Spontaneous development of otitis media in plasminogen-deficient mice

Eriksson, Per; Li, Jinan; Ny, Tor; Hellström, Sten

doi:10.1016/j.ijmm.2006.04.002

Cited by 31 publications

(28 citation statements)

References 60 publications

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“…It should also be noted that plg-deficient mice are more susceptible to the development of otitis media [18]. This could also be seen in the current study, in which four mice developed otitis during the experimental period whereas none of the wt mice did so.…”

Section: Discussionsupporting

confidence: 83%

“…One may speculate that the macrophages and neutrophils pouring out into the myringotomized PT in the plg-deficient mice are unable to function and subsequently new inflammatory cells are continuously recruited to the wound area. Similar interpretations have also been made regarding these inflammatory cells in other plg-deficient wound models [18]. The plg activator (PA) system has been shown to play an important role during wound healing of skin [6].…”

Section: Discussionsupporting

confidence: 53%

“…This could also be seen in the current study, in which four mice developed otitis during the experimental period whereas none of the wt mice did so. Eriksson et al [18] explained the increased susceptibility with a possible decreased functionality of the inflammatory cells used in the host defense mechanism for clearing pathogens out of the middle ear. Their hypothesis is aligned with our speculation on the activation and functionality of inflammatory cells during the healing of TM perforations.…”

Section: Discussionmentioning

confidence: 99%

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Lack of plasminogen does not alter the early inflammatory response following a tympanic membrane perforation: a study in plasminogen-deficient mice

Prestwich¹,

Eriksson³

et al. 2008

Acta Oto-Laryngologica

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Perforation of the TM resulted in early otomicroscopic changes of the pars flaccida (PF) in both genotypes. Infiltration of inflammatory cells to PF and the presence of edema occurred as early as 6 h after the perforation was made, in both plg-deficient and wt mice. Morphometry did not reveal any significant differences between the genotypes concerning the occurrence of inflammatory cells. In contrast to the PF, the PT showed only sparse reactions during the experimental period. Furthermore, the migration pattern of keratinocytes did not differ between the genotypes throughout the experimental period.

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Section: Discussionsupporting

confidence: 83%

Section: Discussionsupporting

confidence: 53%

Section: Discussionmentioning

confidence: 99%

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Lack of plasminogen does not alter the early inflammatory response following a tympanic membrane perforation: a study in plasminogen-deficient mice

Prestwich¹,

Eriksson³

et al. 2008

Acta Oto-Laryngologica

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“…There are a range of in vivo models that simulate chronic infections, such as surface wounds [75,76], subcutaneous wounds [77,78], implant-related (such as catheter, orthopaedic, and dental) [79][80][81][82][83], otitis media [84][85][86], and CF [87][88][89][90] to name but a few. As with all models, some are deemed more applicable than others.…”

Section: In Vivo Investigation Of Biofilmsmentioning

confidence: 99%

The Limitations of In Vitro Experimentation in Understanding Biofilms and Chronic Infection

Roberts

Kragh

Bjarnsholt

et al. 2015

Journal of Molecular Biology

171

153

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We have become increasingly aware that during infection, pathogenic bacteria often grow in multicellular biofilms which are often highly resistant to antibacterial strategies. In order to understand how biofilms form and contribute to infection, in vitro biofilm systems such as microtitre plate assays and flow cells, have been heavily used by many research groups around the world. Whilst these methods have greatly increased our understanding of the biology of biofilms, it is becoming increasingly apparent that many of our in vitro methods do not accurately represent in vivo conditions. Here we present a systematic review of the most widely used in vitro biofilm systems, and we discuss why they are not always representative of the in vivo biofilms found in chronic infections. We present examples of methods that will help us to bridge the gap between in vitro and in vivo biofilm work, so that our bench-side data can ultimately be used to improve bedside treatment.

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“…Furthermore, targeted and induced mutagenesis identified mouse lines that model the pathology of OME (Eya4 tm1Jse ) and CSOM (Fbxo11 transcription factor Eya4 and ubiquitination factor Fxbo11 cause dysmorphologies of the Eustachian tube (ET), suggesting that impaired aeration of the middle ear cavity and clearance of the middle ear secretions is the underlying cause of the OM. Inflammation of the middle ear was also observed in the N-ethyl-N-nitrosourea induced Hush Puppy mutant, in plasminogen-deficient mice (Plg tm1Dco ), and mice of the LP/J inbred strain further underscoring the diverse and complex etiology of otitis media (22)(23)(24)(25).…”

mentioning

confidence: 91%

Ectopic Mineralization in the Middle Ear and Chronic Otitis Media with Effusion Caused by RPL38 Deficiency in the Tail-short (Ts) Mouse

Noben-Trauth

Latoche

2011

Journal of Biological Chemistry

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Inflammation of the middle ear cavity (otitis media) and the abnormal deposition of bone at the otic capsule are common causes of conductive hearing impairment in children and adults. Although a host of environmental factors can contribute to these conditions, a genetic predisposition has an important role as well. Here, we analyze the Tail-short (Ts) mouse, which harbors a spontaneous semi-dominant mutation that causes skeletal defects and hearing loss. By genetic means, we show that the Ts phenotypes arise from an 18-kb deletion/insertion of the Rpl38 gene, encoding a ribosomal protein of the large subunit. We show that Ts mutants exhibit significantly elevated auditory-brain stem response thresholds and reduced distortion-product otoacoustic emissions, in the presence of normal endocochlear potentials and typical inner ear histology suggestive of a conductive hearing impairment. We locate the cause of the hearing impairment to the middle ear, demonstrating over-ossification at the round window ridge, ectopic deposition of cholesterol crystals in the middle ear cavity, enlarged Eustachian tube, and chronic otitis media with effusion all beginning at around 3 weeks after birth. Using specific antisera, we demonstrate that Rpl38 is an ϳ8-kDa protein that is predominantly expressed in mature erythrocytes. Finally, using an Rpl38 cDNA transgene, we rescue the Ts phenotypes. Together, these data present a previously uncharacterized combination of interrelated middle ear pathologies and suggest Rpl38 deficiency as a model to dissect the causative relationships between neo-ossification, cholesterol crystal deposition, and Eustachian tubes in the etiology of otitis media.

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Spontaneous development of otitis media in plasminogen-deficient mice

Cited by 31 publications

References 60 publications

Lack of plasminogen does not alter the early inflammatory response following a tympanic membrane perforation: a study in plasminogen-deficient mice

Lack of plasminogen does not alter the early inflammatory response following a tympanic membrane perforation: a study in plasminogen-deficient mice

The Limitations of In Vitro Experimentation in Understanding Biofilms and Chronic Infection

Ectopic Mineralization in the Middle Ear and Chronic Otitis Media with Effusion Caused by RPL38 Deficiency in the Tail-short (Ts) Mouse

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