Etude de l’interaction Interleukine-10 (il-10) et proteine Inflammatoire des macrophages-1β (MIP-1β/CCL4) aux differents stades du paludisme A Plasmodium falciparum chez l’enfant

Les profils moyens du taux dfhemoglobine (Hb) et de la densite parasitaire (DP) ont permis dfetudier lfinteraction entre IL-10 et MIP-1ƒÀ a travers le dosage plasmatique de ces cytokines par la technique ELISA en sandwich et la determination de leurs profils moyens chez les enfants a chaque stade depaludisme et apres traitement. Les resultats confirment la baisse du taux dfHb lorsque la DP augmente ; la charge parasitaire diminuant avec lfage. La concentration moyenne en IL10 a nettement augmente (p <0,0001) chez les enfants atteints de paludisme comparativement aux enfants temoins negatifs et ceux traites. Cependant la production de IL10 nfa pas evolue au stade paludisme grave ; ce qui a reduit son role anti-inflammatoire et engendre la forte production (p < 0,0001) de MIP-1ƒÀ a ce stade

Etude de la densite erythrocytaire par la methode des grandients de phtalate chez les patients drepanocytaires au Chu-campus de Lome(Togo)

Introduction: The sickle cell disease is a genetic disease of the red blood cell. It results in the presence of haemoglobin S whose essential property is gelation in deoxygenized atmosphere.Objective: To determine the profiles of erythrocyt density of the red blood cells according to the phenotype.Method: The density of the red blood cells was measured by the technique of the phthalate gradients.Result: Forty and one subject AA, 36 SS and 32 SC were included in this study. Compared to the AA group (D50 controls: 1.096 ± 0.003), D50 (average density) is increased in the SS group (D50: 1.1005 ± 0.003) and even more in the SC group (D50: 1.1054 ± 0.0026). The very heavy fractions (F5) were absent in the AA group, low in the SC group (1.54 ± 2.1) and high in the SS group (5.85 ± 4. 99). R60 (variation of density) which was of 0.0071 ± 0.0014 in the AA group, was moderately high in the SC group (0.0086 ± 0.0014) and very high in the SS group (0.014 ± 0.004). The indices of density R60 and F5 are narrowly correlated (R = 0.93) and characterize better the sickle cell disease according to the gravity of the phenotype.Conclusion: R60 and F5 appreciate cellular heterogeneity better. Future research must be harnessed to assemble the interest of the measurement of the erythrocyt density like predictive value of the acute sickle cell disease.Introduction : La drépanocytose est une maladie héréditaire du globule rouge. Elle se traduit par la présence d’hémoglobine S dont la propriété essentielle est la gélification en milieu désoxygéné.Objectifs : Déterminer les profils de densité des érythrocytes en fonction du phénotype hémoglobinique.Matériel et méthodes : La densité des érythrocytes a été mesurée par la technique des gradients de phtalate.Résultats : Quarante et un sujets AA, 36 SS et 32 SC ont été inclus dans cette étude. Par rapport au groupe contrôle AA (D50 : 1,096 ± 0,003), la D50 (densité moyenne) est augmentée chez les SS (D50 : 1,1005 ± 0,003) et encore plus chez les SC (D50 : 1,1054 ± 0,0026). Les fractions très lourdes (F5) étaient absentes chez les AA, faibles chez les SC (1,54 ± 2,1) et élevée chez les SS (5,85 ± 4, 99). La R60 (écart de densité) qui a été de 0,0071 ± 0,0014 chez les AA, était modérément élevée chez les SC (0,0086 ± 0,0014) et très élevée chez les SS (0,014 ± 0,004). Les indices de densité R60 et F5 sont étroitement corrélés (r = 0,93) et caractérisent mieux la drépanocytose selon la gravité du phénotype.Conclusion : La R60 et la F5 apprécient mieux l’hétérogénéité cellulaire. Les recherches futures doivent s’atteler à monter l’intérêt de la mesure de la densité érythrocytaire comme valeur prédictive des crises aiguës drépanocytaire

γδT cells and CD14(+) monocytes are predominant cellular sources of cytokines and chemokines associated with severe malaria

Background. Severe malaria (SM) is associated with high levels of cytokines such as tumor necrosis factor (TNF), interleukin 1 (IL-1), and interleukin 6 (IL-6). The role of chemokines is less clear, as is their cellular source.\ud \ud Methods. In a case-control study of children with SM (n = 200), uncomplicated malaria (UM) (n = 153) and healthy community controls (HC) (n = 162) in Papua, New Guinea, we measured cytokine/chemokine production by peripheral blood mononuclear cells (PBMCs) stimulated with live Plasmodium falciparum parasitized red blood cells (pRBC). Cellular sources were determined. Associations between immunological endpoints and clinical/parasitological variables were tested.\ud \ud Results. Compared to HC and UM, children with SM produced significantly higher IL-10, IP-10, MIP-1 beta m and MCP-2. TNF and MIP-1 α were significantly higher in the SM compared to the UM group. IL-10, IL-6, MIP-1 α, MIP-1 β, and MCP-2 were associated with increased odds of SM. SM syndromes were associated with distinct cytokine/chemokine response profiles compared to UM cases. TNF, MIP-1 β, and MIP-1 α were produced predominantly by monocytes and γδ T cells, and IL-10 by CD4(+) T cells.\ud \ud Conclusions. Early/innate PBMC responses to pRBC in vitro are informative as to cytokines/chemokines associated with SM. Predominant cellular sources are monocytes and gamma delta T cells. Monocyte-derived chemokines support a role for monocyte infiltrates in the etiology of SM

The mucosal inflammatory response to non-typhoidal Salmonella in the intestine is blunted by IL-10 during concurrent malaria parasite infection

Co-infection can markedly alter the response to a pathogen, thereby changing its clinical presentation. For example, non-typhoidal Salmonella (NTS) serotypes are associated with gastroenteritis in immunocompetent individuals. In contrast, individuals with severe pediatric malaria can develop bacteremic infections with NTS, during which symptoms of gastroenteritis are commonly absent. Here, we report that in both a ligated ileal loop model and a mouse colitis model, malaria parasites caused a global suppression of gut inflammatory responses and blunted the neutrophil influx that is characteristic of NTS infection. Further, malaria parasite infection led to increased recovery of S. Typhimurium from the draining mesenteric lymph node of mice. In the mouse colitis model, blunted intestinal inflammation during NTS infection was independent of anemia, but instead required parasite-induced synthesis of IL-10. Blocking of IL-10 in co-infected mice reduced dissemination of S. Typhimurium to the mesenteric lymph node, suggesting that induction of IL-10 contributes to development of disseminated infection. Thus, IL-10 produced during the immune response to malaria in this model contributes to suppression of mucosal inflammatory responses to invasive NTS, which may contribute to differences in the clinical presentation of NTS infection in the setting of malaria