Interactions of α-, β-, and θ-Defensins with Influenza A Virus and Surfactant Protein D

Doss, Mona; White, Mitchell R.; Tecle, Tesfaldet; Gantz, Donald; Crouch, Erika C.; Jung, Grace; Ruchala, Piotr; Waring, Alan J.; Lehrer, Robert I.; Hartshorn, Kevan L.

doi:10.4049/jimmunol.0804049

Cited by 126 publications

(159 citation statements)

References 56 publications

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“…Thus, although this remains to be demonstrated in vivo, iNKT cell-derived IL-22 may be important to sustain the respiratory epithelium and preserve the epithelial barrier during IAV infection. In parallel, IL-22 may promote the synthesis of epithelial cytokines/chemokines as well as antimicrobial peptides, some of which are known to neutralize IAV (93)(94)(95). Through these mechanisms, IL-22 may be of particular significance during IAV pneumonia, a hypothesis that is currently under active investigation.…”

Section: Discussionmentioning

confidence: 99%

Interleukin-22 Is Produced by Invariant Natural Killer T Lymphocytes during Influenza A Virus Infection

Paget

Ivanov

Fontaine

et al. 2012

Journal of Biological Chemistry

156

168

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Background: Invariant natural killer T (iNKT) cells play a beneficial role during experimental influenza A virus (IAV) infection.Results: iNKT cells produce IL-22 during infection, and IL-22 prevents the IAV-triggered cell death of pulmonary epithelium. Conclusion: IL-22 produced by iNKT cells might be important during IAV infection.Significance: Understanding how iNKT cells function during IAV infection might be instrumental to control IAV-associated pathogenesis.

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Section: Discussionmentioning

confidence: 99%

Interleukin-22 Is Produced by Invariant Natural Killer T Lymphocytes during Influenza A Virus Infection

Paget

Ivanov

Fontaine

et al. 2012

Journal of Biological Chemistry

156

168

View full text Add to dashboard Cite

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“…Human -defensin-1 (retrocyclin-1) inhibits HIV-1 entry by binding to CD4 and gp120 receptors (50,51), and studies have indicated that the disulfide bonds and cyclic backbone have a role in receptor binding (52). -Defensins are also able to inhibit adhesion and entry of herpes simplex virus by binding a glycoprotein (53), and influenza A virus by inducing viral aggregation (54). Potent anti-inflammatory and antisepsis activities of RTDs have recently been reported, and studies suggest that RTD-1 inhibits the release of proinflammatory cytokines and tumor necrosis factors (42).…”

Section: The Role Of the Disulfide Bonds And The Circular Backbone Inmentioning

confidence: 99%

The Cyclic Cystine Ladder in θ-Defensins Is Important for Structure and Stability, but Not Antibacterial Activity

Conibear

Rosengren

Daly

et al. 2013

Journal of Biological Chemistry

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Background: -Defensins are antimicrobial peptides comprising a cyclic backbone and three disulfide bonds. Results: -Defensins retain antibacterial and membrane-binding activity, but lose structure and stability when the disulfide bonds are removed. Conclusion: Disulfide bonds are important for the stability and structure of -defensins, but not antibacterial activity. Significance: Understanding the role of disulfide bonds and cyclization in -defensins facilitates applications as peptide drug scaffolds.

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“…Two important proteins of the innate immune system in the gas exchange portion of the lung are surfactant proteins A and D (Haagsman et al, 2008;Pastva et al, 2007), both of which have been reported to be important in controlling viral infections (Doss et al, 2009;Leth-Larsen et al, 2007). BALF samples from SDAV and control rats were assayed for surfactant proteins SP-A and SP-D using ELISA (Fig.…”

Section: Rat Lung Infection By Sdav Induces Expression Of Cytokines Lmentioning

confidence: 99%

Rat respiratory coronavirus infection: replication in airway and alveolar epithelial cells and the innate immune response

Funk

Manzer

Miura

et al. 2009

Journal of General Virology

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The rat coronavirus sialodacryoadenitis virus (SDAV) causes respiratory infection and provides a system for investigating respiratory coronaviruses in a natural host. A viral suspension in the form of a microspray aerosol was delivered by intratracheal instillation into the distal lung of 6-8-weekold Fischer 344 rats. SDAV inoculation produced a 7 % body weight loss over a 5 day period that was followed by recovery over the next 7 days. SDAV caused focal lesions in the lung, which were most severe on day 4 post-inoculation (p.i.). Immunofluorescent staining showed that four cell types supported SDAV virus replication in the lower respiratory tract, namely Clara cells, ciliated cells in the bronchial airway and alveolar type I and type II cells in the lung parenchyma. In bronchial alveolar lavage fluid (BALF) a neutrophil influx increased the population of neutrophils to 45 % compared with 6 % of the cells in control samples on day 2 after mock inoculation. Virus infection induced an increase in surfactant protein SP-D levels in BALF of infected rats on days 4 and 8 p.i. that subsided by day 12. The concentrations of chemokines MCP-1, LIX and CINC-1 in BALF increased on day 4 p.i., but returned to control levels by day 8. Intratracheal instillation of rats with SDAV coronavirus caused an acute, self-limited infection that is a useful model for studying the early events of the innate immune response to respiratory coronavirus infections in lungs of the natural virus host. INTRODUCTIONThe large volume of air inhaled each day and the extensive surface area of the lung makes the respiratory system especially vulnerable to airborne infectious agents. These pathogens include many respiratory viruses such as influenza virus, respiratory syncytial virus, rhinovirus and coronaviruses (CoVs). Respiratory tract infections are the leading cause of infectious disease globally (WHO, 2004). The outbreak of severe acute respiratory syndrome (SARS) in [2002][2003] emphasized the vulnerability of humans to respiratory virus diseases and the potential for high morbidity and mortality in viral infections of the lower respiratory tract. The aetiological agent of SARS was identified as a coronavirus (SARS-CoV) derived from an animal reservoir (Fouchier et al., 2003). Besides human infections, CoVs cause respiratory, enteric and neurological infections in a variety of birds and mammals (Weiss & Navas-Martin, 2005). Five human CoVs have been identified to date, all of which cause respiratory tract infections. Human CoVs 229E and OC43 were first identified in the 1960s, and they cause up to 15-35 % of the adult colds in otherwise healthy individuals (Kahn & McIntosh, 2005). After the discovery of SARS-CoV, two additional human CoVs were identified, NL63 and HKU1 (van der Hoek et al., 2004;Woo et al., 2005). On a global basis, the human CoVs 229E, OC43, HKU1 and NL63 are estimated to cause approximately 10 % of all hospitalizations of children for respiratory tract infections (Gerna et al., 2007;Vabret et al., 2008).A number of animal mod...

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Interactions of α-, β-, and θ-Defensins with Influenza A Virus and Surfactant Protein D

Cited by 126 publications

References 56 publications

Interleukin-22 Is Produced by Invariant Natural Killer T Lymphocytes during Influenza A Virus Infection

Interleukin-22 Is Produced by Invariant Natural Killer T Lymphocytes during Influenza A Virus Infection

The Cyclic Cystine Ladder in θ-Defensins Is Important for Structure and Stability, but Not Antibacterial Activity

Rat respiratory coronavirus infection: replication in airway and alveolar epithelial cells and the innate immune response

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