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Objective and design This double-blind cross-over study compared the potential of bilastine, cetirizine, and fexofenadine to relieve the symptoms of allergic rhinitis. Subjects and methods Seventy-five allergic volunteers were challenged with grass pollen in the Vienna Challenge Chamber (VCC) on two consecutive days of allergen provocation; 6 h on day 1 and 4 h day 2. Bilastine 20 mg, cetirizine 10 mg, fexofenadine 120 mg, or placebo were taken orally 2 h after the start of provocation on day 1 only. Total nasal symptom scores, the global symptom scores, nasal secretions, and eye symptoms were assessed on both day 1 and day 2. Results and conclusions Bilastine had a rapid onset of action, within 1 h, and a long duration of action, greater than 26 h. Cetirizine was similar. Fexofenadine was similar on day 1 but less effective on day 2, indicating a shorter duration of action. Bilastine, like cetirizine and fexofenadine, was safe and well tolerated in this study.

Intranasal (i.n.) infections preferentially generate Th17 cells. We explored the basis for this anatomic preference by tracking polyclonal CD4⁺ T cells specific for an MHC class II-bound peptide from the mucosal pathogenStreptococcus pyogenes. S. pyogenesMHC class II-bound peptide-specific CD4⁺ T cells were first activated in the cervical lymph nodes following i.n. inoculation and then differentiated into Th17 cells.S. pyogenes-induced Th17 formation depended on TGF-β1 from dendritic cells and IL-6 from a CD301b⁺ dendritic cell subset located in the cervical lymph nodes but not the spleen. Thus, the tendency of i.n. infection to induce Th17 cells is related to cytokine production by specialized dendritic cells that drain this site.

Innate immunity responds to pathogens by producing alarm signals and activating pathways that make host cells inhospitable for pathogen replication. The intracellular bacterium Burkholderia thailandensis invades the cytosol, hijacks host actin, and induces cell fusion to spread to adjacent cells, forming multinucleated giant cells (MNGCs) which promote bacterial replication. We show that type I interferon (IFN) restricts macrophage MNGC formation during B. thailandensis infection. Guanylate-binding proteins (GBPs) expressed downstream of type I IFN were required to restrict MNGC formation through inhibition of bacterial Arp2/3-dependent actin motility during infection. GTPase activity and the CAAX prenylation domain were required for GBP2 recruitment to B. thailandensis, which restricted bacterial actin polymerization required for MNGC formation. Consistent with the effects in in vitro macrophages, Gbp2-/-, Gbp5-/-, GbpChr3-KO mice were more susceptible to intranasal infection with B. thailandensis than wildtype mice. Our findings reveal that IFN and GBPs play a critical role in restricting cell-cell fusion and bacteria-induced pathology during infection.

Context.— The sinonasal tract is frequently affected by a variety of nonneoplastic inflammatory disease processes that are often multifactorial in their etiology but commonly have a molecular genetic component. Objective.— To review the molecular genetics of a variety of nonneoplastic inflammatory diseases of the sinonasal tract. Data Sources.— Inflammatory lesions of the sinonasal tract can be divided into 3 main categories: (1) chronic rhinosinusitis, (2) infectious diseases, and (3) autoimmune diseases/vasculitides. The molecular diagnosis and pathways of a variety of these inflammatory lesions are currently being elucidated and will shed light on disease pathogenesis and treatment. Conclusions.— The sinonasal tract is frequently affected by inflammatory lesions that arise through complex interactions of environmental, infectious, and genetic factors. Because these lesions are all inflammatory in nature, the molecular pathology surrounding them is most commonly due to upregulation and down-regulation of genes that affect inflammatory responses and immune regulation.

The concentrations of C-reactive protein (CRP), serum amyloid A, haptoglobin (Hp) and α1-acid glycoprotein were measured in dogs with clinical signs of nasal disease and compared with those of healthy dogs in order to determine the expression of these proteins in cases of canine nasal disease. A significant difference (P<0.001) between the symptomatic group and the control group was found for both CRP and Hp. Among the animals with nasal disease, a significant intergroup difference (P<0.05) was found in the expression of Hp between dogs with aspergillosis and those with chronic rhinitis.

Nasal cytology is a very useful diagnostic tool in nasal disorders, being able to detect both the cellular modifications of the nasal epithelium caused by either allergen exposure or irritative stimuli (that may be physical or chemical, acute or chronic), or inflammation. Over these past few years, nasal cytology has allowed to identify new disorders, such as the non-allergic rhinitis with eosinophils (NARES), the non-allergic rhinitis with mast cells (NARMA), the non-allergic rhinitis with neutrophils (NARNE), and the non-allergic rhinitis with eosinophils and mast cells (NARESMA). The rhinocytogram is actually able to distinguish the different forms of allergic rhinitis and to suggest the appropriate treatment, such as antinflammatory drugs or allergen immunotherapy. The technique is easy to perform and nasal cytology is therefore particularly suitable even for children. Such a consideration suggests the utility of a systematic use of nasal cytology in the diagnostic work-up of nasal disorders in children, in order to reach a proper defined diagnosis and to set a rational therapeutic approach: in facts, these two elements are fundamental in order to prevent from complications and to improve the patient’s quality of life.

A case of mucocutaneous nasal histoplasmosis in an immunocompetent host is described below. A 30-year-old male had a broadened nose with swelling and repeated blockage of nasal passages for the past six months. Diagnosis was made on the basis of histological demonstration of characteristic yeast cells of Histoplasma capsulatum var. capsulatum occurring within histiocytes and extracellularly in stained smears of fine needle aspirates and biopsy from the lesions in ala of the nose and perioral region. The patient showed appreciable regression of lesions after three weeks of itraconazole therapy but was not available for re-assessment.

Mucormycosis is a form of fulminant invasive fungal infection of the sinonasal tract that often extends to the orbit, brain, palate, and skin. It is caused by members of the order Mucorales, and it is considered to be the most fatal fungal infection known to man because it is rapidly disseminated by the blood vessels. It is most commonly associated with diabetic ketoacidosis, hematologic malignancies, acquired immunodeficiency syndrome, and immunosuppressive therapy. This rare opportunistic infection exists in many forms, the most common of which is rhinocerebral mucormycosis. Treatment includes aggressive surgical debridement of the necrotic tissue combined with systemic antifungal therapy. In this case report, we describe the successful management of rhinoorbital mucormycosis, a subtype of the rhinocerebral variety, secondary to Rhizopus oryzae that developed in a patient with lymphoma. We review the diagnostic work-up and discuss the literature with respect to the presentation, pathophysiology, management, and outcome of the disease.