Interferon-alpha in viral and bacterial gastroenteritis: a comparison with C-reactive protein and interleukin-6

Mangiarotti, P.; Moulin, F.; Palmer, P.; Ravilly, S.; Raymond, J.; Gendrel, D.

doi:10.1080/08035259950169206

Cited by 9 publications

(11 citation statements)

References 6 publications

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“…Other enteroviruses including astroviruses, noroviruses, and adenoviruses are also frequent causes of diarrhea episodes in children [38]. Th1 responses and inflammation play important roles in anti-enteroviral immunity [39,40] and are associated with local production of IFN-␣ [41,42]. It is therefore conceivable that IFN-␣ production as a result of a viral infection would lead to a shift toward Th1 responses and reinstruct previously tolerogenic DCs to prime gluten-specific T cells and support inflammation instead of sustaining oral tolerance.…”

Section: Type I Interferons and Virusesmentioning

confidence: 99%

Celiac Disease—Sandwiched between Innate and Adaptive Immunity

2006

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Section: Type I Interferons and Virusesmentioning

confidence: 99%

Celiac Disease—Sandwiched between Innate and Adaptive Immunity

2006

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“… † Direct comparison between viral and bacterial infections revealed higher circulating levels in viral infections [74]. N.D.: not detected.…”

Section: Plasma Inflammatory Profiles In Viral and Bacterial Infectionsmentioning

confidence: 99%

IL-1β/IL-6/CRP and IL-18/ferritin: Distinct Inflammatory Programs in Infections

et al. 2016

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The host inflammatory response against infections is characterized by the release of pro-inflammatory cytokines and acute-phase proteins, driving both innate and adaptive arms of the immune response. Distinct patterns of circulating cytokines and acute-phase responses have proven indispensable for guiding the diagnosis and management of infectious diseases. This review discusses the profiles of acute-phase proteins and circulating cytokines encountered in viral and bacterial infections. We also propose a model in which the inflammatory response to viral (IL-18/ferritin) and bacterial (IL-6/CRP) infections presents with specific plasma patterns of immune biomarkers.

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“…A recent study of total human peripheral blood mononuclear cells (PBMCs) exposed to RRV or human rotavirus indicated that both myeloid DCs and pDCs are susceptible to infection, and that infection results in the secretion of IFNa, presumably from pDCs [42]. While increased levels of IFNa have also been correlated with a positive clinical outcome in infected children [43,44], several rotaviruses, including RRV, have recently been demonstrated to antagonize the production of type I IFN through the degradation of interferon regulatory factors (IRF)3, IRF5, and IRF7, and the inhibition of NFkB activation, by a viral nonstructural protein, NSP1 [45,46,47,48].…”

Section: Introductionmentioning

confidence: 99%

Rotavirus Structural Proteins and dsRNA Are Required for the Human Primary Plasmacytoid Dendritic Cell IFNα Response

Deal

Jaimes²,

Crawford³

et al. 2010

PLoS Pathog

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Rotaviruses are the leading cause of severe dehydrating diarrhea in children worldwide. Rotavirus-induced immune responses, especially the T and B cell responses, have been extensively characterized; however, little is known about innate immune mechanisms involved in the control of rotavirus infection. Although increased levels of systemic type I interferon (IFNα and β) correlate with accelerated resolution of rotavirus disease, multiple rotavirus strains, including rhesus rotavirus (RRV), have been demonstrated to antagonize type I IFN production in a variety of epithelial and fibroblast cell types through several mechanisms, including degradation of multiple interferon regulatory factors by a viral nonstructural protein. This report demonstrates that stimulation of highly purified primary human peripheral plasmacytoid dendritic cells (pDCs) with either live or inactivated RRV induces substantial IFNα production by a subset of pDCs in which RRV does not replicate. Characterization of pDC responses to viral stimulus by flow cytometry and Luminex revealed that RRV replicates in a small subset of human primary pDCs and, in this RRV-permissive small subset, IFNα production is diminished. pDC activation and maturation were observed independently of viral replication and were enhanced in cells in which virus replicates. Production of IFNα by pDCs following RRV exposure required viral dsRNA and surface proteins, but neither viral replication nor activation by trypsin cleavage of VP4. These results demonstrate that a minor subset of purified primary human peripheral pDCs are permissive to RRV infection, and that pDCs retain functionality following RRV stimulus. Additionally, this study demonstrates trypsin-independent infection of primary peripheral cells by rotavirus, which may allow for the establishment of extraintestinal viremia and antigenemia. Importantly, these data provide the first evidence of IFNα induction in primary human pDCs by a dsRNA virus, while simultaneously demonstrating impaired IFNα production in primary human cells in which RRV replicates. Rotavirus infection of primary human pDCs provides a powerful experimental system for the study of mechanisms underlying pDC-mediated innate immunity to viral infection and reveals a potentially novel dsRNA-dependent pathway of IFNα induction.

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Interferon-alpha in viral and bacterial gastroenteritis: a comparison with C-reactive protein and interleukin-6

Cited by 9 publications

References 6 publications

Celiac Disease—Sandwiched between Innate and Adaptive Immunity

Celiac Disease—Sandwiched between Innate and Adaptive Immunity

IL-1β/IL-6/CRP and IL-18/ferritin: Distinct Inflammatory Programs in Infections

Rotavirus Structural Proteins and dsRNA Are Required for the Human Primary Plasmacytoid Dendritic Cell IFNα Response

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