Influenza A Inhibits TH17-mediated Immunity Which Is Required For Host Defense Against Staphylococcus Aureus Pneumonia

Alcorn, John F.; Kudva, Anupa; Crowe, Christopher R.; Scheller, Erich V.; Kolls, Jay K.

doi:10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a5085

C92. Il-17 in Lung Immunity, Friend or Foe? 2010

DOI: 10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a5085

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Influenza A Inhibits TH17-mediated Immunity Which Is Required For Host Defense Against Staphylococcus Aureus Pneumonia

John F. Alcorn¹,

Anupa Kudva²,

Christopher R. Crowe³

et al.

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2011

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“…Cytokines more typically associated with T cell signaling cascades are important in the clearance of extracellular bacteria from the airways. Mice with mutations in the Th17 cascade (interleukin-17A [IL-17A] or -F and IL-22) appear to have impaired staphylococcal clearance from the lung, despite increased cytokine production and increased inflammation (1). In contrast, the type I interferon (IFN) cascade contributes directly to pulmonary pathology in response to S. aureus.…”

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Participation of CD11c ⁺ Leukocytes in Methicillin-Resistant Staphylococcus aureus Clearance from the Lung

et al. 2011

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Staphylococcus aureus causes especially severe pulmonary infection, associated with high morbidity and mortality. In addition to the effects of specific virulence factors, it appears that the intensity of the host proinflammatory response, particularly in the initial stages of infection, contributes substantially to pulmonary damage. We tested the hypothesis that the CD11c ؉ leukocytes are important in the host response to pulmonary infection with methicillin-resistant S. aureus (MRSA) USA300. Clodronate-induced depletion of the alveolar macrophage population resulted in increased numbers of dendritic cells (DCs) and CD4؉ cells in bronchoalveolar lavage (BAL) fluid and was associated with significantly increased mortality by 18 h following S. aureus inoculation but had no effect on bacterial load or polymorphonuclear leukocyte (PMN) numbers in the lung. These clodronate-treated mice also had increased expression of interleukin-17A/F (IL-17A/F) and Staphylococcus aureus bacteria, particularly the epidemic methicillin-resistant USA300 strains, have recently been associated with severe invasive pneumonias in previously well individuals, as well as being a complication of influenza (15). These pneumonias are characterized by a predominant polymorphonuclear leukocyte (PMN) response with significant areas of necrosis and hemorrhage (6). Numerous studies have addressed which of the several virulence factors expressed by the USA300 strains are most important in the pathogenesis of pulmonary infection. In the C57BL/6J mouse model of acute pneumonia, the contributions of ␣-hemolysin (Hla) (3) and protein A (SpA) (8) have been well documented. The importance of Panton-Valentine leukocidin (PVL) has also been confirmed in a rabbit model of infection; rabbits, like humans, have highly PVL-susceptible leukocytes (6). Besides the direct toxicity of staphylococcal toxins, some of the pathological consequences of staphylococcal virulence factors are due to the intensity of the host immune response. Both Tnfr1 Ϫ/Ϫ (8) and Ifnar Ϫ/Ϫ (17) mice are highly resistant to S. aureus pneumonia and even to the USA300 strains expressing these virulence factors, suggesting that the intensity of the host immune response to infection is critical in the pathogenesis of severe pneumonia.Exactly which components of the innate immune response contribute to lethality in these models of acute S. aureus pneumonia has not been clearly delineated. PMNs have long been thought to be critical for efficient staphylococcal clearance (19,22), and the increased incidence of severe staphylococcal infection in humans with disorders of PMN function or activation, such as chronic granulomatous disease (10, 12), confirm this observation. PMNs themselves can also contribute to the pathology associated with staphylococcal infection. A substantial component of the lung pathology associated with S. aureus USA300 pneumonia has been attributed to the PVL-associated release of cytotoxic components from PMN granules (5). In models of soft tissue infection, the importance ...

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Participation of CD11c ⁺ Leukocytes in Methicillin-Resistant Staphylococcus aureus Clearance from the Lung

et al. 2011

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Influenza A Inhibits TH17-mediated Immunity Which Is Required For Host Defense Against Staphylococcus Aureus Pneumonia

Cited by 1 publication

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Participation of CD11c ⁺ Leukocytes in Methicillin-Resistant Staphylococcus aureus Clearance from the Lung

Participation of CD11c ⁺ Leukocytes in Methicillin-Resistant Staphylococcus aureus Clearance from the Lung

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Influenza A Inhibits TH17-mediated Immunity Which Is Required For Host Defense Against Staphylococcus Aureus Pneumonia

Cited by 1 publication

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Participation of CD11c + Leukocytes in Methicillin-Resistant Staphylococcus aureus Clearance from the Lung

Participation of CD11c + Leukocytes in Methicillin-Resistant Staphylococcus aureus Clearance from the Lung

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Participation of CD11c ⁺ Leukocytes in Methicillin-Resistant Staphylococcus aureus Clearance from the Lung

Participation of CD11c ⁺ Leukocytes in Methicillin-Resistant Staphylococcus aureus Clearance from the Lung