Peter Hellings

Staphylococcus aureus enterotoxin B facilitates allergic sensitization in experimental asthma

Background Staphylococcus aureus Enterotoxin B (SEB) has immunomodulatory effects in allergic airway disease. The potential contribution of SEB to the sensitization process to allergens remains obscure.

Staphylococcus aureus enterotoxin B augments granulocyte migration and survival via airway epithelial cell activation

To cite this article: Huvenne W, Callebaut I, Reekmans K, Hens G, Bobic S, Jorissen M, Bullens DMA, Ceuppens JL, Bachert C, Hellings PW. Staphylococcus aureus enterotoxin B augments granulocyte migration and survival via airway epithelial cell activation. Allergy 2010; 65: 1013–1020.

Exacerbation of cigarette smoke-induced pulmonary inflammation by Staphylococcus aureus enterotoxin B in mice

BackgroundCigarette smoke (CS) is a major risk factor for the development of COPD. CS exposure is associated with an increased risk of bacterial colonization and respiratory tract infection, because of suppressed antibacterial activities of the immune system and delayed clearance of microbial agents from the lungs. Colonization with Staphylococcus aureus results in release of virulent enterotoxins, with superantigen activity which causes T cell activation.ObjectiveTo study the effect of Staphylococcus aureus enterotoxin B (SEB) on CS-induced inflammation, in a mouse model of COPD.MethodsC57/Bl6 mice were exposed to CS or air for 4 weeks (5 cigarettes/exposure, 4x/day, 5 days/week). Endonasal SEB (10 μg/ml) or saline was concomitantly applied starting from week 3, on alternate days. 24 h after the last CS and SEB exposure, mice were sacrificed and bronchoalveolar lavage (BAL) fluid and lung tissue were collected.ResultsCombined exposure to CS and SEB resulted in a raised number of lymphocytes and neutrophils in BAL, as well as increased numbers of CD8+ T lymphocytes and granulocytes in lung tissue, compared to sole CS or SEB exposure. Moreover, concomitant CS/SEB exposure induced both IL-13 mRNA expression in lungs and goblet cell hyperplasia in the airway wall. In addition, combined CS/SEB exposure stimulated the formation of dense, organized aggregates of B- and T- lymphocytes in lungs, as well as significant higher CXCL-13 (protein, mRNA) and CCL19 (mRNA) levels in lungs.ConclusionsCombined CS and SEB exposure aggravates CS-induced inflammation in mice, suggesting that Staphylococcus aureus could influence the pathogenesis of COPD.

Nasal corticosteroid treatment reduces substance P levels in tear fluid in allergic rhinoconjunctivitis

BACKGROUNDnThe mechanisms underlying conjunctival symptom reduction by nasal corticosteroids in allergic rhinoconjunctivitis are unknown. A naso-ocular reflex may be present.nnnOBJECTIVEnTo study the effects of nasal fluticasone furoate (FF) on conjunctival symptoms and substance P and histamine levels in tear fluid after nasal grass pollen provocation (GPP).nnnMETHODSnA double-blind placebo-controlled study was performed in 26 grass pollen-allergic patients. A selective GPP was performed during the grass pollen season after 2 weeks of FF or placebo treatment. Nasal and conjunctival symptoms were scored using a visual analog scale (VAS), and tear fluid was collected for measuring substance P and histamine using an enzyme-linked immunosorbent assay.nnnRESULTSnCompared with placebo, FF reduced conjunctival symptom scores during the pollen season (-1.75 [-2.75, 0.20] vs 0.0 [0.0, 0.0]; P = .01) and after GPP at 15 minutes (0.05 [-0.42, 1.52] vs 2.05 [0.62, 3.62]; P < .001) and 1 hour (-0.45 [-1.75, 0.1] vs 0.05 [-0.97, 1.85]; P < .01). Treatment with FF decreased substance P levels in tear fluid (44.11 [32.81, 61.02] vs 65.26 [48.62, 79.73] pg/mg protein; P = .0098). Histamine levels in tear fluid showed a GPP-induced increase in the placebo group (7.26 [3.12, 9.69] vs 5.71 [2.05, 7.00] ng/mg protein; P = .02), but not in the FF group (6.77 [3.43, 13.00] vs 5.24 [3.18, 7.06] ng/mg protein; P = .08).nnnCONCLUSIONnFF nasal spray reduced conjunctival symptoms in grass pollen-allergic patients in parallel with lower substance P levels in tear fluid. These data help in understanding the reduction of conjunctival symptoms by intranasal anti-inflammatory therapy.

Conjunctival effects of a selective nasal pollen provocation

To cite this article: Callebaut I, Spielberg L, Hox V, Bobic S, Jorissen M, Stalmans I, Scadding G, Ceuppens JL, Hellings PW. Conjunctival effects of a selective nasal pollen provocation. Allergy 2010; 65: 1173–1181.

Transient swelling of the Schneiderian membrane after transversal sinus augmentation: a pilot study

OBJECTIVEnThe predictability and simplicity of the Summers technique for sinus floor elevation encouraged many clinicians to consider this new approach. The impact of such intervention on the sinus mucosa has, however, not been explored extensively. This pilot study followed the response of the Schneiderian membrane, longitudinally, via cone-beam CT images.nnnMATERIAL AND METHODSnTen consecutive patients (five women, mean age 58.7xa0years) referred for implant therapy in the posterior part of the maxilla, in combination with a trans-alveolar sinus floor elevation (13 sinuses involved), were enrolled. CBCT images were taken prior to and at 1xa0week and 1xa0month after surgery. The changes in thickness of the Schneiderian membrane were scored at nine standardized points per sinus using reformatted cross-sectional images.nnnRESULTSnOne week after sinus floor elevation, the Schneiderian membrane showed a significant swelling of 9.2xa0mm in the middle (SD 0.3; Pxa0<xa00.005), 7.2xa0mm medially (SD 2.5; Pxa0<xa00.005) and 3.9xa0mm laterally (SD 0,3; Pxa0<xa00.05), respectively, resulting in an overall mean of 6.7xa0mm (SD 2.6), which fully disappeared 3xa0weeks later. This swelling involved the entire floor of the sinus and not only the augmented area.nnnCONCLUSIONSnWithin the limitations of this pilot study, one can conclude that the Schneiderian membrane responds with a significant transient swelling (5-10× its size) during the first weeks of healing.

Laryngeal effects of nasal allergen provocation in singers with allergic rhinitis

In spite of our recent insight into nasobronchial interaction mechanisms in allergic airway disease, the association between allergic rhinitis and voice complaints remains obscure. To evaluate the effects of nasal allergen provocation and seasonal grass pollen exposure on subjective and objective laryngeal parameters in singers with and without allergic rhinitis, an observational case control study was conducted. Prior to the pollen season, six grass pollen allergic and six non-allergic semiprofessional singers were exposed to nebulized sham solution and grass pollen extract (HAL°) in rising concentrations. After 3 min, 60xa0min and 24xa0h, nasal and laryngeal complaints were evaluated by the use of a visual analog scale (VAS). Laryngeal parameters like voice appearance (video stroboscopic images), voice range profile and subjective (GRBAS) and objective (jitter, shimmer, H/N, DSI) voice quality were evaluated before provocation, after 60xa0min and 24xa0h. During the pollen season, the allergic singers were re-evaluated. Results showed that in allergic singers both nasal (TNS of 4.0xa0±xa02.4 vs. 0.0xa0±xa00.0, pxa0<xa00.05) and laryngeal complaints (TLS of 1.4xa0±xa01.1 vs. 0.0xa0±xa00.2, pxa0<xa00.05) were induced at 3xa0min after the provocation. The induced laryngeal complaints were the feeling of laryngeal irritation, secretions and globus. No change in voice quality or stroboscopy score was measured. During the pollen season, laryngeal complaints were present (TLS of 2.4xa0±xa02.4) in allergic singers, without evidence for objective voice and laryngeal changes. In conclusion, we here demonstrate the rapid induction of laryngeal complaints in allergic singers by nasal allergen provocation and during the pollen season. There was no subject reported or investigator measured change in voice quality. No change in stroboscopy score was measured.

Vascular endothelial growth factor receptor 1 expression in nasal polyp tissue

Edema represents a key feature of nasal polyp (NP) disease. Members of the vascular endothelial growth factor (VEGF) family may be involved, but the precise role of VEGF‐A, VEGF‐B, placental growth factor (PlGF), and their receptors VEGFR1 and VEGFR2 in NP edema formation remains elusive.