Bordetella pseudohinzii targets cilia and impairs tracheal cilia-driven transport in naturally acquired infection in mice.

Several species of the Gram-negative genus Bordetella are the cause of respiratory infections in mammals and birds, including whooping cough (pertussis) in humans. Very recently, a novel atypical species, Bordetella pseudohinzii, was isolated from laboratory mice. These mice presented no obvious clinical symptoms but elevated numbers of neutrophils in bronchoalveolar lavage fluid and inflammatory signs in histopathology. We noted that this species can occur at high prevalence in a mouse facility despite regular pathogen testing according to the FELASA-recommendations. Affected C57BL/6 J mice had, in addition to the reported pulmonary alterations, tracheal inflammation with reduced numbers of ciliated cells, slower ciliary beat frequency, and largely (>50%) compromised cilia-driven particle transport speed on the mucosal surface, a primary innate defence mechanism. In an in vitro-model, Bordetella pseudohinzii attached to respiratory kinocilia, impaired ciliary function within 4 h and caused epithelial damage within 24 h. Regular testing for this ciliotropic Bordetella species and excluding it from colonies that provide mice for lung research shall be recommended. On the other hand, controlled colonization and infection with Bordetella pseudohinzii may serve as an experimental model to investigate mechanisms of mucociliary clearance and microbial strategies to escape from this primary innate defence response.

Electrophysiological characterization of chloride secretion across the jejunum and colon of pigs as affected by age and weaning.

Hypersecretion of chloride can cause diarrhea, a disease frequently occurring in young pigs, particularly around weaning. We investigated the contribution of different channels to intestinal Cl(-) secretion as influenced by age and weaning. Jejunal and colonic epithelia from 4-month-old pigs and 4-week-old piglets were incubated in Ussing chambers and stimulated by carbachol and forskolin. Changes in short-circuit currents were taken as measure of electrogenic net Cl(-) secretion. DIDS or NPPB served to inhibit Ca-activated Cl(-)-channels and outwardly rectifying Cl(-)-channels (ORCC) or cystic fibrosis transmembrane regulator (CFTR), respectively. Depolarizing the basolateral membrane allowed to examine the influence of K(+)-channels on Cl(-) secretion. Forskolin-stimulated Cl(-) secretion was mediated by CFTR. ORCC were not involved. Carbachol-induced Cl(-) secretion could be ascribed to an enhanced driving force due to the opening of K(+)-channels, whereas Ca-dependent Cl(-) channels seemed not to be involved. In jejunum, piglets showed higher Cl(-) secretion than pigs. Two days after weaning forskolin induced an I (sc) overshoot and a faster increase in G (t). In colon, Cl(-) secretion was neither influenced by age nor by weaning. The data suggest a disposition of porcine jejunum for a higher Cl(-) secretion in young and freshly weaned piglets, which might be a natural defense mechanism as well as a predisposing factor for diarrhea.