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Otitis media (OM), or middle ear inflammation, is the most common paediatric disease and leads to significant morbidity. Although understanding of underlying disease mechanisms is hampered by complex pathophysiology it is clear that epithelial abnormalities underpin the disease. There is currently a lack of a well-characterised in vitro model of the middle ear (ME) epithelium that replicates the complex cellular composition of the middle ear. Here, we report the development of a novel in vitro model of mouse middle ear epithelial cells (mMECs) at an air–liquid interface (ALI) that recapitulates the characteristics of the native murine ME epithelium. We demonstrate that mMECs undergo differentiation into the varied cell populations seen within the native middle ear. Proteomic analysis confirmed that the cultures secrete a multitude of innate defence proteins from their apical surface. We showed that the mMECs supported the growth of the otopathogen, nontypeable Haemophilus influenzae (NTHi), suggesting that the model can be successfully utilised to study host–pathogen interactions in the middle ear. Overall, our mMEC culture system can help to better understand the cell biology of the middle ear and improve our understanding of the pathophysiology of OM. The model also has the potential to serve as a platform for validation of treatments designed to reverse aspects of epithelial remodelling that underpin OM development.

Summary Background During 2016–2018, 15 critically ill neonatal foals with acute respiratory distress associated with Chlamydia psittaci infection were presented to three referral hospitals in New South Wales. Chlamydia psittaci has not previously been associated with the development of neonatal respiratory disease. Objectives To investigate and describe the clinical features and outcome of C. psittaci infection in neonatal foals. Study design Multicentre retrospective case series. Methods The clinical, clinicopathological, necropsy and histological features of 15 foals with confirmed C. psittaci infection were reviewed and reported. Results Thirteen foals with C. psittaci infection died or were subjected to euthanasia within 36 h of hospitalisation and two foals survived to discharge. Findings during post‐mortem examination of nonsurviving foals included bronchopneumonia, pulmonary congestion, hepatic congestion and hepatic inflammation. Detection of C. psittaci was achieved using polymerase chain reaction (PCR) testing of swabs of nasal secretions (4/6) and rectal mucosa (5/7) from live foals, lung tissues of foals at necropsy (11/14) and foetal membranes (4/5). Main limitations Small numbers of confirmed cases of neonatal C. psittaci infection and inconsistent sampling methods. Conclusions Chlamydia psittaci should be considered a differential diagnosis for neonatal foals with signs of severe systemic disease, including equine neonatal acute respiratory distress syndrome (EqNARDS). Chlamydia psittaci is a zoonotic pathogen and a personal protective equipment (PPE) should be worn for the management of foals with suspected or confirmed infection.

Otitis Media (OM) is characterized by epithelial abnormalities and defects in innate immunity in the middle ear (ME). Although, BPIFA1, a member of the BPI fold containing family of putative innate defence proteins is abundantly expressed by the ME epithelium and SNPs in Bpifa1 have been associated with OM susceptibility, its role in the ME is not well characterized. We investigated the role of BPIFA1 in protection of the ME and the development of OM using murine models. Loss of Bpifa1 did not lead to OM development. However, deletion of Bpifa1 in Evi1Jbo/+ mice, a model of chronic OM, caused significant exacerbation of OM severity, thickening of the ME mucosa and increased collagen deposition, without a significant increase in pro-inflammatory gene expression. Our data suggests that BPIFA1 is involved in maintaining homeostasis within the ME under steady state conditions and its loss in the presence of inflammation, exacerbates epithelial remodelling leading to more severe OM.