Pediatric recurrent respiratory tract infections: when and how to explore the immune system? (About 53 cases)

Recurrent respiratory tract infections are one of the most frequent reasons for pediatric visits and hospitalization. Causes of this pathology are multiple ranging from congenital to acquired and local to general. Immune deficiencies are considered as underlying conditions predisposing to this pathology. Our work is about to determine when and how to explore the immune system when facing recurrent respiratory infections. This was based on the records of 53 children hospitalized at the pediatrics unit of Hassan II University Hospital, Fez Morocco. Thirty boys and 23 girls with age ranging from 5 months to 12 years with an average age of 2 years were involved in this study. Bronchial foreign body was the main etiology in children of 3 to 6 year old. Gastro-esophageal reflux, which in some cases is a consequence of chronic cough, as well as asthma were most frequent in infants (17 and 15% respectively). Immune deficiency was described in 7.5% of patients and the only death we deplored in our series belongs to this group. Recurrent respiratory tract infections have multiple causes. In our series they are dominated by foreign body inhalation and gastroesophageal reflux, which in some cases is a consequence of a chronic cough. Immune deficiency is not frequent but could influence the prognosis. Therefore immune explorations should be well codified.Pan African Medical Journal 2016; 2

Single Polarization Transmission on Polished Panda- Type Polarization Maintaining Optical Fiber

High polarization dependent loss on polished Polarization Maintaining Panda-type-fiber is reported. We report on these observations and on the analysis of such a phenomena. We believe that the polarization dependent loss is due to the energy transfer of the fundamental mode to higher order modes of the polished fiber part. Depending on the polarization, beating between these modes induces a polarization dependence on the transmission. As an application, we have been able to show experimentally and theoretically extinction ratio of 30 dB with 1 dB of excess loss for the transmitted polarization over 1 cm of polished panda-type fiber

The Arab world's contribution to solid waste literature: a bibliometric analysis

BACKGROUND: Environmental and health-related effects of solid waste material are considered worldwide problems. The aim of this study was to assess the volume and impact of Arab scientific output published in journals indexed in the Science Citation Index (SCI) on solid waste. METHODS: We included all the documents within the SCI whose topic was solid waste from all previous years up to 31 December 2012. In this bibliometric analysis we sought to evaluate research that originated from Arab countries in the field of solid waste, as well as its relative growth rate, collaborative measures, productivity at the institutional level, and the most prolific journals. RESULTS: A total of 382 (2.35 % of the overall global research output in the field of solid waste) documents were retrieved from the Arab countries. The annual number of documents published in the past three decades (1982–2012) indicated that research productivity demonstrated a noticeable rise during the last decade. The highest number of articles associated with solid waste was that of Egypt (22.8 %), followed by Tunisia (19.6), and Jordan (13.4 %). the total number of citations over the analysed years at the date of data collection was 4,097, with an average of 10.7 citations per document. The h-index of the citing articles was 31. Environmental science was the most researched topic, represented by 175 (45.8 %) articles. Waste Management was the top active journal. The study recognized 139 (36.4 %) documents from collaborations with 25 non-Arab countries. Arab authors mainly collaborated with countries in Europe (22.5 %), especially France, followed by countries in the Americas (9.4 %), especially the USA. The most productive institution was the American University of Beirut, Lebanon, with 6.3 % of total publications. CONCLUSIONS: Despite the expected increase in solid waste production from Arab world, research activity about solid waste is still low. Governments must invest more in solid waste research to avoid future unexpected problems. Finally, since solid waste is a multidisciplinary science, research teams in engineering, health, toxicology, environment, geology and others must be formulated to produce research in solid waste from different scientific aspects

Anthrax Edema Toxin Modulates PKA- and CREB-Dependent Signaling in Two Phases

Background: Anthrax edema toxin (EdTx) is an adenylate cyclase which operates in the perinuclear region of host cells. However, the action of EdTx is poorly understood, especially at molecular level. The ability of EdTx to modulate cAMPdependent signaling was studied in Jurkat T cells and was compared with that of other cAMP-rising agents: Bordetella pertussis adenylate cyclase toxin, cholera toxin and forskolin. Methodology/Principal Findings: EdTx caused a prolonged increase of the intracellular cAMP concentration. This led to nuclear translocation of the cAMP-dependent protein kinase (PKA) catalytic subunit, phosphorylation of cAMP response element binding protein (CREB) and expression of a reporter gene under control of the cAMP response element. Neither p90 ribosomal S6 kinase nor mitogen- and stress-activated kinase, which mediate CREB phosphorylation during T cell activation, were involved. The duration of phospho-CREB binding to chromatin correlated with the spatio-temporal rise of cAMP levels. Strikingly, EdTx pre-treated T cells were unresponsive to other stimuli involving CREB phosphorylation such as addition of forskolin or T cell receptor cross-linking. Conclusions/Significance: We concluded that, in a first intoxication phase, EdTx induces PKA-dependent signaling, which culminates in CREB phosphorylation and activation of gene transcription. Subsequently CREB phosphorylation is impaired and therefore T cells are not able to respond to cues involving CREB. The present data functionally link the perinuclea

Analysis of anemia induced by lymphocytic choriomeningitis virus

Le virus de la chorioméningite lymphocitaire (LCMV), prototype de la famille des Arenaviridae, provoque une infection naturelle chez la souris. L’injection intracérébrale de ce virus à des souris C3HeB/FeJ entraîne une anémie hémolytique. Bloquée par le cyclophosphamide, cette anémie a été considérée comme étant de nature auto-immune. Dans ce travail nous avons étudié les points suivants : 1- nature des autoanticorps anti-érythrocytaires ; 2- modulation des réponses immunes induite par le LCMV et son rôle dans le processus auto-immunitaire ; 3- effet des différences génétiques entre les couches de souris dans le développement de l’anémie. 1- Les autoanticorps anti-érythrocytaires détectés dans les souris anémiques pourraient être le facteur médiateur de la maladie. Pour mieux les caractériser, nous avons d’abord identifié la cible antigénique de ces autoanticorps. Nos résultats montrent que la Bande 3, molécule transporteuse d’anions à la surface des globules rouges, est l’antigène de surface le plus souvent reconnu par les anticorps anti-érythrocytaires. 2- Nous avons également étudié les mécanismes par lesquels le LCMV induit la production d’autoanticorps et, par voie de conséquence le développement de l’anémie. Nous avons ainsi analysé le rôle de la modulation des réponses immunes, induites par le LCMV, dans le processus auto-immunitaire ? Nos résultats indiquent que le LCMV provoque une stimulation générale du système immunitaire qui se traduit par une augmentation de la sécrétion de cytokines, une prolifération importante des lymphocytes B et une hypergammaglubolinémie. Cette activation polyclonale des lymphocytes B n’est cependant pas suffisante pour expliquer le développement de la réponse auto-immune. En outre, nous montré que le virus favorise la différenciation de la sous-population Th1 des lymphocytes T auxiliaires aux dépens des cellules Th2. cette réponse Th1 est accompagnée d’une prédominance des immuglobulines de sous-classe IgG2a. Vues les propriétés particulières de cette sous-classe d’IgG à savoir, l’activation du complément, l’opsonisation via les récepteurs Fc et la médiation de la cytotoxicité dépendant des anticorps, nos résultats suggèrent qu’en favorisant le réponse Th1, le LCMV augmente la pathogénicité des autoanticorps entraînant ainsi le développement de l’anémie. 3- Différents travaux ont suggéré que la pathologie induite par le LCMV dépend du patrimoine génétique de l’hôte. Nous avons examiné le développement de l’anémie dans différentes souches de souris après infection par le LCMV. La plupart des souches infectées deviennent anémiques et produisent des anticorps anti-globules rouges. Cependant, chez les souris CBA/Ht, l’anémie s’avère indépendante de la production des autoanticorps. Nous avons étudié l’implication de divers mécanismes dans l’étiologie de la maladie chez ces animaux. Nos résultats indiquent qu’une aplasie centrale combinée à un retard de restauration de l’hématopoïèse, ainsi qu’une forte activation des macrophages pourraient être les médiateurs de la maladies chez le CBA/Ht. En conclusion, le LCMV induit une anémie par des mécanismes différents selon le souche de souris utilisées, 1- réponse auto-immune chez les souris C3HeB/FeJ, 2- aplasie centrale et probablement une activation des macrophages chez les souris CBA/HtTen years ago a model of autoimmune haemolytic anemia was established in C3HeB/FeJ mice infected with the ‘Docile’ strain of Lymphocytic Choriomeningitis Virus (LCMV). Several questions emerged from this model : 1- nature of the anti-red cell autoantibodies; 2- modulation of immune responses triggered by LCMV and its role in the autoimmune process; 3- effect of genetic differences between strains of mice on the development of the disease 1- Anti-erythrocyte autoantibodies have been suggested to be the promoters of the pathophysiological process. To have more insights into these autoantibodies we first determined the autoantigen target on the RBC surface. Our results indicated that Band 3, an anion channel, was the major red blood cell protein recognized by anti-erythrocyte autoantibodies 2- We also studied the role of the LCMV-induced modulation of immune responses in this disorder. Our results indicated that LCMV triggered a general stimulation of the immune system that because manifest by an increased cytokine secretion, an important B cell proliferation and hypergammaglobulinemia. Such a polyclonal B cell activation has been suggested to be necessary for the development of anemia but it appears to be insufficient. We further demonstrate that LCMV stimulated T helper cells to differentiate towards the Th1 subpopulation at the expense of the Th2 subset. This was accompanied by an IgG2a preponderance in the anti-erythrocyte autoantibody response. Generally, IgG2a antibodies absorb to macrophages via Fc receptor at a very high rate, readily activate complement and are highly efficient in ADCC (antibody dependent cell-mediated cytotoxicity) situations, we can postulate that favoring of the Th1 response could not only result in an enhancement of autoantibody pathogenicity but also could be one of the mechanisms by which LCMV triggers the autoimmune disorder. 3- Since the pathology induced by LCMV had previously been shown to depend on the genetic background of the infected host we expanded the spectrum of inbred mice for their predisposition to develop LCMV-induced anemia. The majority of the strains infected with LCMV displayed an anemia accompanied by anti-erythrocyte autoantibody production. However in CBA/Ht mice anemia seems to be independent of the autoantibody response. Since, macrophages have been suggested to play a key role in the development of anemia both in mice and humans. We analyzed their possible role in our system. On the other hand, several reports have described hematopoietic alterations after LCMV infection. Our data argue in favour of both a central aphasia as well as macrophage activation as the promoters of the disease in CBA/Ht mice. Therefore, LCMV triggers anemia by different mechanisms in different mice; i.e. autoimmune responses as well as bone marrow aplasia in association with macrophage activationThèse de doctorat en sciences biomédicales (Immunologie virale) -- UCL, 199

Involvement of CD4+ cells in lymphocytic choriomeningitis virus-induced autoimmune anaemia and hypergammaglobulinaemia

Development of pathology varies widely between different strains of mice after intracerebral inoculation with the so-called 'docile' isolate of Lymphocytic Choriomeningitis (LCM) virus. The C3HeB/FeJ and B10. Br/SgSnJ mouse strains have been of special interest because they display autoimmune haemolytic anaemia with varying degrees of apparent immunological involvement. In this report, we examined the role of CD4+ T helper cells in this autoimmune response by treating mice with the CD4-specific GK1.5 monoclonal antibody. We also determined if polyclonal activation of B lymphocytes, induced either by LCM virus or by lactate dehydrogenase-elevating virus, another well known B cell activator, correlated with the development of anaemia in these mice. Our results strengthened the central role of the immune system in the anaemia in C3H mice by showing that depletion of CD4+ cells largely, if not completely, abrogated this anti-erythrocyte autoimmune reaction. As reported by others, we found that the anaemia was more mild in B10.BR mice than in C3H mice. However, we could not confirm the difference in the degree of B lymphocyte polyclonal activation between these mice. Furthermore, lactate dehydrogenase-elevating virus had no apparent effect on erythrocytes, even though this virus also induced a sharp increase in plasma IgG levels