Lethal influenza infection: Is a macrophage to blame?

Research output: Contribution to journalReview article

4 Citations (Scopus)

Abstract

Alveolar macrophages (AMs) are critical for immunity against influenza A virus (IAV) infection. Depletion, hyporeactivity, and disruption of AM development and differentiation are all associated with lethal IAV infection. AMs drive the innate immune response that limits IAV infection. AMs are crucial for steady-state homeostasis of pulmonary surfactant, and in turn surfactant proteins regulate AMs and participate in host defense against IAV. Known factors that are necessary for AM function and differentiation in vivo include surfactant proteins, the growth factor GM-CSF, the hormone receptor PPARγ, and the transcription factors PU.1 and Bach2. Although PU.1 and PPARγ are downstream effectors of GM-CSF, Bach2 works independently. GM-CSF and Bach2-deficient AMs have phenotypes with immature or alternatively activated states of differentiation, respectively, and both extremes are unsuitable for surfactant homeostasis. The activation state of AMs and the local microenvironment may determine the development of symptomatic versus asymptomatic IAV infection in different individuals.

Original languageEnglish (US)
Pages (from-to)1425-1428
Number of pages4
JournalExpert Review of Anti-Infective Therapy
Volume13
Issue number12
DOIs
StatePublished - Dec 2 2015

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Alveolar Macrophages
Human Influenza
Macrophages
Influenza A virus
Virus Diseases
Infection
Surface-Active Agents
Peroxisome Proliferator-Activated Receptors
Granulocyte-Macrophage Colony-Stimulating Factor
Homeostasis
Granulocyte-Macrophage Colony-Stimulating Factor Receptors
Pulmonary Surfactants
Innate Immunity
Immunity
Intercellular Signaling Peptides and Proteins
Proteins
Hormones
Phenotype

All Science Journal Classification (ASJC) codes

  • Microbiology
  • Microbiology (medical)
  • Virology
  • Infectious Diseases

Cite this

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title = "Lethal influenza infection: Is a macrophage to blame?",
abstract = "Alveolar macrophages (AMs) are critical for immunity against influenza A virus (IAV) infection. Depletion, hyporeactivity, and disruption of AM development and differentiation are all associated with lethal IAV infection. AMs drive the innate immune response that limits IAV infection. AMs are crucial for steady-state homeostasis of pulmonary surfactant, and in turn surfactant proteins regulate AMs and participate in host defense against IAV. Known factors that are necessary for AM function and differentiation in vivo include surfactant proteins, the growth factor GM-CSF, the hormone receptor PPARγ, and the transcription factors PU.1 and Bach2. Although PU.1 and PPARγ are downstream effectors of GM-CSF, Bach2 works independently. GM-CSF and Bach2-deficient AMs have phenotypes with immature or alternatively activated states of differentiation, respectively, and both extremes are unsuitable for surfactant homeostasis. The activation state of AMs and the local microenvironment may determine the development of symptomatic versus asymptomatic IAV infection in different individuals.",
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Lethal influenza infection : Is a macrophage to blame? / Halstead, E. Scott; Chroneos, Zissis C.

In: Expert Review of Anti-Infective Therapy, Vol. 13, No. 12, 02.12.2015, p. 1425-1428.

Research output: Contribution to journalReview article

TY - JOUR

T1 - Lethal influenza infection

T2 - Is a macrophage to blame?

AU - Halstead, E. Scott

AU - Chroneos, Zissis C.

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Y1 - 2015/12/2

N2 - Alveolar macrophages (AMs) are critical for immunity against influenza A virus (IAV) infection. Depletion, hyporeactivity, and disruption of AM development and differentiation are all associated with lethal IAV infection. AMs drive the innate immune response that limits IAV infection. AMs are crucial for steady-state homeostasis of pulmonary surfactant, and in turn surfactant proteins regulate AMs and participate in host defense against IAV. Known factors that are necessary for AM function and differentiation in vivo include surfactant proteins, the growth factor GM-CSF, the hormone receptor PPARγ, and the transcription factors PU.1 and Bach2. Although PU.1 and PPARγ are downstream effectors of GM-CSF, Bach2 works independently. GM-CSF and Bach2-deficient AMs have phenotypes with immature or alternatively activated states of differentiation, respectively, and both extremes are unsuitable for surfactant homeostasis. The activation state of AMs and the local microenvironment may determine the development of symptomatic versus asymptomatic IAV infection in different individuals.

AB - Alveolar macrophages (AMs) are critical for immunity against influenza A virus (IAV) infection. Depletion, hyporeactivity, and disruption of AM development and differentiation are all associated with lethal IAV infection. AMs drive the innate immune response that limits IAV infection. AMs are crucial for steady-state homeostasis of pulmonary surfactant, and in turn surfactant proteins regulate AMs and participate in host defense against IAV. Known factors that are necessary for AM function and differentiation in vivo include surfactant proteins, the growth factor GM-CSF, the hormone receptor PPARγ, and the transcription factors PU.1 and Bach2. Although PU.1 and PPARγ are downstream effectors of GM-CSF, Bach2 works independently. GM-CSF and Bach2-deficient AMs have phenotypes with immature or alternatively activated states of differentiation, respectively, and both extremes are unsuitable for surfactant homeostasis. The activation state of AMs and the local microenvironment may determine the development of symptomatic versus asymptomatic IAV infection in different individuals.

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