Search

Introduction L’argan est tres utilise en cosmetologie depuis quelques annees, notamment pour ses proprietes supposees benefiques pour la sante. Nous rapportons ici les premiers cas de rhinites et d’asthmes professionnels decrit chez des agents de production d’une societe de fabrication d’actifs pour cosmetiques, en lien avec la manipulation de poudre d’argan. Methode Neuf patients travaillant dans une entreprise de production d’actifs pour cosmetiques ont ete explores suite a l’apparition chez 4 d’entre eux de symptomes ORL et/ou respiratoires en relation avec la manipulation de poudre d’argan. Tous etaient occasionnellement amene a manipuler de l’argan sous forme de poudre et de liquide, sans mesure de protection respiratoire specifique. Tous ont repondu a un questionnaire medical et professionnel, puis ont beneficie d’examens complementaires comprenant : un suivi de debit expiratoire de pointe (DEP), un test de provocation bronchique a la metacholine, une recherche d’IgE specifique de l’argan par immunoblot , des prick-tests a l’argan et a divers autres allergenes vegetaux. Pour ceux suspects de presenter un asthme professionnel, un test de provocation bronchique realiste avec de la poudre d’argan a ete realise. Enfin, une recherche de sequences peptidiques analogues a d’autres vegetaux a ete realisee par analyse en spectrometrie de masse. Resultats Sur les 4 agents symptomatiques, 3 presentaient des prick-tests positifs pour au moins un allergene standard et la noisette. Deux des 3 avaient egalement un prick-test positif a l’argan. Les 3 agents rapportant des symptomes d’asthme presentaient un test de provocation bronchique realiste positif a la poudre d’argan. Sept sequences proteiques etaient identifiees par immunoblotting de la poudre d’argan avec le serum de patients sensibilises. En revanche, aucune sequence n’etait mise en evidence lors de l’application de la meme technique sur un extrait liquide d’argan, suggerant la denaturation des proteines allergeniques par le processus de transformation. L’identification des proteines par comparaison avec des banques de donnees d’extraits allergeniques vegetaux, la sensibilisation associee a la noisette documentee par prick-test et les tests Elisa d’inhibition des IgE de l’argan par un extrait de noisette suggeraient le role allergenique de 2 proteines en particulier : une viciline et une globuline 11 S. Conclusion Une exposition habituelle a de fortes concentrations d’argan sous forme de poudre semble pouvoir favoriser l’apparition d’allergies respiratoires IgE mediees. Il semble important de proteger efficacement et de surveiller medicalement les salaries amenes a manipuler ce type de substance.

Introduction: Moringa oleifera is a small native tree of North West India. Many bioactive compounds of Moringa have recently been isolated, leading to industrial and medicinal uses worldwide. We report the first case of occupational asthma (OA) to Moringa. Patient, Methods and Results: A 32 year-old cosmetic factory technician (without allergy history) exposed into the workplace to a powder of Moringa seed progressively complained of rhinitis and respiratory symptoms. Initial investigations (patient still working) didn9t show baseline airway obstruction (FEV1=4.15L, 96% of predicted value; FEV1/FVC%=81%), exhaled nitric oxide fraction ( F eno) was increased to 91.21 ppb, methacholine challenge showed nonspecific bronchial hyperresponsiveness (22% decrease of FEV1), and the Oasys II score was 3.29. Specific inhalation challenge (SIC) to Moringa seed powder showed immediate positive reaction (21% decrease of FEV1). Sputum eosinophil counts and F eno evaluated at baseline and 24h after SIC showed an increase of eosinophils from 6% to 62%, and an increase of F eno from 32.37 to 94.34 ppb. The prick-tests to a 10% solution of Moringa seed powder was positive while we observed negative control prick tests in 4 volunteers never exposed. OA to Moringa seed was retained and the patient removed from further exposure to the implicated agent into the workplace. Conclusion: Moringa has shown numerous health benefits rapidly leading the cosmetic industry to incorporate Moringa as a compound of various products (moisturizers or skin ointment). New cases of allergy could therefore appear regarding to the increasing consumption of Moringa worldwide, as suggested by our description of the first case of OA to Moringa.

Background: ω-5 gliadin is a major allergen in exercise-induced wheat allergy (EIWA), but it is also implicated in immediate-type reactions to wheat. An ImmunoCAP assay to measure ω-5 gliadin-specific IgE has become available. This study aimed to evaluate this new biological test in wheat allergy diagnosis and to also determine if it was able to discriminate EIWA from other types of wheat allergy. Methods: Sixty-one patients with wheat allergy were divided into 3 groups as a function of their symptoms (EIWA, immediate-type reactions and atopic dermatitis). These patients underwent skin prick tests with purified ω gliadins and ImmunoCAP to wheat flour, gluten and recombinant ω-5 gliadin. Results: The experimental data showed that 78% of EIWA patients had a positive skin prick test to natural ω-5 gliadin and the same proportion had detectable specific IgE to recombinant ω-5 gliadin, indicating that ω-5 gliadin is the main allergen, but not the only one, in our population. Additionally, we showed that this detection was not EIWA specific since ω-5 gliadin-specific IgE was detected in 30% of other patients who had a wheat allergy. These results lead to a positive predictive value of 37.5% and to a negative predictive value of 91%. Conclusions: Although not specific to EIWA, the new ImmunoCAP ω-5 gliadin is an important biological test because of its negative predictive value. In case of food-dependent exercise-induced allergy, the absence of ω-5 gliadin-specific IgE will almost completely exclude the implication of wheat.

Virtually all cancer biological attributes are heterogeneous. Because of this, it is currently difficult to reconcile results of cancer transcriptome and proteome experiments. It is also established that cancer somatic mutations arise at rates higher than suspected, but yet are insufficient to explain all cancer cell heterogeneity. We have analyzed sequence variations of 17 abundantly expressed genes in a large set of human ESTs originating from either normal or cancer samples. We show that cancer ESTs have greater variations than normal ESTs for >70% of the tested genes. These variations cannot be explained by known and putative SNPs. Furthermore, cancer EST variations were not random, but were determined by the composition of the substituted base (b0) as well as that of the bases located upstream (up to b − 4) and downstream (up to b + 3) of the substitution event. The replacement base was also not randomly selected but corresponded in most cases (73%) to a repetition of b − 1 or of b + 1. Base substitutions follow a specific pattern of affected bases: A and T substitutions were preferentially observed in cancer ESTs. In contrast, cancer somatic mutations [Sjoblom T, et al. (2006) Science 314:268–274] and SNPs identified in the genes of the current study occurred preferentially with C and G. On the basis of these observations, we developed a working hypothesis that cancer EST heterogeneity results primarily from increased transcription infidelity.

In HIV-1 infected cells transcription of the integrated provirus generates the single full length 9 kb viral RNA, a major fraction of which is spliced to produce the single-spliced 4 kb RNAs and the multiple-spliced 2 kb RNAs. These spliced RNAs are the messengers for the Env glycoproteins and the viral regulatory factors. The cellular SR and hnRNP proteins were shown in vitro to control alternative splicing by binding cis-regulatory elements on the viral RNA. To better understand in vivo the role of the SR proteins on HIV-1 genomic RNA splicing and virion production, we used a human cell line expressing high levels of complete HIV-1 and either one of the ASF/SF2, SC35, and 9G8 SR proteins. Results show that over-expressing SR proteins caused a large reduction of genomic RNA and that each SR protein modified the viral 9 kb RNA splicing pattern in a specific mode. In fact, ASF/SF2 increased the level of Vpr RNA while SC35 and 9G8 caused a large increase in Tat RNA. As expected, overexpressing SR proteins caused a strong reduction of total Gag made. However, we observed by immuno-confocal microscopy an accumulation of Gag at the plasma membrane and in intracellular compartments while there is a dramatic reduction of Env protein made in most cells. Due to the negative impact of the SR proteins on the levels of genomic RNA and HIV-1 structural proteins much less virions were produced which retained part of their infectivity. In conclusion, SR proteins can down-regulate the late steps of HIV-1 replication.

International audience; Retroviral protein production depends upon alternative splicing of the viral transcript. The HIV-1 acceptor site A7 is required for tat and rev mRNA production. Production of the Tat transcriptional activator is highly controlled because of its apoptotic properties. Two silencer elements (ESS3 and ISS) and two enhancer elements (ESE2 and ESE3/(GAA)3) were previously identified at site A7. hnRNP A1 binds ISS and ESS3 and is involved in the inhibitory process, ASF/SF2 activates site A7 utilisation. Here, by using chemical and enzymatic probes we established the 2D structure of the HIV-1(BRU) RNA region containing site A7 and identified the RNA segments protected in nuclear extract and by purified hnRNP A1. ISS, ESE3/(GAA)3 and ESS3 are located in three distinct stem-loop structures (SLS1, 2 and 3). As expected, hnRNP A1 binds sites 1, 2 and 3 of ISS and ESS3b, and oligomerises on the polypurine sequence upstream of ESS3b. In addition, we discovered an unidentified hnRNP A1 binding site (AUAGAA), that overlaps ESE3/(GAA)3. On the basis of competition experiments, hnRNP A1 has a stronger affinity for this site than for ESS3b. By insertion of (GAA)3 alone or preceded by the AUA trinucleotide in a foreign context, the AUAGAA sequence was found to modulate strongly the (GAA)3 splicing enhancer activity. Cross-linking experiments on these heterologous RNAs and the SLS2-SLS3 HIV-1 RNA region, in nuclear extract and with recombinant proteins, showed that binding of hnRNP A1 to AUA(GAA)3 strongly competes the association of ASF/SF2 with (GAA)3. In addition, disruption of AUA(GAA)3 demonstrated a key role of this sequence in hnRNP A1 cooperative binding to the ISS and ESS3b inhibitors and hnRNP A1 oligomerisation on the polypurine sequence. Thus, depending on the cellular context ([ASF/SF2]/[hnRNP A1] ratio), AUA(GAA)3 will activate or repress site A7 utilisation and can thus be considered as a Janus splicing regulator.