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

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

Distinct Host-Dependent Pathogenic Mechanisms Leading to a Similar Clinical Anemia After Infection with Lymphocytic Choriomeningitis Virus

The Docile strain of lymphocytic choriomeningitis virus (LCMV) induces anemia in a number of inbred strains of mice, including C3HeB/FeJ and CBA/Ht animals. A difference in the kinetics of anemia and in compensatory reticulocytosis suggested that impaired erythropoiesis was the major pathogenic mechanism involved in CBA/Ht mice, but not in C3HeB/FeJ mice. In both mouse strains an antierythrocyte autoantibody production that depended on the presence of functional CD4+ T lymphocytes was observed. Although depletion of T helper lymphocytes prevented anemia in C3HeB/FeJ mice, this treatment largely failed to inhibit the development of the disease in CBA/Ht animals. This observation indicated that the antierythrocyte autoimmune response induced by the infection was at least partly responsible for the anemia of C3HeB/FeJ mice, but not of CBA/Ht mice. Erythrophagocytosis was enhanced in both mouse strains after LCMV infection, but did not appear to be a major cause of anemia. These data clearly indicate that similar disease profiles induced by the same virus in two different host strains can be the result of distinctly different mechanisms

Distinct host-dependent pathogenic mechanisms leading to a similar clinical anemia after infection with lymphocytic choriomeningitis virus.

The Docile strain of lymphocytic choriomeningitis virus (LCMV) induces anemia in a number of inbred strains of mice, including C3HeB/FeJ and CBA/Ht animals. A difference in the kinetics of anemia and in compensatory reticulocytosis suggested that impaired erythropoiesis was the major pathogenic mechanism involved in CBA/Ht mice, but not in C3HeB/FeJ mice. In both mouse strains an antierythrocyte autoantibody production that depended on the presence of functional CD4+ T lymphocytes was observed. Although depletion of T helper lymphocytes prevented anemia in C3HeB/FeJ mice, this treatment largely failed to inhibit the development of the disease in CBA/Ht animals. This observation indicated that the antierythrocyte autoimmune response induced by the infection was at least partly responsible for the anemia of C3HeB/FeJ mice, but not of CBA/Ht mice. Erythrophagocytosis was enhanced in both mouse strains after LCMV infection, but did not appear to be a major cause of anemia. These data clearly indicate that similar disease profiles induced by the same virus in two different host strains can be the result of distinctly different mechanisms

Moroccan Lagoon Microbiomes

Lagoons are fragile marine ecosystems that are considerably affected by anthropogenic pollutants. We performed a spatiotemporal characterization of the microbiome of two Moroccan lagoons, Marchica and Oualidia, both classified as Ramsar sites, the former on the Mediterranean coast and the latter on the Atlantic coast. We investigated their microbial diversity and abundance using 16S rRNA amplicon- and shotgun-based metagenomics approaches during the summers of 2014 and 2015. The bacterial microbiome was composed primarily of Proteobacteria (25–53%, 29–29%), Cyanobacteria (34–12%, 11–0.53%), Bacteroidetes (24–16%, 23–43%), Actinobacteria (7–11%, 13–7%), and Verrucomicrobia (4–1%, 15–14%) in Marchica and Oualidia in 2014 and 2015, respectively. Interestingly, 48 strains were newly reported in lagoon ecosystems, while eight unknown viruses were detected in Mediterranean Marchica only. Statistical analysis showed higher microbial diversity in the Atlantic lagoon than in the Mediterranean lagoon and a robust relationship between alpha diversity and geographic sampling locations. This first-ever metagenomics study on Moroccan aquatic ecosystems enriched the national catalog of marine microorganisms. They will be investigated as candidates for bioindication properties, biomonitoring potential, biotechnology valorization, biodiversity protection, and lagoon health assessment

Moroccan Lagoon Microbiomes

Lagoons are fragile marine ecosystems that are considerably affected by anthropogenic pollutants. We performed a spatiotemporal characterization of the microbiome of two Moroccan lagoons, Marchica and Oualidia, both classified as Ramsar sites, the former on the Mediterranean coast and the latter on the Atlantic coast. We investigated their microbial diversity and abundance using 16S rRNA amplicon- and shotgun-based metagenomics approaches during the summers of 2014 and 2015. The bacterial microbiome was composed primarily of Proteobacteria (25–53%, 29–29%), Cyanobacteria (34–12%, 11–0.53%), Bacteroidetes (24–16%, 23–43%), Actinobacteria (7–11%, 13–7%), and Verrucomicrobia (4–1%, 15–14%) in Marchica and Oualidia in 2014 and 2015, respectively. Interestingly, 48 strains were newly reported in lagoon ecosystems, while eight unknown viruses were detected in Mediterranean Marchica only. Statistical analysis showed higher microbial diversity in the Atlantic lagoon than in the Mediterranean lagoon and a robust relationship between alpha diversity and geographic sampling locations. This first-ever metagenomics study on Moroccan aquatic ecosystems enriched the national catalog of marine microorganisms. They will be investigated as candidates for bioindication properties, biomonitoring potential, biotechnology valorization, biodiversity protection, and lagoon health assessment