{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,13]],"date-time":"2026-10-13T13:43:41Z","timestamp":1791899021204,"version":"4.3.4"},"reference-count":25,"publisher":"Microbiology Society","issue":"1","funder":[{"DOI":"10.13039\/100006686","name":"Miami University","doi-asserted-by":"crossref","id":[{"id":"10.13039\/100006686","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2021,1,1]]},"abstract":"\n Introduction.<\/jats:bold> Infections with the respiratory pathogen \n \n Mycoplasma pneumoniae<\/jats:ext-link>\n <\/jats:named-content>\n <\/jats:italic> are often chronic, recurrent and resistant, persisting after antibiotic treatment. \n \n M. pneumoniae<\/jats:ext-link>\n <\/jats:named-content>\n <\/jats:italic> grown on glass forms protective biofilms, consistent with a role for biofilms in persistence. These biofilms consist of towers of bacteria interspersed with individual adherent cells.<\/jats:p>\n \n Hypothesis\/Gap Statement.<\/jats:bold> A tissue culture model for \n \n M. pneumoniae<\/jats:ext-link>\n <\/jats:named-content>\n <\/jats:italic> biofilms has not been described or evaluated to address whether growth, development and resistance properties are consistent with persistence in the host. Moreover, it is unclear whether the \n \n M. pneumoniae<\/jats:ext-link>\n <\/jats:named-content>\n <\/jats:italic> cells in the biofilm towers and individual bacterial cells have distinct roles in disease.<\/jats:p>\n \n Aim.<\/jats:bold> We evaluated the properties of biofilms of \n \n M. pneumoniae<\/jats:ext-link>\n <\/jats:named-content>\n <\/jats:italic> grown on the immortalized human bronchial epithelial cell line BEAS-2B in relation to persistence in the host. We observed nucleation of biofilm towers and the disposition of individual cells in culture, leading to a model of how tower and individual cells contribute to infection and disease.<\/jats:p>\n \n Methodology.<\/jats:bold> With submerged BEAS-2B cells as a substrate, we evaluated growth and development of \n \n M. pneumoniae<\/jats:ext-link>\n <\/jats:named-content>\n <\/jats:italic> biofilms using scanning electron microscopy and confocal laser scanning microscopy. We characterized resistance to erythromycin and complement using minimum inhibitory concentration assays and quantification of colony forming units. We monitored biofilm tower formation using time-lapse microscopic analysis of host-cell-free \n \n M. pneumoniae<\/jats:ext-link>\n <\/jats:named-content>\n <\/jats:italic> cultures.<\/jats:p>\n \n Results.<\/jats:bold> Bacteria grown on host cells underwent similar development to those grown without host cells, including tower formation, rounding and incidence of individual cells outside towers. Erythromycin and complement significantly reduced growth of \n \n M. pneumoniae<\/jats:ext-link>\n <\/jats:named-content>\n <\/jats:italic>. Towers formed exclusively from pre-existing aggregates of bacteria. We discuss a model of the \n \n M. pneumoniae<\/jats:ext-link>\n <\/jats:named-content>\n <\/jats:italic> biofilm life cycle in which protective towers derive from pre-existing aggregates, and generate individual cytotoxic cells.<\/jats:p>\n \n Conclusion<\/jats:bold>\n \n .<\/jats:bold> M. pneumoniae<\/jats:italic> can form protective biofilms in a tissue culture model, implicating biofilms in chronic infections, with aggregates of \n \n M. pneumoniae<\/jats:ext-link>\n <\/jats:named-content>\n <\/jats:italic> cells being important for establishing infections.<\/jats:p>","DOI":"10.1099\/jmm.0.001266","type":"journal-article","created":{"date-parts":[[2020,11,10]],"date-time":"2020-11-10T15:47:23Z","timestamp":1605023243000},"source":"Crossref","is-referenced-by-count":17,"title":["Modelling persistent Mycoplasma pneumoniae biofilm infections in a submerged BEAS-2B bronchial epithelial tissue culture model"],"prefix":"10.1099","volume":"70","author":[{"given":"Monica","family":"Feng","sequence":"first","affiliation":[{"name":"Present address: Department of Medicine, Albert Einstein Medical College, Bronx, NY 10461, USA"},{"name":"Department of Microbiology, Miami University, Oxford, OH 45056, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Amanda C.","family":"Burgess","sequence":"additional","affiliation":[{"name":"Department of Microbiology, Miami University, Oxford, OH 45056, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rachel R.","family":"Cuellar","sequence":"additional","affiliation":[{"name":"Department of Microbiology, Miami University, Oxford, OH 45056, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3673-8149","authenticated-orcid":false,"given":"Nathan R.","family":"Schwab","sequence":"additional","affiliation":[{"name":"Department of Microbiology, Miami University, Oxford, OH 45056, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2606-5481","authenticated-orcid":false,"given":"Mitchell F.","family":"Balish","sequence":"additional","affiliation":[{"name":"Department of Microbiology, Miami University, Oxford, OH 45056, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"345","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1128\/CMR.00114-16"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1128\/JCM.00400-10"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.3109\/00365549209052607"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1007\/s00203-011-0749-y"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1099\/mic.0.064782-0"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1016\/j.ijmm.2018.01.007"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1099\/mic.0.000928"},{"key":"R8","volume-title":"Immunology of Biofilms 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