The cartilage of the trachea provides a flexible rigidity that maintains an open airway to and from the lungs at all times. It is divided into three lobes, an upper, middle, and a lower, by two fissures, one oblique and one horizontal. Type I cells provide 95% of the surface area of each alveoli and are flat “ squamous “, and Type II cells generally cluster in the corners of the alveoli and have a cuboid al shape. 9 Despite this, cells occur in a roughly equal ratio of 1:1 or 6:4. 7 9 types I are squamous epithelial cells that make up the alveolar wall structure. The diaphragm contracts and pushes itself into the abdominal cavity, increasing the volume of the thoracic cavity and expanding the lungs to draw in fresh atmospheric air. Alveoli are found in small clusters called alveolar lacs at the end of the terminal bronchiole. The heart then sends the oxygenated filled with oxygen blood out to all the cells in the body. The interstitium walls between air lacs become scarred, making the lungs stiff and causing shortness of breath. The visceral pleura forms the inner layer of the membrane covering the outside surface of the lungs. The lungs together weigh approximately 1.3 kilograms 2.9 lb, and the right is heavier.
As part of the research group’s work to explore the roles of sugar molecules in health and disease, they found that keratan sulfate, a large negatively charged saccharide found in the small airway of the lung, is decreased in mice that have been exposed to cigarette smoke. They wondered if this decrease might be associated with the damage that smoking causes to the lung. Taniguchi says, “We are not absolutely sure of the mechanism through which smoking leads to a reduction in keratan sulfate, but felt that clearly the reduction is important in thinking about glycan-based strategies for combating emphysema and COPD.” They wondered whether the keratan sulfate might be playing a protective Thanking You role in COPD. To test the hypothesis, they prepared a repeating disaccharide element of keratan sulfate, named L4, and administered it into two mouse models of emphysema — one a model of emphysema triggered by the enzyme elastase, and the other an exacerbation of smoking-induced emphysema triggered by LPS, a toxin found in bacterial cell walls. In the first model, they found that that treatment with L4 prevented destruction of the alveoli — the small air sacs in lungs that are used to exchange gases, and in addition that it reduced the infiltration of a type of Ta white blood cell called neutrophils, which is symptomatic of an inflammatory response, as well as levels of inflammatory cytokines and tissue-degrading enzymes. Although L4 was shown to inhibit these enzymes, they did not find any ability of L4 to directly reduce the production of cytokines or reactive oxygen species, so concluded that the action was also being done indirectly, through mechanisms involving the neutrophils. In the exacerbation model, they found that the L4 administration prevented the influx of neutrophils. According to Taniguchi, “We found that L4 was as effective as dexamethasone in reducing neutrophil infiltration. This is very exciting, because dexamethasone, the treatment currently used for COPD, is a steroid medication that can have serious side effects and can in some cases make the outcome worse.
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