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Biomedical subjects

G Hens

Publications and source records attributed to G Hens.

17 recordsLinked to original sources

Aggravation of bronchial eosinophilia in mice by nasal and bronchial exposure to Staphylococcus aureus enterotoxin B.

BACKGROUND: The role of bacterial enterotoxins like Staphylococcus aureus enterotoxin B (SEB) in allergic asthma remains unknown. We used a mouse model of airway allergy to study the effects of nasal or bronchial contact with SEB on bronchial allergic inflammation. METHODS: The features of allergic asthma were induced in ovalbumin (OVA)-sensitized mice (days 1-13) by repeated exposures to nebulized OVA (days 33-37). Nasal or bronchial application of SEB was performed on three occasions (days 33-35-37), and the effects on bronchial inflammation, IgE titres and expression levels of mRNA for T helper type 2 cytokines and other inflammatory mediators were evaluated. RESULTS: Both nasal and bronchial SEB enhanced the allergen-induced bronchial inflammation, as reflected by more eosinophilic inflammation in the airway lumen and in bronchial tissue. Aggravation of experimental asthma correlated with higher expression of mRNA for IL-5, IL-4, IFN-gamma, IL-12 p40, eotaxin-1 and TGF-beta in bronchi. In addition, nasal SEB elevated concentrations of IL-4, IL-5 and IFN-gamma in serum and bronchial SEB increased titres of OVA-specific and total IgE in serum. CONCLUSION: Our data illustrate the potential of both nasal as well as bronchial SEB to aggravate several features of allergic asthma in a mouse model.

Acute Disease↗

The nose: gatekeeper and trigger of bronchial disease.

The nose is strategically placed at the entrance of the airway. Nose breathing takes place under physiologic circumstances and protects the lower airways from exposure to unconditioned air and exogenous particles. Alternatively, nasal disease may have a negative impact on lower airway biology, being involved in aggravation of bronchial disease. The interaction between upper and lower airway disease has been recognized for centuries. Due to the increase in prevalence of allergic diseases during the last decades, new interest has been gained in understanding the mechanisms underlying the interaction between rhinitis and asthma. Nowadays, allergic rhinitis and asthma are considered part of a global airway disease, with both diagnostic and therapeutic consequences for every day clinical practice. Besides allergy, other inflammatory conditions of the upper airways are associated with lower airway disease via unknown mechanisms. Viral rhinitis often coincides with exacerbations of bronchial disease, chronic sinus disease with or without nasal polyps frequently relates to bronchial dysfunction and occupational rhinitis and asthma are often present in the same individuals. In spite of the clinical relevance of considering the airway as one organ with major involvement of disease in upper, lower or both parts, many clues to understand the pathology still remain to be explored. This manuscript aims at providing a comprehensive overview of the current knowledge on the interaction between nasal disease and lower airway biology and stresses the importance of further research on this important matter.

Bronchi↗

Chronic maxillary atelectasis.

Chronic maxillary atelectasis (CMA) is characterized by a reduced maxillary sinus volume due to an inward bowing of one or more of the sinus walls. The disorder is probably caused by an obstruction of the maxillary ostium, leading to a persistent negative pressure within the sinus lumen. To provide insight into the epidemiology, pathogenesis and treatment of this disorder, a retrospective study of twelve cases that met radiographic criteria of CMA was carried out. The patients were equally divided between both sexes and were on average 25 years old. Five of the twelve patients were under eighteen years of age. The patients had chronic sinonasal complaints except two, who had a "silent sinus syndrome", characterized by enophthalmos associated with a marked sinus deformation. This is the first report of CMA associated with a benign nasal tumour and also of CMA following cicatrisation due to nasal packing for bleeding after endoscopic sinus surgery. All patients were treated surgically by creating a middle meatal antrostomy, thus restoring sinus ventilation. To conclude, CMA is rare and probably underestimated, especially in the paediatric population. Different entities causing a complete ostial occlusion can lead to CMA. Endoscopically restoring maxillary sinus ventilation is the recommended treatment.

Adult↗

Progeroid syndrome with facial teleangiectatic erythema, posterior subcapsular cataracts, calcification of basal ganglia and atrium septum defect type 2.

In this report we present the long-term follow-up findings in a young female born to consanguineous parents with the unique association of (1) a progeroid syndrome, (2) facial dysmorphism with relative microcephaly, triangular face, retrognathism and skin erythema, (3) bilateral posterior cataracts, (4) basal ganglia calcifications and (5) atrium septum defect type 2. Intelligence is borderline. Clinical evolution after normal puberty was positive with regression of the facial erythematous changes. Over the years differential diagnosis included progeria, hypohidrotic ectodermal dysplasia, Rothmund-Thompson syndrome, Cockayne syndrome, Bloom syndrome, but the clinical spectrum of abnormalities and the evolution with age were not compatible with one of these diagnoses. Parental consanguinity is in favour of autosomal recessive inheritance.

Abnormalities, Multiple↗