The role of inflammation in respiratory impairment during Pneumocystis carinii pneumonia

Peter Y. Hahn, Andrew Harold Limper

Research output: Contribution to journalArticle

16 Citations (Scopus)

Abstract

Pneumocystis carinii remains an important cause of pneumonia in immunosuppressed hosts. Severe Pneumocystis pneumonia is characterized by an intense neutrophilic inflammatory response resulting in gas exchange abnormalities, diffuse alveolar damage, and respiratory failure. The inflammatory response directed against P. carinii involves a complex series of interactions between alveolar macrophages, CD4+ T lymphocytes, polymorphonuclear cells, and their various products. CD4+ T lymphocytes are crucial to host defense against P. carinii. Alveolar macrophages also provide essential functions that significantly enhance clearance of P. carinii infection. In addition, host proteins play an important role in augmenting the host inflammatory responses to this organism. Although essential for effective clearance of infection, excessive inflammatory responses also predispose the host to the development of lung injury and respiratory compromise. Understanding the complex processes involved in the host inflammatory response and its potential for causing lung injury may enable development of novel therapeutic approaches for this and other important fungal lung infections.

Original languageEnglish (US)
Pages (from-to)40-47
Number of pages8
JournalSeminars in Respiratory Infections
Volume18
Issue number1
DOIs
StatePublished - Mar 2003

Fingerprint

Pneumocystis carinii
Pneumocystis Pneumonia
Alveolar Macrophages
Lung Injury
Inflammation
Pneumocystis Infections
T-Lymphocytes
Mycoses
Immunocompromised Host
Respiratory Insufficiency
Pneumonia
Gases
Lung
Infection
Proteins
Therapeutics

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine
  • Microbiology (medical)

Cite this

The role of inflammation in respiratory impairment during Pneumocystis carinii pneumonia. / Hahn, Peter Y.; Limper, Andrew Harold.

In: Seminars in Respiratory Infections, Vol. 18, No. 1, 03.2003, p. 40-47.

Research output: Contribution to journalArticle

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