Skip to main content Accessibility help
×
Hostname: page-component-78c5997874-94fs2 Total loading time: 0 Render date: 2024-11-05T16:33:47.481Z Has data issue: false hasContentIssue false

20 - Lung

from PART V - INFLAMMATORY DISEASES/HISTOLOGY

Published online by Cambridge University Press:  05 April 2014

Bruce D. Levy
Affiliation:
Brigham and Women's Hospital and Harvard Medical School
Charles N. Serhan
Affiliation:
Harvard Medical School
Peter A. Ward
Affiliation:
University of Michigan, Ann Arbor
Derek W. Gilroy
Affiliation:
University College London
Get access

Summary

Inflammation in the lung is common in both physiologic responses as well as many respiratory illnesses. In particular, chronic inflammation is associated with a variety of prevalent disorders, including asthma, chronic obstructive pulmonary disease, bronchiectasis, and interstitial lung diseases [1 – 3]. For purposes of host defense, an overexuberant inflammatory response can also lead to respiratory disorders. For example, inhalation of pathogens, toxins, or specific allergens initiates an acute inflammatory response that characterizes acute exacerbations of bronchiectasis, COPD, and asthma [1, 4]. Perhaps the most extensively investigated example of acute inflammation and its spontaneous resolution is pneumonia. In this chapter, a common clinical presentation of pneumonia is provided with examples of its radiographic appearance and histology during both the initiation and resolution phases of the illness.

Bea Coffin is a 56-year-old woman who presents with a new cough and dyspnea. She has felt ill for about 3 days. Her cough is productive of blood-tinged green phlegm. She has also had fevers, chills, and sweats that are getting worse. The symptoms began with the sudden onset of right sided chest pain that makes it difficult to take a deep breath. She has tried acetaminophen and an expectorant, but these interventions have not been successful in controlling her symptoms. She is a lifelong nonsmoker and has no significant past medical history.

Type
Chapter
Information
Publisher: Cambridge University Press
Print publication year: 2010

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

1. Cowburn, A.S., Condliffe, A.M., Farahi, N., Summers, C., and Chilvers, E.R. 2008. Advances in neutrophil biology: clinical implications. Chest 134:606–612.CrossRefGoogle ScholarPubMed
2. Galli, S.J., Tsai, M., and Piliponsky, A.M. 2008. The development of allergic inflammation. Nature 454:445–454.CrossRefGoogle ScholarPubMed
3. Sutherland, E.R., and Cherniack, R.M. 2004. Management of chronic obstructive pulmonary disease. N Engl J Med 350:2689–2697.CrossRefGoogle ScholarPubMed
4. Kim, E.Y., Battaile, J.T., Patel, A.C., et al. 2008. Persistent activation of an innate immune response translates respiratory viral infection into chronic lung disease. Nat Med 14:633–640.CrossRefGoogle ScholarPubMed
5. Mizgerd, J.P. 2008. Acute lower respiratory tract infection. N Engl J Med 358:716–727.CrossRefGoogle ScholarPubMed
6. Armstrong, G.L., Conn, L.A., and Pinner, R.W. 1999. Trends in infectious disease mortality in the United States during the 20th century. JAMA 281:61–66.CrossRefGoogle ScholarPubMed
7. Waite, S., Jeudy, J., and White, C.S. 2006. Acute lung infections in normal and immunocompromised hosts. Radiol Clin North Am 44:295–315, ix.CrossRefGoogle ScholarPubMed
8. Ware, L.B., and Matthay, M.A. 2000. The acute respiratory distress syndrome. N Engl J Med 342:1334–1349.CrossRefGoogle ScholarPubMed
9. Farver, C.F. 2008. Bacterial diseases. In Pulmonary Pathology, Zander, D. S. and Farver, C.F. (eds.), pp. 167–203. Philadelphia: Churchill Livingstone Elsevier.Google Scholar
10. Mizgerd, J.P., and Skerrett, S.J. 2008. Animal models of human pneumonia. Am J Physiol Lung Cell Mol Physiol 294:L387–L398.CrossRefGoogle ScholarPubMed
11. Serhan, C.N., Brain, S.D., Buckley, C.D., et al. 2007. Resolution of inflammation: state of the art, definitions and terms. FASEB J 21:325–332.CrossRefGoogle ScholarPubMed
12. Serhan, C.N., Chiang, N., and Van Dyke, T.E. 2008. Resolving inflammation: dual anti-inflammatory and pro-resolution lipid mediators. Nat Rev Immunol 8:349–361.CrossRefGoogle ScholarPubMed
13. Levy, B.D., Clish, C.B., Schmidt, B., Gronert, K., and Serhan, C.N. 2001. Lipid mediator class switching during acute inflammation: signals in resolution. Nat Immunol 2:612–619.CrossRefGoogle ScholarPubMed
14. Fukunaga, K., Kohli, P., Bonnans, C., Fredenburgh, L.E., and Levy, B.D. 2005. Cyclooxygenase 2 plays a pivotal role in the resolution of acute lung injury. J Immunol 174:5033–5039.CrossRefGoogle Scholar
15. Machado, F.S., Johndrow, J.E., Esper, L., et al. 2006. Antiinflammatory actions of lipoxin A4 and aspirin-triggered lipoxin are SOCS-2 dependent. Nat Med 12:330–334.CrossRefGoogle ScholarPubMed
16. Canny, G., Levy, O., Furuta, G.T., et al. 2002. Lipid mediator-induced expression of bactericidal/permeability-increasing protein (BPI) in human mucosal epithelia. Proc Natl Acad Sci USA 99:3902–3907.CrossRefGoogle Scholar
17. Bruns, A.H., Oosterheert, J.J., Prokop, M., Lammers, J.W., Hak, E., and Hoepelman, A.I. 2007. Patterns of resolution of chest radiograph abnormalities in adults hospitalized with severe community-acquired pneumonia. Clin Infect Dis 45:983–991.CrossRefGoogle ScholarPubMed
Levy, B.D., Clish, C.B., Schmidt, B., Gronert, K., and Serhan, C.N. 2001. Lipid mediator class switching during acute inflammation: signals in resolution. Nat Immunol 2:612–619.CrossRefGoogle ScholarPubMed
Mizgerd, J.P. 2008. Acute lower respiratory tract infection. N Engl J Med 358:716–727.CrossRefGoogle ScholarPubMed
Schwab, J.M., Chiang, N., Arita, M., and Serhan, C.N. 2007. Resolvin E1 and protectin D1 activate inflammation-resolution programmes. Nature 447:869–874.CrossRefGoogle ScholarPubMed
Serhan, C.N., Brain, S.D., Buckley, C.D., et al. 2007. Resolution of inflammation: state of the art, definitions and terms. FASEB J 21:325–332.CrossRefGoogle ScholarPubMed

Save book to Kindle

To save this book to your Kindle, first ensure [email protected] is added to your Approved Personal Document E-mail List under your Personal Document Settings on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part of your Kindle email address below. Find out more about saving to your Kindle.

Note you can select to save to either the @free.kindle.com or @kindle.com variations. ‘@free.kindle.com’ emails are free but can only be saved to your device when it is connected to wi-fi. ‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.

Find out more about the Kindle Personal Document Service.

Available formats
×

Save book to Dropbox

To save content items to your account, please confirm that you agree to abide by our usage policies. If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account. Find out more about saving content to Dropbox.

Available formats
×

Save book to Google Drive

To save content items to your account, please confirm that you agree to abide by our usage policies. If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account. Find out more about saving content to Google Drive.

Available formats
×