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Abdelouahab Bellou

Publications and source records attributed to Abdelouahab Bellou.

8 recordsLinked to original sources
PubMed2005

Costimulation: critical pathways in the immunologic regulation of asthma.

T cells play an important role in the pathogenesis of allergy and asthma. T-cell receptor engagement by antigenic peptides presented to major histocompatibility complex (MHC) class II molecules and activation of costimulatory molecules are crucial in the regulation of T-cell immune responses. Costimulatory molecules are responsible for second signals that induce T-cell activation and proliferation. The best characterized costimulatory pathways include CD80/CD86 interacting with CD28, and a number of additional costimulatory molecules have recently been identified, including members of the tumor necrosis family. The positive signals induced by these molecules are counterbalanced by other members of the costimulatory family, including cytotoxic T lymphocyte-associated antigen (CTLA)-4, programmed death (PD)-1, and B and T lymphocyte attenuator (BTLA), which dampen immune responses. In this review, we describe the fundamental properties of costimulatory molecules and address the influence of costimulatory signals on allergic responses.

Antigens, CD↗
PubMed2005

Performance of magnetic resonance angiography in suspected acute pulmonary embolism.

Pulmonary embolism (PE) is a common and potentially fatal disorder. Non-specific findings make the clinical diagnosis of PE difficult. To assess the diagnostic value and inter-observer agreement of magnetic resonance angiography (MRA) in a cohort of patients with suspected PE, we conducted a prospective clinical study. MRA was compared for sensitivity and specificity to a diagnostic strategy including clinical probability, D-dimer testing, spiral CT, ultrasound leg compression and pulmonary angiography. A total of 89 patients with clinically suspected PE were included: the clinical probability of PE was intermediate or high in 78, and low in the remaining 11. All patients underwent monoor multi-slice spiral CT and MRA with gadolinium injection (both within 24 hours of entry to the study). Anticoagulation was withheld in patients concerned about the strategy. All subjects were followed up for 3 months. MRA was read independently by two experienced teams of radiologists: one local and one from another university centre. Spiral CT was positive in 62 of 63 cases of confirmed PE. No patient with negative CT findings was positive ultrasonographically. Only one patient with a negative CT (and negative ultrasound) had a recurrent thromboembolic event. The first team diagnosed PE with MRA in 47 cases, with a sensitivity of 71% and a specificity of 92%; the second team obtained the diagnosis in 23 cases, with a sensitivity of 31% and a specificity of 85%. Inter-observer agreement between MRA reading was low: Kappa = 0.16 (-0.01 to 0.33); p = 0.07. In conclusion, compared with a non-invasive strategy based on spiral CT, the diagnostic value of MRA is limited by poor inter-observer agreement.

Acute Disease↗
PubMed2004

Toll-like receptor 4 or 2 agonists decrease allergic inflammation.

Toll-like receptors (TLRs) recognize highly conserved microbial molecular patterns, such as found in endotoxin. This study tested whether TLR4 and TLR2 stimulation in vivo would modulate subsequent adaptive (allergic) immune responses. We analyzed the effects of pulmonary administration of a TLR4 agonist, lipid A (LpA), and two TLR2 agonists, peptidoglycan (Ppg) and PamCys, in a murine model of allergic inflammation. The TLR agonists were administered during allergen sensitization or challenge. Both TLR agonists decreased the allergen-induced pulmonary recruitment of eosinophils when administered at sensitization or challenge. When given before sensitization, the TLR4 and TLR2 agonists decreased additional allergen-induced parameters of inflammation (pulmonary eosinophilia, bronchoalveolar lavage IL-13, total serum IgE, and airway hyperresponsiveness). Interestingly, TLR4 and TLR2 agonists decreased the number of CD4+ cells in the lung. Also, at the site of local allergen stimulation, the draining thoracic lymph nodes, allergen-induced lymphocyte proliferation, and IL-13 secretion were decreased by administration of LpA and Ppg. These data provide a distinct example of the modulation of adaptive (allergic) responses by non-antigen-dependent stimuli. Our findings also demonstrate that both TLR4 and TLR2 agonists decrease allergic responses, supporting the concept that exposure to bacterial components under defined conditions may protect against allergic disease.

Administration, Inhalation↗
PubMed2004

TLR2 and TLR4 stimulation differentially induce cytokine secretion in human neonatal, adult, and murine mononuclear cells.

Toll-like receptor 2 (TLR2) and TLR4 signaling may induce differential secretion of T helper 1 (Th1) and Th2 cytokines, potentially influencing the development of autoimmune or atopic diseases. To date, the influence of the type of stimulus, timing, and dose of TLR2 and TLR4 ligands on cytokine secretion has not been well established. We tested whether the innate stimuli peptidoglycan (Ppg, TLR2 agonist) and lipid A (LpA, TLR4 agonist) differentially affect the secretion of interleukin-13 (IL-13) (Th2) and interferon-gamma (IFN-gamma) (Th1). Further, we examined the influence of the maturity of the immune system, species, dose, and timing of stimuli in human cord and adult peripheral blood mononuclear cells (PBMC) and murine cells in vitro and in vivo. Stimulation with Ppg induced the secretion of both IL-13 and IFN-gamma, influenced by time and dose in neonates, adults, and mice. In contrast, stimulation with LpA induced primarily time-independent and dose-independent production of IFN-gamma. Pulmonary administration of Ppg in vivo in mice resulted in secretion of IL-13, whereas administration of LpA resulted in secretion of IFN-gamma in bronchoalveolar lavage (BAL). Therefore, TLR2 and TLR4 stimuli differentially influence IL-13 and IFN-gamma secretion in neonates, adults, and mice, supporting a critical role for innate stimuli in the modulation of cytokine responses.

Adult↗
PubMed2003

Spectrum of acute allergic diseases in an emergency department: an evaluation of one years' experience.

OBJECTIVE: There is limited available literature on the incidence of allergic diseases in ED. The objective of this study was to investigate the clinical records of patients admitted to the ED with a suspected allergic reaction. METHODS: A 1 year retrospective study was carried out and data were collected from the patients' computerized medical reports. RESULTS: A total of 324 patients were admitted for an allergic event. Of those, 165 patients (50.9%) were female and their mean age was 55 +/- 18.5 years. Diagnoses included: asthma in 100 patients (30.9%); hymenoptera allergy in 78 patients (24.1%); food allergy in 31 patients (9.5%); drug allergy in 25 patients (7.7%); and allergic conjunctivitis in 12 patients (3.7%). No diagnosis was found in the medical records of 78 patients (24.1%). Anaphylactic shock was observed in 12 patients (3.7%) with a diagnosis of food allergy (six cases), drug allergy (three cases) and hymenoptera allergy (three cases). Ninety patients (27.7%) were hospitalized in the following units: 38 in allergy unit (42.2%); 20 in intensive care unit (22.2%); 10 in pulmonary unit (11.1%); eight in the dermatology unit (8.9%); six in the internal medicine unit (6.7%); and eight in other units (8.9%). Overall, 42 patients (12.9%) were evaluated by an allergologist after ED discharge with positive allergy results in 28 cases (66.6%). CONCLUSIONS: Acute allergic diseases are not rare in ED, representing 1% of the annual visits in our series. A low rate of allergologist referral was observed. Emergency physicians must work closely with allergologists to ensure a better evaluation, long-term care and preventive management of patients with allergic diseases admitted to the ED.

Acute Disease↗
PubMed2003

Constitutive nitric oxide synthase inhibition combined with histamine and serotonin receptor blockade improves the initial ovalbumin-induced arterial hypotension but decreases the survival time in brown norway rats anaphylactic shock.

Anaphylactic shock accidents after allergen exposure are frequent. After immunization with ovalbumin (OVA), a common dietary constituent, we evaluated the efficacy of pretreatment with histamine-receptor or serotonin-receptor blockers administered alone or in combination with a nitric oxide synthase inhibitor (L-NAME) on OVA-induced anaphylactic shock in Brown Norway rats. Animals were allocated to the following groups (n = 6 each): control (0.9% saline); diphenydramine (15 mg kg(-1)); cimetidine (20 mg kg(-1)); diphenydramine + cimetidine; dihydroergotamine (50 microg kg(-1)); diphenydramine + cimetidine + dihydroergotamine; L-NAME (100 mg/kg) alone or associated with diphenydramine, cimetidine, diphenydramine + cimetidine, dihydroergotamine, or diphenydramine + cimetidine + dihydroergotamine. Mean arterial blood pressure (MABP), heart rate (HR), and survival time were monitored for 60 min following treatment. The shock was initiated with i.v. OVA. The MABP drop after i.v. OVA was worsened by diphenydramine and was modestly attenuated by cimetidine, dihydroergotamine, or both together. L-NAME potentiated slightly the effects of cimetidine and dihydroergotamine by lessening the initial MABP decrease, but this transient effect was not sufficient to prevent the final collapse or to improve survival time. Decreased vasodilatory (prostaglandins E2), increased vasoconstrictory (thromboxane B2) prostaglandins, and unchanged leukotriene C4 concentrations were contributory to the overall hemodynamic changes. Thus, the combined blockade of vasodilator mediators (histamine, serotonin, and nitric oxide) slowed the MABP drop in anaphylactic shock, but did not improve survival. More studies are needed to understand these discordant effects.

Anaphylaxis↗
PubMed2003

Toll receptors modulate allergic responses: interaction with dendritic cells, T cells and mast cells.

PURPOSE OF REVIEW: The discovery of Toll-like receptors has generated much interest in understanding the impact of innate immunity on adaptive immune responses, including allergic diseases. RECENT FINDINGS: Recent studies suggest that Toll-like receptor pathways may mediate interactions between dendritic cells, T lymphocytes and mast cells, thus modulating allergic immune responses. Toll-like receptor signaling triggers dendritic cell maturation, which primes naive T lymphocytes towards specific T helper cell types 1 and 2 immune responses. Although a T helper cell type 1/2 balance may be important in modulating allergic responses, T regulatory cells that suppress certain immune responses may be critical in immune regulation. SUMMARY: With the identification of different subsets of dendritic cells and the discovery of Toll-like receptors on T regulatory cells and mast cells, the manipulation of Toll-like receptor signaling may lead to novel therapeutic options in allergic diseases.

Dendritic Cells↗