Mast cells initiate early anti-Listeria host defences

Gekara, Nelson O.; Weiß, Siegfried

doi:10.1111/j.1462-5822.2007.01033.x

Cited by 40 publications

(52 citation statements)

References 45 publications

(29 reference statements)

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“…Mast cells are known to be ready sources of several proinflammatory cytokines that are released rapidly to initiate antibacterial host defenses (20,22,(36)(37)(38)(39).We now show that mast cells also can elicit type I IFNs but only in response to viral infection. As shown in this study, during L. monocytogenes infection strong type I IFN signaling attenuates mast cell-dependent neutrophil recruitment that is required for bacterial clearance.…”

Section: Discussionmentioning

confidence: 70%

“…However, whether mast cells also contribute to type I IFN production and how type I IFNs modulate early inflammatory responses such as neutrophil mobilization is undetermined. As shown previously (22), mice depleted of mast cells were impaired in the production of the proinflammatory cytokine TNF-α ( Fig. S1) and exhibited diminished ability to mount neutrophil recruitment ( Fig.…”

Section: Ifn-β Impairs Mast Cell-dependent Mobilization Of Neutrophilmentioning

confidence: 72%

“…Infection with bacteria is accompanied by a rapid influx of neutrophils that mediate bacterial clearance from the site of infection. Previously we showed that, in the case of L. monocytogenes, this early innate immune response is caused by proinflammatory cytokines such as TNF-α rapidly released from mast cell granules (22). In addition to proinflammatory cytokines, type I IFNs constitute a key host response induced by L. monocytogenes.…”

Section: Ifn-β Impairs Mast Cell-dependent Mobilization Of Neutrophilmentioning

confidence: 99%

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Mast cells elicit proinflammatory but not type I interferon responses upon activation of TLRs by bacteria

Dietrich¹,

Rohde

Geffers³

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

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Balanced induction of proinflammatory and type I IFN responses upon activation of Toll-like receptors (TLRs) determines the outcome of microbial infections and the pathogenesis of autoimmune and other inflammatory diseases. Mast cells, key components of the innate immune system, are known for their debilitating role in allergy and autoimmunity. However, their role in antimicrobial host defenses is being acknowledged increasingly. How mast cells interact with microbes and the nature of responses triggered thereby is not well characterized. Here we show that in response to TLR activation by Gram-positive and -negative bacteria or their components, mast cells elicit proinflammatory but not type I IFN responses. We demonstrate that in mast cells, bound bacteria and TLR ligands remain trapped at the cell surface and do not undergo internalization, a prerequisite for type I IFN induction. Such cells, however, can elicit type I IFNs in response to vesicular stomatitis virus which accesses the cytosolic retinoic acid-inducible gene I receptor. Although important for antiviral immunity, a strong I IFN response is known to contribute to pathogenesis of several bacterial pathogens such as Listeria monocytogenes . Interestingly, we observed that the mast cell-dependent neutrophil mobilization upon L. monocytogenes infection is highly impaired by IFN-β. Thus, the fact that mast cells, although endowed with the capacity to elicit type I IFNs in response to viral infection, elicit only proinflammatory responses upon bacterial infection shows that mast cells, key effector cells of the innate immune system, are well adjusted for optimal antibacterial and antiviral responses.

show abstract

Section: Discussionmentioning

confidence: 70%

Section: Ifn-β Impairs Mast Cell-dependent Mobilization Of Neutrophilmentioning

confidence: 72%

Section: Ifn-β Impairs Mast Cell-dependent Mobilization Of Neutrophilmentioning

confidence: 99%

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Mast cells elicit proinflammatory but not type I interferon responses upon activation of TLRs by bacteria

Dietrich¹,

Rohde

Geffers³

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

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show abstract

“…For example, anti-histamines block histamine whether it has been secreted from mast cells or non-mast cells and antibodies that neutralize SCF 36 or block c-Kit 37,38 can result in the depletion of mast cells in vivo, but may also influence other cell types that express c-Kit.…”

Section: Other Approachesmentioning

confidence: 99%

Immunomodulatory mast cells: negative, as well as positive, regulators of immunity

2008

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“…Since then, a large number of reports have shown similar findings, i.e., that MC deficiency results in a markedly elevated susceptibility to a host of different bacterial insults. For example, MC-deficient mice are much more sensitive to infection caused by Citrobacter rodentium (62), Helicobacter felis (63), Listeria monocytogenes (17), Pseudomonas aeruginosa (50), and invasive group A streptococci (10) than are corresponding WT animals.…”

mentioning

confidence: 99%

Infection of Mast Cells with Live Streptococci Causes a Toll-Like Receptor 2- and Cell-Cell Contact-Dependent Cytokine and Chemokine Response

2010

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Mast cells initiate early anti-Listeria host defences

Cited by 40 publications

References 45 publications

Mast cells elicit proinflammatory but not type I interferon responses upon activation of TLRs by bacteria

Mast cells elicit proinflammatory but not type I interferon responses upon activation of TLRs by bacteria

Immunomodulatory mast cells: negative, as well as positive, regulators of immunity

Infection of Mast Cells with Live Streptococci Causes a Toll-Like Receptor 2- and Cell-Cell Contact-Dependent Cytokine and Chemokine Response

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