Immune homeostasis in the respiratory tract and its impact on heterologous infection

Wissinger, Erika; Goulding, John; Hussell, Tracy

doi:10.1016/j.smim.2009.01.005

Cited by 83 publications

(86 citation statements)

References 128 publications

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“…Alveolar macrophages that can produce interleukin-10 and transforming growth factor-b to restrain the inflammatory response in the lung may be responsible for this inhibitory effect on the activation of lung NK cells. 25 As an important part of the innate immune system, NK cells play critical roles in protecting the host against tumours and pathogens. 26,27 However, increasing evidence suggests that NK-cell activation can lead to tissue injury during the inflammatory response.…”

Section: Discussionmentioning

confidence: 99%

Lung natural killer cells in mice: phenotype and response to respiratory infection

Wang

Zheng

et al. 2012

Immunology

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SummaryNatural killer (NK) cells have a specialized function in peripheral organs, which is determined by the organ-specific niches. We have attempted to explore whether lung NK cells display a particular phenotype according to their function in the unique pulmonary environment in health or during respiratory infection in mice. In healthy mice, higher frequencies of NK cells among lymphocytes were detected in the lung than in other tissues (lymph node, bone marrow, spleen, blood and liver), and lung NK cells maintained a more mature phenotype, implying that lung NK cells were critical for the pulmonary immune response. However, lung NK cells expressed higher levels of inhibitory receptors and lower levels of activating receptors, migration/adhesion-associated molecules and co-stimulatory molecules than splenic NK cells, implying that lung NK cells were quiescent, and the activation of lung NK cells was tightly regulated by the pulmonary environment in health. During respiratory infection, lung NK cells could be activated and express functional molecules (CD107a and interferon-c) to take part in the response to infection quickly. These results suggested that the unique pulmonary environment promotes the development of NK cells with a lung-specific phenotype.

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Section: Discussionmentioning

confidence: 99%

Lung natural killer cells in mice: phenotype and response to respiratory infection

Wang

Zheng

et al. 2012

Immunology

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“…To shift the "immune rheostat" (reviewed in Ref. 49) toward a pathological state of inflammation like that observed in our hands, these mechanisms must be overcome. Recent work by Shahangian et al (22) may provide a clue to explain this phenomenon.…”

Section: Discussionmentioning

confidence: 93%

Dysregulated Macrophage-Inflammatory Protein-2 Expression Drives Illness in Bacterial Superinfection of Influenza

Zavitz¹,

Bauer²,

Gaschler³

et al. 2010

The Journal of Immunology

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Influenza virus infection is a leading cause of death and disability throughout the world. Influenza-infected hosts are vulnerable to secondary bacterial infection, however, and an ensuing bacterial pneumonia is actually the predominant cause of influenza-attributed deaths during pandemics. A number of mechanisms have been proposed by which influenza may predispose to superinfection with an unrelated or heterologous pathogen, but the subsequent interaction between the host, virus, and bacteria remains an understudied area. In this study, we develop and examine a novel model of heterologous pulmonary infection in which an otherwise subclinical Bordetella parapertussis infection synergizes with an influenza virus infection to yield a life-threatening secondary pneumonia. Despite a profound pulmonary inflammatory response and unaltered viral clearance, bacterial clearance was significantly impaired in heterologously infected mice. No deficits were observed in pulmonary or systemic adaptive immune responses or the viability or function of infiltrating inflammatory cells to explain this phenomenon, and we provide evidence that the onset of severe pulmonary inflammation actually precedes the increased bacterial burden, suggesting that exacerbated inflammation is independent of bacterial burden. To that end, neutralization of the ELR+ inflammatory chemokine MIP-2 (CXCL2/GRO-β) attenuated the inflammation, weight loss, and clinical presentation of heterologously infected mice without impacting bacterial burden. These data suggest that pulmonary inflammation, rather than pathogen burden, is the key threat during bacterial superinfection of influenza and that selective chemokine antagonists may be a novel therapeutic intervention in cases of bacterial superinfection of influenza.

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“…On the other hand, excessive inflammation may cause tissue or organ damage. The avian flu virus, SARS virus, and RSV often causes lung infections, and infection of the central nervous system (Ruckwardt et al, 2009;Wissinger et al, 2009). The mechanism by which viral infection initiates the production of a large number of inflammatory cytokines has not been elucidated so far.…”

Section: Discussionmentioning

confidence: 99%

Interleukin-17 enhances the removal of respiratory syncytial virus in mice by promoting neutrophil migration and reducing interferon-gamma expression

Zhang

Zhou

2016

Genet. Mol. Res.

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ABSTRACT. The aim of this study was to observe the effect of interleukin (IL)-17 on early immune response and inflammation in the lungs of respiratory syncytial virus (RSV)-infected mice. Specific pathogen-free BALB/c mice were randomly assigned to control, RSV-infected, RSVinfected with phosphate-buffered saline, and RSV-infected + IL-17 intervention groups. The RSV infection model was set up by nasal mucosa immunization. The intervention group was provided with restructured IL-17 (intranasal). The viral load and cytokine concentrations in the lung tissues and broncho-alveolar lavage fluid (BALF) were determined by real-timepolymerase chain reaction and enzyme-linked immunosorbent assay.

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Immune homeostasis in the respiratory tract and its impact on heterologous infection

Cited by 83 publications

References 128 publications

Lung natural killer cells in mice: phenotype and response to respiratory infection

Lung natural killer cells in mice: phenotype and response to respiratory infection

Dysregulated Macrophage-Inflammatory Protein-2 Expression Drives Illness in Bacterial Superinfection of Influenza

Interleukin-17 enhances the removal of respiratory syncytial virus in mice by promoting neutrophil migration and reducing interferon-gamma expression

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