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Regulation of Lung Immunity: Significance of the Cytokine Environment

  • Nicholas W. Lukacs
  • Theodore Standiford
  • Cory Hogaboam
  • Steven L. Kunkel
Chapter
  • 88 Downloads
Part of the Molecular and Cellular Biology of Critical Care Medicine book series (MCCM, volume 1)

Abstract

The disruption of lung structure and pulmonary function can be a devastating event leading to acute deteriorating health and chronic respiratory illness (1, 2, 3, 4). Regulation of lung function is maintained by intricate mechanisms that promote a balance between host defenses against injurious events and reactive inflammatory responses. An excessive inflammatory response can result in acute lung injury (ALI), leading to organ dysfunction. The development and regulation of inflammation and immune responses within the lung are dependent upon several complex interactions including the nature of the infectious agent, structural cell production of chemotactic factors, activation of recruited leukocytes, and release of specific cytokines. The cytokine responses that occur in the lung dictate the nature of ensuing activation events and the type of immune response that subsequently occurs. For example, if an infectious or noxious foreign agent initiates a response that predominantly induces a Th1 type response characterized by high levels of IL-12 and IFN-γ, an environment may be initiated that would augment subsequent anti-pathogen immune responses within the lung. In contrast, if a foreign agent induces a predominant Th2 type response, then subsequent responses may be skewed. The Th2 response may alter the ability to clear intracellular pathogens and increase the host’s susceptibility to developing allergic responses. This chapter will address the influence of early cytokine production on the nature of the subsequent immune responses.

Keywords

Respiratory Syncytial Virus Acute Lung Injury Chemokine Receptor Acute Respiratory Distress Syndrome Respiratory Syncytial Virus Infection 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Springer Science+Business Media New York 2001

Authors and Affiliations

  • Nicholas W. Lukacs
    • 1
  • Theodore Standiford
    • 1
  • Cory Hogaboam
    • 1
  • Steven L. Kunkel
    • 1
  1. 1.Department of Pathology and Division of Pulmonary and Critical Care MedicineUniversity of Michigan Medical SchoolUSA

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