The innate immune rheostat: Influence on lung inflammatory disease and secondary bacterial pneumoniaCitation formats

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The innate immune rheostat: Influence on lung inflammatory disease and secondary bacterial pneumonia. / Hussell, Tracy; Cavanagh, Mary M.

In: Biochemical Society Transactions, Vol. 37, No. 4, 2009, p. 811-813.

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Hussell, Tracy ; Cavanagh, Mary M. / The innate immune rheostat: Influence on lung inflammatory disease and secondary bacterial pneumonia. In: Biochemical Society Transactions. 2009 ; Vol. 37, No. 4. pp. 811-813.

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@article{4f12b35a46d74d5dbfdcbf09c6e871dc,
title = "The innate immune rheostat: Influence on lung inflammatory disease and secondary bacterial pneumonia",
abstract = "The activity of innate immunity is not simply dictated by the presence of an antigen but also by the balance between negative regulatory and immune potentiator pathways. Even in the absence of antigen, innate immunity can 'inflame' if negative regulators are absent. This resting state is adaptable and dictated by environmental influences, host genetics and past infection history. A return to homoeostasis post inflammation may therefore not leave the tissue in an identical state to that prior to the inflammatory event. This adaptability makes us all unique and also explains the variable outcome experienced by a diverse population to the same inflammatory stimulus. Using murine models we have identified that influenza virus causes a long-term modification of the lung microenvironment by a de-sensitization to bacterial products and an increase in the myeloid negative regulator CD200R (CD200 receptor). These two events prevent subsequent inflammatory damage while the lung is healing, but also they may predispose to bacterial colonization of the lower respiratory tract should regulatory mechanisms overshoot. In the extreme, this leads to bacterial pneumonia, sepsis and death. A deeper understanding of the consequences arising from innate immune cell alteration during influenza infection and the subsequent development of bacterial complications has important implications for future drug development. {\circledC} The Authors Journal compilation. {\circledC} 2009 Biochemical Society.",
keywords = "CD200 receptor, Influenza, Innate immunity, Lung inflammatory disease, Negative regulator, Secondary bacterial pneumonia",
author = "Tracy Hussell and Cavanagh, {Mary M.}",
note = "1 UO1 AI070232-01, NIAID NIH HHS, United StatesP171/03/C1/048, Medical Research Council, United Kingdom",
year = "2009",
doi = "10.1042/BST0370811",
language = "English",
volume = "37",
pages = "811--813",
journal = "Biochemical Society. Transactions",
issn = "0300-5127",
publisher = "Portland Press Ltd",
number = "4",

}

RIS

TY - JOUR

T1 - The innate immune rheostat: Influence on lung inflammatory disease and secondary bacterial pneumonia

AU - Hussell, Tracy

AU - Cavanagh, Mary M.

N1 - 1 UO1 AI070232-01, NIAID NIH HHS, United StatesP171/03/C1/048, Medical Research Council, United Kingdom

PY - 2009

Y1 - 2009

N2 - The activity of innate immunity is not simply dictated by the presence of an antigen but also by the balance between negative regulatory and immune potentiator pathways. Even in the absence of antigen, innate immunity can 'inflame' if negative regulators are absent. This resting state is adaptable and dictated by environmental influences, host genetics and past infection history. A return to homoeostasis post inflammation may therefore not leave the tissue in an identical state to that prior to the inflammatory event. This adaptability makes us all unique and also explains the variable outcome experienced by a diverse population to the same inflammatory stimulus. Using murine models we have identified that influenza virus causes a long-term modification of the lung microenvironment by a de-sensitization to bacterial products and an increase in the myeloid negative regulator CD200R (CD200 receptor). These two events prevent subsequent inflammatory damage while the lung is healing, but also they may predispose to bacterial colonization of the lower respiratory tract should regulatory mechanisms overshoot. In the extreme, this leads to bacterial pneumonia, sepsis and death. A deeper understanding of the consequences arising from innate immune cell alteration during influenza infection and the subsequent development of bacterial complications has important implications for future drug development. © The Authors Journal compilation. © 2009 Biochemical Society.

AB - The activity of innate immunity is not simply dictated by the presence of an antigen but also by the balance between negative regulatory and immune potentiator pathways. Even in the absence of antigen, innate immunity can 'inflame' if negative regulators are absent. This resting state is adaptable and dictated by environmental influences, host genetics and past infection history. A return to homoeostasis post inflammation may therefore not leave the tissue in an identical state to that prior to the inflammatory event. This adaptability makes us all unique and also explains the variable outcome experienced by a diverse population to the same inflammatory stimulus. Using murine models we have identified that influenza virus causes a long-term modification of the lung microenvironment by a de-sensitization to bacterial products and an increase in the myeloid negative regulator CD200R (CD200 receptor). These two events prevent subsequent inflammatory damage while the lung is healing, but also they may predispose to bacterial colonization of the lower respiratory tract should regulatory mechanisms overshoot. In the extreme, this leads to bacterial pneumonia, sepsis and death. A deeper understanding of the consequences arising from innate immune cell alteration during influenza infection and the subsequent development of bacterial complications has important implications for future drug development. © The Authors Journal compilation. © 2009 Biochemical Society.

KW - CD200 receptor

KW - Influenza

KW - Innate immunity

KW - Lung inflammatory disease

KW - Negative regulator

KW - Secondary bacterial pneumonia

U2 - 10.1042/BST0370811

DO - 10.1042/BST0370811

M3 - Article

VL - 37

SP - 811

EP - 813

JO - Biochemical Society. Transactions

JF - Biochemical Society. Transactions

SN - 0300-5127

IS - 4

ER -