University of Science and Technology Houari Boumediene | Laraba-Djebari F.,Pasteur Institute of Algeria
NeuroImmunoModulation | Year: 2013

Objective: Kaliotoxin (KTX) is a neurotoxin purified from Androctonus scorpion venom. Purification and pharmacological and immunological characterization of this neurotoxin has been extensively studied, but its biological effects have not. The ability of KTX to induce neuropathophysiological and immuno-inflammatory effects was investigated. Methods: NMRI mice were injected with a sublethal dose of KTX (20 ng/20 g of body weight) or saline solution via the intra-cerebro-ventricular route. Tissue damage and immunological biomarkers such as eosinophil peroxidase (EPO), myeloperoxidase (MPO), and nitric oxide (NO) were analyzed in serum, brain, lung, and heart tissue. Protein levels, LDH, and CPK activities were also determined in serum 24 h after injection. Results: In this study, KTX injection induced severe alterations in the cerebral cortex, myocardium, and pulmonary parenchyma. Tissue damage was correlated with seric increase in creatine kinase and lactate dehydrogenase activities. KTX also induced an immuno-inflammatory response distinguished by cell infiltration characterized by a significant increase in EPO and MPO activities in the brain, heart, and lungs. This infiltration was also associated with an increase in albumin, , β-, and γ-globulin fractions, and NO release. Conclusion: KTX binding to its targets in CNS (Kv1.1 and Kv1.3 channels) may induce severe modifications in the structure and function of various organs associated with the activation of immuno-inflammatory reactions. © 2012 S. Karger AG, Basel. Source

Ait-Lounis A.,University of Science and Technology Houari Boumediene | Ait-Lounis A.,Pasteur Institute of Algeria | Laraba-Djebari F.,University of Science and Technology Houari Boumediene | Laraba-Djebari F.,Pasteur Institute of Algeria
PLoS Neglected Tropical Diseases | Year: 2012

Background: Scorpion venom induces systemic inflammation characterized by an increase in cytokine release and chemokine production. There have been few experimental studies assessing the effects of scorpion venom on adipose tissue function in vivo. Methodology/Principal Findings: To study the adipose tissue inflammation (ATI) induced by Androctonus australis hector (Aah) venom and to assess possible mechanisms of ATI, mice (n = 6, aged 1 month) were injected with Aah (0.45 mg/kg), toxic fraction of Aah (FTox-G50; 0.2 mg/kg) or saline solution (control). Inflammatory responses were evaluated by ELISA and cell sorting analyses in adipose tissue 45 minutes and 24 hours after injection. Quantitative real-time PCR was used to assess the regulation of genes implicated in glucose uptake. The titers of selected inflammatory cytokines (IL-1β, IL-6 and TNF-α) were also determined in sera and in insulin target tissues. The serum concentration of IL-1β rose 45 minutes after envenomation and returned to basal level after 24 hours. The pathophysiological effects of the venom after 24 hours mainly involved M1-proinflammatory macrophage infiltration in adipose tissue combined with high titers of IL-1β, IL-6 and TNF-α. Indeed, TNF-α was strongly induced in both adipose tissue and skeletal muscle. We studied the effects of Aah venom on genes implicated in insulin-stimulated glucose uptake. Insulin induced a significant increase in the expression of the mRNAs for hexokinase 2 and phosphatidylinositol 3-kinase in both skeletal muscle and adipose tissue in control mice; this upregulation was completely abolished after 24 hours in mice envenomed with Aah or FTox-G50. Conclusions/Significance: Our findings suggest that Aah venom induces insulin resistance by mechanisms involving TNF-α-dependent Map4k4 kinase activation in the adipose tissue. © 2012 Ait-Lounis, Laraba-Djebari. Source

Sebia-Amrane F.,University of Science and Technology Houari Boumediene | Sebia-Amrane F.,Pasteur Institute of Algeria | Laraba-Djebari F.,University of Science and Technology Houari Boumediene | Laraba-Djebari F.,Pasteur Institute of Algeria
Inflammation | Year: 2013

The inflammatory response induced by Vipera lebetina venom (VLV) in the mice hind paw was evaluated by paw edema value and vascular permeability changes. The edema was produced in a dose- and time-dependent manner. This response was maximal within 2 h and disappeared after 24 h The minimum edema-forming dose was estimated at 0.8 μg/20 g body weight. Microscopic examination confirmed that VLV also induces skin structure alterations with collagen fiber dissociation and polynuclear infiltration, which is characteristic of edema formation. The induced edema with VLV (1 μg/paw) could be due to the release of pharmacological active substances at the site of injection. Histamine, serotonine, and arachidonate metabolites may play important roles in the vasoactive and edematic effect of VLV since pretreatment of mice with cromoglycate, cyproheptadine, ibuprofen, loratidine, and indomethacin significantly reduced the edema formation (77, 63, 57, 45, and 43 %, respectively). The obtained results demonstrate that the induced edema and vasodilatation by this venom may be triggered and maintained by different pharmacological mechanisms, since cromoglycate and cyproheptadine were the most active inhibitors of the edema. The relationships between histamine and serotonin release from mast cells and arachidonate metabolites activation could be the main step in edema-forming and the induced vasodilatation by the venom. © 2012 Springer Science+Business Media New York. Source

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