Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040586 (tracheobronchitis)
 449 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mycoplasma pneumoniae is a small bacterium without a cell wall that causes tracheobronchitis and atypical pneumonia in humans. It has also been associated with chronic conditions, such as arthritis, and extrapulmonary complications, such as encephalitis. Although the interaction of mycoplasmas with respiratory epithelial cells is a critical early phase of pathogenesis, little is known about the cascade of events initiated by infection of respiratory epithelial cells by mycoplasmas. Previous studies have shown that M. pneumoniae can induce proinflammatory cytokines in several different study systems including cultured murine and human monocytes. In this study, we demonstrate that M. pneumoniae infection also induces proinflammatory cytokine expression in A549 human lung carcinoma cells. Infection of A549 cells resulted in increased levels of interleukin-8 (IL-8) and tumor necrosis factor alpha mRNA, and both proteins were secreted into culture medium. IL-1 beta mRNA also increased after infection and IL-1 beta protein was synthesized, but it remained intracellular. In contrast, levels of IL-6 and gamma interferon mRNA and protein remained unchanged or undetectable. Using protease digestion and antibody blocking methods, we found that M. pneumoniae cytoadherence is important for the induction of cytokines. On the other hand, while M. pneumoniae protein synthesis and DNA synthesis do not appear to be prerequisites for the induction of cytokine gene expression, A549 cellular de novo protein synthesis is responsible for the increased cytokine protein levels. These results suggest a novel role for lung epithelial cells in the pathogenesis of M. pneumoniae infection and provide a better understanding of M. pneumoniae pathology at the cellular level.
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PMID:Regulation of proinflammatory cytokines in human lung epithelial cells infected with Mycoplasma pneumoniae. 1206 6

Interleukin-1beta (IL-1beta) is a major proinflammatory cytokine that is involved in many important cellular functions such as proliferation, differentiation, and activation of different cell types. Its mature form is released from the cells in response to various bacterial and viral infections, and it plays a significant role in host defense. Mycoplasma pneumoniae is a small bacterium without a cell wall that causes tracheobronchitis and atypical pneumonia in humans following attachment to respiratory epithelium, as well as extrapulmonary infections. Very little is known about the role of cytokines in pathogenesis or the response of target cells to M.pneumoniae attachment. The purpose of this study was to investigate the ability of M. pneumoniae to induce IL-1beta in human lung epithelial carcinoma A549 and in human monocytic U937 cell lines. Following M. pneumoniae infection, both IL-1beta mRNA and protein were induced in A549 cells vs. no induction in uninfected cells; however, the protein remained inside the A549 cells. Similarly, M. pneumoniae infection strongly increased mRNA and extracellular protein levels in U937 cells, which unlike A549 cells did exhibit baseline constitutive levels. De novo IL-1beta protein expression was verified by cycloheximide studies. M. pneumoniae infection did not affect constitutive caspase-1 mRNA or protein levels in either cell line. Reduced caspase-1 activity in A549 cell lysates suggests the presence of an endogenous caspase-1 inhibitory component in the A549 cells. These collective data confirm previous studies that show that M. pneumoniae is a potent inducer of cytokines following adherence to host target cells, and establish that IL-1beta release in response to M. pneumoniae infection is cell-type specific, thus emphasizing the importance of carefully considering multiple cell types in M. pneumoniae pathogenesis studies involving both immune cells and cytokine release patterns.
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PMID:Interleukin-1beta responses to Mycoplasma pneumoniae infection are cell-type specific. 1262 Mar 81

In their review article the authors overview the primary and secondary pulmonary complications of rheumatoid arthritis with the help of bibliographic data. They emphasize the pulmonological complications of disease modifying antirheumatic drugs used for the pharmaceutical therapy of rheumatoid arthritis, of which they discuss the methotrexate induced pulmonary diseases. Methotrexate participates nearly in all of additive double and triple--O'Dell-scheme--combined disease modifying antirheumatic drugs therapy. Because of that, the early detection of drug-induced pulmonological complications is important. For rheumatologists the treatment of methotrexate resistant rheumatoid arthritis is always getting a higher and higher challenge. Biological therapeutical drugs act as cytokine antagonists, by blocking TNF-alpha and, compared to disease modifying antirheumatic drugs, they can more effectively inhibit the progression of the disease. These are the biological response modifiers. Their main representatives are infliximab, adalimumab, and etanercept. At the end, the authors discuss secondary pulmonary complications caused by biological response modifiers, e.g. the biological response modifiers associated pulmonary tuberculosis, bacterial tracheobronchitis, bacterial pneumonia, bronchiectasia, pulmonary oedema, rapid fibrosing alveolitis, and coccidioidomycosis. At 3% of patients with rheumatoid arthritis, treated with biological response modifiers, who live in Arizona, California, Nevada, pulmonary and systemic mycosis--coccidioidomycosis can appear with a 15% of mortality. As a consequence of frequent earthquakes, the spores getting into the air from the ground infect immunosuppressed patients treated with biological response modifiers. The authors draw attention to the fact that patients who receive biological therapy and travel to the above-mentioned endemic or earthquake-active regions, have a potential high risk, so it is indispensable that they are informed by the doctor. Testing and use of newer and newer groups of biological response modifiers are expected in the near future in the therapy of rheumatoid arthritis. Nowadays--in patients, who are non-reactive for TNF-alpha inhibitor treatment--the use of B-lymphocyte inhibitor rituximab, characteristic in non-Hodgkin lymphoma therapy is possible. The pulmonary complications of rheumatoid arthritis therapy of that cytokine are not known yet. Today, antirheumatic therapy results in a significant improvement of patients' life-quality, whilst the more and more modern therapeutical methods cause more complications.
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PMID:[The pulmonological manifestations of rheumatoid arthritis]. 1861 67

Bacterial pneumonia and tracheobronchitis are diagnosed frequently following lung transplantation. The diseases share clinical signs of inflammation and are often difficult to differentiate based on culture results. Microbiome and host immune-response signatures that distinguish between pneumonia and tracheobronchitis are undefined. Using a retrospective study design, we selected 49 bronchoalveolar lavage fluid samples from 16 lung transplant recipients associated with pneumonia (n = 8), tracheobronchitis (n = 12) or colonization without respiratory infection (n = 29). We ensured an even distribution of Pseudomonas aeruginosa or Staphylococcus aureus culture-positive samples across the groups. Bayesian regression analysis identified non-culture-based signatures comprising 16S ribosomal RNA microbiome profiles, cytokine levels and clinical variables that characterized the three diagnoses. Relative to samples associated with colonization, those from pneumonia had significantly lower microbial diversity, decreased levels of several bacterial genera and prominent multifunctional cytokine responses. In contrast, tracheobronchitis was characterized by high microbial diversity and multifunctional cytokine responses that differed from those of pneumonia-colonization comparisons. The dissimilar microbiomes and cytokine responses underlying bacterial pneumonia and tracheobronchitis following lung transplantation suggest that the diseases result from different pathogenic processes. Microbiomes and cytokine responses had complementary features, suggesting that they are closely interconnected in the pathogenesis of both diseases.
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PMID:Looking Beyond Respiratory Cultures: Microbiome-Cytokine Signatures of Bacterial Pneumonia and Tracheobronchitis in Lung Transplant Recipients. 2669 65