Global secretome characterization of A549 human alveolar epithelial carcinoma cells during Mycoplasma pneumoniae infection

Li, Shuxian; Li, Xuejing; Wang, Yingshuo; Yang, Jun; Chen, Zhimin; Shan, Shiguang

doi:10.1186/1471-2180-14-27

Cited by 18 publications

(16 citation statements)

References 61 publications

(84 reference statements)

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“…Studies have shown that M. pneumoniae can invade A549 lung cancer cells, evidenced by its detection in the cytoplasm and nucleus, and the invasive ability depends on the duration and temperature of infection (24). In cell culture in vitro , M. pneumoniae has been shown to invade non-phagocytes, survive for >6 months and synthesize DNA inside cells (7).…”

Section: Direct Damage Mechanismsmentioning

confidence: 99%

Insights into the pathogenesis of Mycoplasma pneumoniae

Liu

et al. 2016

Molecular Medicine Reports

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Mycoplasma are the smallest prokaryotic microbes present in nature. These wall-less, malleable organisms can pass through cell filters, and grow and propagate under cell-free conditions in vitro. Of the pathogenic Mycoplasma Mycoplasma pneumoniae has been examined the most. In addition to primary atypical pneumonia and community-acquired pneumonia with predominantly respiratory symptoms, M. pneumoniae can also induce autoimmune hemolytic anemia and other diseases in the blood, cardiovascular system, gastrointestinal tract and skin, and can induce pericarditis, myocarditis, nephritis and meningitis. The pathogenesis of M. pneumoniae infection is complex and remains to be fully elucidated. The present review aimed to summarize several direct damage mechanisms, including adhesion damage, destruction of membrane fusion, nutrition depletion, invasive damage, toxic damage, inflammatory damage and immune damage. Further investigations are required for determining the detailed pathogenesis of M. pneumoniae.

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Section: Direct Damage Mechanismsmentioning

confidence: 99%

Insights into the pathogenesis of Mycoplasma pneumoniae

Liu

et al. 2016

Molecular Medicine Reports

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“…With the aim to evidence differences between the two groups, this analysis resulted in the identification of 15‐lipoxygenase‐derived ω‐3 and ω‐6 oxylipins as the most prominent different components, thus suggesting their role in allergic inflammation. LC‐MS/MS was also applied by other authors: (i) to compare the level of lysophosphatidic acids (LPAs) in idiopathic pulmonary fibrosis patients versus healthy controls ; (ii) to identify novel biomarkers and pathological mediators of disorder in subjects after subsegmental exposure ; (iii) to characterize the global secretome of A549 human alveolar epithelial carcinoma cells during Mycoplasma pneumoniae infection ; (iv) to compare the proteomes of patients with moderate and stable chronic obstructive pulmonary disease (COPD) versus healthy controls and (v) to identify proteins that differentiate survivors from nonsurvivors of acute respiratory distress syndrome . This differentiation was also investigated by Evans et al.…”

Section: Analysis Of Human Fluids Collected By Invasive Methodsmentioning

confidence: 99%

Recent applications of CE‐ and HPLC‐MS in the analysis of human fluids

et al. 2015

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The present review intends to cover the literature on the use of CE-/LC-MS for the analysis of human fluids, from 2010 until present. It has been planned to provide an overview of the most recent practical applications of these techniques to less extensively used human body fluids, including, bronchoalveolar lavage fluid, synovial fluid, nipple aspirate, tear fluid, breast fluid, amniotic fluid, and cerumen. Potential pitfalls related to fluid collection and sample preparation, with particular attention to sample clean-up procedures, and methods of analysis, from the research laboratory to a clinical setting will also be addressed. While being apparent that proteomics/metabolomics represent the most prominent approaches for global identification/quantification of putative biomarkers for a variety of human diseases, evidence is also provided of the suitability of these sophisticated techniques for the detection of heterogeneous components carried by these fluids.

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“…The first involves engagement with the TLRs, notably TLR2 [128][129][130], leading to the up-regulation of IL-12, IFNγ and other pro-inflammatory cytokines [131,132]. Interestingly, Mycoplasma species infection leads to the generation of a wide range of DAMPs including those normally released following cellular necrosis [133]. Mycoplasma antigens are also capable of activating the inflammasome [134,135], with subsequent elevation of IL-1α, IL-18, and ROS levels and a concomitant decline in the mitochondrial membrane potential [136][137][138].…”

Section: Mycoplasmamentioning

confidence: 99%

The Putative Role of Viruses, Bacteria, and Chronic Fungal Biotoxin Exposure in the Genesis of Intractable Fatigue Accompanied by Cognitive and Physical Disability

Morris¹,

Berk

Walder

et al. 2015

Mol Neurobiol

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Patients who present with severe intractable apparently idiopathic fatigue accompanied by profound physical and or cognitive disability present a significant therapeutic challenge. The effect of psychological counseling is limited, with significant but very slight improvements in psychometric measures of fatigue and disability but no improvement on scientific measures of physical impairment compared to controls. Similarly, exercise regimes either produce significant, but practically unimportant, benefit or provoke symptom exacerbation. Many such patients are afforded the exclusionary, non-specific diagnosis of chronic fatigue syndrome if rudimentary testing fails to discover the cause of their symptoms. More sophisticated investigations often reveal the presence of a range of pathogens capable of establishing life-long infections with sophisticated immune evasion strategies, including Parvoviruses, HHV6, variants of Epstein-Barr, Cytomegalovirus, Mycoplasma, and Borrelia burgdorferi. Other patients have a history of chronic fungal or other biotoxin exposure. Herein, we explain the epigenetic factors that may render such individuals susceptible to the chronic pathology induced by such agents, how such agents induce pathology, and, indeed, how such pathology can persist and even amplify even when infections have cleared or when biotoxin exposure has ceased. The presence of active, reactivated, or even latent Herpes virus could be a potential source of intractable fatigue accompanied by profound physical and or cognitive disability in some patients, and the same may be true of persistent Parvovirus B12 and mycoplasma infection. A history of chronic mold exposure is a feasible explanation for such symptoms, as is the presence of B. burgdorferi. The complex tropism, life cycles, genetic variability, and low titer of many of these pathogens makes their detection in blood a challenge. Examination of lymphoid tissue or CSF in such circumstances may be warranted.

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Global secretome characterization of A549 human alveolar epithelial carcinoma cells during Mycoplasma pneumoniae infection

Cited by 18 publications

References 61 publications

Insights into the pathogenesis of Mycoplasma pneumoniae

Insights into the pathogenesis of Mycoplasma pneumoniae

Recent applications of CE‐ and HPLC‐MS in the analysis of human fluids

The Putative Role of Viruses, Bacteria, and Chronic Fungal Biotoxin Exposure in the Genesis of Intractable Fatigue Accompanied by Cognitive and Physical Disability

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