Mycoplasma pneumoniae host–pathogen studies in an air–liquid culture of differentiated human airway epithelial cells

Mycoplasma pneumoniae as an Under- Recognized Agent of Vasculitic Disorders

“…Following an initial droplet infection to the lower respiratory tract below the larynx, M. pneumoniae begins to propagate on the respiratory surface with ciliated epithelium [Krunkosky et al, 2007]. This event facilitates non-specific recognition of the organism by the innate immunity of the host through Toll-like receptors 1, 2, and 6, among which Tolllike receptor 2 plays a major role in initiating intracellular signal transmission [Shimizu, 2005].…”

“…pneumoniae, following its passive transfer into the circulation through the gaps that result from direct yet modest injury to the respiratory epithelial cells, is delivered to the distant vessels and organs, where it activates various inflammatory substances which then elicit vasculitis. These inflammatory substances include interleukin-8, tumor necrosis factor-, macrophage inflammatory peptide-1 [Hardy et al, 2001], intercellular adhesion molecule-1 [Krunkosky et al, 2007], and regulated upon activation, normal T cells expression and secreted [Dakhama et al, 2003], among others. Tumor necrosis factor-has been observed to be induced by M. pneumoniae in vitro from an early period of investigation [Arai et al, 1990;Kita et al, 1992].…”

Current Status of the Mollicute (Mycoplasma) Lung Disease: Pathogenesis, Diagnostics, Treatment and Prevention

“…This structure, termed the tip organelle, functions both as an attachment organelle and as the leading end in gliding motility [Baseman et al, 1995;Razin, 1999;Rottem, 2003;Svenstrup et al, 2002]. Host-pathogen studies in an air-liquid culture of differentiated human airway epithelial cells revealed that the microorganism bounds initially to ciliated epithelial cells, but colonization become more evently distributed over the entire surface with time [Krunkosky et al, 2007]. We recently studied the adherence of U. urealyticum to a respiratory epithelial cell line, as a virulence factor for lung disease.…”

“…As the key processes occurring in all respiratory diseases are the exacerbation of lung inflammation and injury, most of the in vitro models have be en developed to study the inflammatory response mediated primarily by cytokines. Different studies have demonstrated that the release of Interleukin (IL)-2, IL-6 RANTES, ICAM-1, TGF-1 and TNF- by human nasal epithelial cells and peripheral monocytes infected with M. pneumoniae could be implicated in the asthma exacerbation in children and may play a role in the pathogenesis of chronic asthma [Dakhama et al, 2003;Kazachkov et al, 2002;Krunkosky et al, 2007]. Additionally, it has been recently demonstrated that M. pneumoniae infection induces reactive oxygen species and DNA damage in human lung cells [Sun et al, 2008].…”

Lung Diseases - Selected State of the Art Reviews

“…As the key processes occurring in all respiratory diseases are the exacerbation of lung inflammation and injury, most of the in vitro models have been developed to study the inflammatory response mediated primarily by cytokines. Different studies have demonstrated that the release of Interleukin (IL)-2, IL-6 RANTES, ICAM-1, TGF-β1 and TNF- by human nasal epithelial cells and peripheral monocytes infected with M. pneumoniae could be implicated in the asthma exacerbation in children and may play a role in the pathogenesis of chronic asthma [Dakhama et al, 2003;Kazachkov et al, 2002;Krunkosky et al, 2007]. Additionally, it has been recently demonstrated that M. pneumoniae infection induces reactive oxygen species and DNA damage in human lung cells [Sun et al, 2008].…”