Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0010200 (cough)
 23,843 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Southwest Metropolitan Mexico City (SWMMC) preadolescent children have been exposed to a highly polluted urban atmosphere most of their lives. The main objective of this study was to determine by nasal lavage (NAL) the acute inflammatory nasal influx elicited in these children upon exposure to three different polluted days. Ozone, the main criteria pollutant for SWMMC, varied both in the number of hours above the National Ambient Air Quality Standard (NAAQS), which is 0.12 ppm as a 1-h maximum concentration not to be exceeded more than once per year, and in the maximal concentrations in the preceding three NAL sampling dates. Nasal neutrophilic influx, the surface expression of the B2 integrin CD11b on the nasal polymorphonuclear leukocytes (PMNs), rhinoscopic findings, respiratory symptoms, and nasal cytologies were evaluated in the 38 exposed children and in the 28 control children living in a nonpolluted Pacific coast port. SWMMC children had an average daily outdoor exposure of 7.7 h and complained of nasal mucus secretion, epistaxis, intermittent nasal obstruction, diurnal cough episodes, and chest discomfort. Nasal mucosal atrophy by rhinoscopy was present in 37/38, and all children had an abnormal nasal cytology. Exposed children had significantly higher nasal PMNs and nasal PMN-CD11b expression than controls. PMN median values in exposed children were higher than controls on all sampling dates (November 12, p < .001; November 17, p < .001; and November 24, p < .00001). Interestingly, a lower nasal neutrophilic response (p < .0004) was recorded in the SWMMC children 18 h after exposure to the highest O3 concentrations (up to 0.307 ppm) and the largest number of hours with O3 > 0.12 ppm (7 h). The question of a competing inflammatory response at the bronchioalveolar level with structural damage is raised. These NAL findings underscore the need to restrict outdoor activity in SWMMC children during the months of greater potential exposure to ozone.
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PMID:Nasal inflammatory responses in children exposed to a polluted urban atmosphere. 764 30

Transmission of Mycobacterium tuberculosis from one individual to another usually is associated with episodes of coughing. The bacteria leave the environment of the lung cavity of the infected person and travel in droplets to reach the recipient's respiratory tract. Therefore, at the time that the bacteria encounter alveolar cells (macrophages and epithelial cells) in the new host, they express virulence determinants that are regulated by the environmental conditions in the infected person. To determine if those environmental conditions encountered in the lung cavity (hyperosmolarity, acidic pH, and low oxygen tension, among others) would influence the uptake of M. tuberculosis by the recipient's alveolar macrophages, M. tuberculosis H37Rv was incubated under several conditions for different periods of time, washed at 4 degrees C, and used to infect human monocyte-derived macrophages. While increased osmolarity had no effect on M. tuberculosis uptake compared to the uptake of bacteria grown on 7H10 Middlebrook medium, both acidic pH and anaerobiosis increased the uptake of the H37Rv strain four- to sixfold. Using anti-CD11b receptor blocking antibodies or mannoside to inhibit the uptake of M. tuberculosis by macrophages, we determined that while uptake of M. tuberculosis cultured on 7H10 medium was inhibited 77% +/- 6% in the presence of anti-CD11b antibody, the antibody had no effect on the uptake of M. tuberculosis incubated at pH 6.0 and was associated with 27% inhibition of M. tuberculosis previously exposed to anaerobic conditions. The mannose receptor was also not involved with invasion after exposure to acidic conditions, and mannoside resulted in only 32% inhibition of uptake by macrophages of M. tuberculosis exposed to anaerobiosis. Uptake by macrophages also resulted in the secretion of significantly lower amounts of interleukin-12 and tumor necrosis factor alpha than that by macrophages infected with a strain cultured under laboratory conditions. M. tuberculosis cultured under the pH and oxygen concentration found in the granuloma expresses a large number of proteins that are different from the proteins expressed by bacteria grown under laboratory conditions. The results suggest that M. tuberculosis in vivo may be adapted to gain access to the intracellular environment in a very efficient fashion and may do so by using different receptors from the complement and mannose receptors.
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PMID:Mycobacterium tuberculosis uptake by recipient host macrophages is influenced by environmental conditions in the granuloma of the infectious individual and is associated with impaired production of interleukin-12 and tumor necrosis factor alpha. 1237 1

Bordetella pertussis, the causative agent of whopping cough, produces an adenylate cyclase toxin (CyaA) that plays a key role in the host colonization by targeting innate immune cells which express CD11b/CD18, the cellular receptor of CyaA. CyaA is also able to invade non-phagocytic cells, via a unique entry pathway consisting in a direct translocation of its catalytic domain across the cytoplasmic membrane of the cells. Within the cells, CyaA is activated by calmodulin to produce high levels of cyclic adenosine monophosphate (cAMP) and alter cellular physiology. In this study, we explored the effects of CyaA toxin on the cellular and molecular structure remodeling of A549 alveolar epithelial cells. Using classical imaging techniques, biochemical and functional tests, as well as advanced cell mechanics method, we quantify the structural and functional consequences of the massive increase of intracellular cyclic AMP induced by the toxin: cell shape rounding associated to adhesion weakening process, actin structure remodeling for the cortical and dense components, increase in cytoskeleton stiffness, and inhibition of migration and repair. We also show that, at low concentrations (0.5 nM), CyaA could significantly impair the migration and wound healing capacities of the intoxicated alveolar epithelial cells. As such concentrations might be reached locally during B. pertussis infection, our results suggest that the CyaA, beyond its major role in disabling innate immune cells, might also contribute to the local alteration of the epithelial barrier of the respiratory tract, a hallmark of pertussis.
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PMID:Functional and structural consequences of epithelial cell invasion by Bordetella pertussis adenylate cyclase toxin. 3239 46