Erratum for Maler et al., “Key Role of the Scavenger Receptor MARCO in Mediating Adenovirus Infection and Subsequent Innate Responses of Macrophages”

Maler, Mareike D.; Nielsen, Peter; Stichling, Nicole; Bar‐Sela, Gil; Ruzsics, Zsolt; Wood, Connor; Engelhard, Peggy; Suomalainen, Maarit; Győry, Ildikó; Huber, Michael; Müller–Quernheim, Joachim; Schamel, Wolfgang W. A.; Gordon, Siamon; Jakob, Thilo; Martin, Stefan F.; Jahnen‐Dechent, Willi; Greber, Urs F.; Freudenberg, Marina A.; Fejér, György

doi:10.1128/mbio.01445-17

Cited by 11 publications

(7 citation statements)

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“…2 c). In vitro experiments confirmed that only Ad-exposed wt, but not MARCO −/− alveolar macrophage-like MPI cells, the latter lacking the sensitizing IFN-αβ response to Ad [ 17 ], overproduce IFN-αβ following LPS stimulation (shown in Fig. 2 d).…”

Section: Resultsmentioning

confidence: 75%

“…S2, bottom left) or RPM ( Fig. 3 ) show impaired Ad uptake and IFN-αβ response ([ 17 ] and Fig. 2 b), which excludes an IFN-αβ-mediated autocrine sensitizing effect.…”

Section: Resultsmentioning

confidence: 99%

“…Since macrophages and cDC are major immune cell targets for Ad entry and subsequent production of the sensitizing IFN-αβ in intraperitoneally infected mice, we first aimed to identify the receptor involved in Ad uptake and sensitization. Several paths of adenovirus entry into macrophages, such as direct uptake via β3 integrin and MARCO [ 17 , 18 ] and indirect uptake via receptors for soluble factors binding to the virus, were described in the past. The latter include natural antibodies, complement proteins C3 and C4, and coagulation factor X [ 68 ].…”

Section: Discussionmentioning

confidence: 99%

“…In mice, MARCO expression is restricted to macrophages in the splenic marginal zone, lung alveoli, and to distinct populations of macrophages in lymph nodes [ 69 , 70 ]. Notably, BMM and RAW 264.7 cells, two types of mouse cells frequently used in macrophage studies, do not express MARCO, and as a consequence, BMM do not produce IFN-αβ after exposure to Ad [ 17 ]. MARCO can, however, be induced on non-expressing macrophages by infection, such as on MARCO-negative Kupffer cells in the liver after exposure to the bacillus Calmette-Guerin or during bacterial sepsis [ 71 ].…”

Section: Discussionmentioning

confidence: 99%

“…Conventional dendritic cells (cDC) and macrophages in the spleen and macrophages in the liver are the main cells taking up adenovirus in intraperitoneally infected mice, and CD11c + CD11b + cDCs in the spleen are the major source of a robust IFN-αβ response [ 16 ]. In our previous in vitro experiments, using blocking antibodies and macrophages generated from knockout mice, and in over-expression studies, we have shown that the macrophage receptor with collagenous structure (MARCO), a member of the class A scavenger receptors, is a major macrophage receptor for Ad with hexon, a major Ad capsid protein, as its binding partner [ 17 , 18 ]. MARCO is expressed only on a small number of macrophage subsets such as alveolar (AM) [ 19 ] and spleen marginal zone macrophages (MZM) [ 20 ] but can be induced in macrophages normally not expressing MARCO by some inflammatory stimuli [ 21 ].…”

Section: Introductionmentioning

confidence: 99%

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Type I interferon, induced by adenovirus or adenoviral vector infection, regulates the cytokine response to LPS in a macrophage type-specific manner

Maler,

Zwick,

Kallfass

et al. 2024

J Innate Immun

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In mice, adenovirus (Ad)-elicited IFN-ab mediates the overproduction of LPS stimulated cytokines such as TNFa and IL-6. We found that Ad infection also mediates the overproduction of IFN-ab itself and enables its production in splenic marginal zone macrophages, which don’t produce IFN-ab in response to LPS alone. We show the importance of the scavenger receptor MARCO for Ad uptake and cytokine overproduction in vivo, and the differential contribution of infection and rIFN-b to LPS-induced cytokine response in macrophage subsets. TNF-a and IL-6 responses are enhanced in alveolar macrophages and alveolar macrophage-like lines, but downregulated in bone-marrow-derived and peritoneal macrophages, which correlates with the absence and presence of the anti-inflammatory IL-10 response. The IFN-ab response to LPS is enhanced in all four macrophage types. In Ad-infected mice, the rough LPS chemotype-induced TNF-a production partially depends on the LPS co-receptor CD14, while the IL-10 response is independent of CD14. The IFN-ab responses are strictly CD14-dependent, and partly IRF-3-independent. Upregulated TNF-a and IL-6, and downregulated IL-10 responses to LPS were also found in human blood treated ex vivo with SARS-CoV-2 adenovirus vaccine or rIFN-b. The altered reactivity of cytokine-producing cells to the ubiquitously present LPS could promote adverse effects of viral infection or vaccination.

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Section: Resultsmentioning

confidence: 75%

“…S2, bottom left) or RPM ( Fig. 3 ) show impaired Ad uptake and IFN-αβ response ([ 17 ] and Fig. 2 b), which excludes an IFN-αβ-mediated autocrine sensitizing effect.…”

Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Type I interferon, induced by adenovirus or adenoviral vector infection, regulates the cytokine response to LPS in a macrophage type-specific manner

Maler,

Zwick,

Kallfass

et al. 2024

J Innate Immun

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Adenoviral strategies to overcome innate cellular responses to infection

Sohn

Hearing

2019

FEBS Letters

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Viruses alter host cell processes to optimize their replication cycle. Human adenoviruses (Ad) encode proteins that promote viral macromolecular synthesis and counteract innate and adaptive responses to infection. The focus of this review is on how Ad evades innate cellular responses to infection, including an interferon (IFN) response and a DNA damage response (DDR). Ad blocks the IFN response by inhibiting cytoplasmic signaling pathways and the activation of IFN-stimulated genes (ISGs), as well as the functions of ISG products, such as PML. Ad also inhibits DDR sensors, for instance, the Mre11-Rad50-Nbs1 complex, and DDR effectors like DNA ligase IV. These innate cellular responses impact many different viruses, and studies on Ad have provided broad insight into these areas.

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Innate immunity to adenovirus: lessons from mice

2019

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Adenovirus is a highly evolutionary successful pathogen, as it is widely prevalent across the animal kingdom, infecting hosts ranging from lizards and frogs to dolphins, birds, and humans. Although natural adenovirus infections in humans rarely cause severe pathology, intravenous injection of high doses of adenovirus-based vectors triggers rapid activation of the innate immune system, leading to cytokine storm syndrome, disseminated intravascular coagulation, thrombocytopenia, and hepatotoxicity, which individually or in combination may cause morbidity and mortality. Much of the information on exactly how adenovirus activates the innate immune system has been gathered from mouse experimental systems. Intravenous administration of adenovirus to mice revealed mechanistic insights into cellular and molecular components of the innate immunity that detect adenovirus particles, activate pro-inflammatory signaling pathways and cytokine production, sequester adenovirus particles from the bloodstream, and eliminate adenovirus-infected cells. Collectively, this information greatly improved our understanding of mechanisms of activation of innate immunity to adenovirus and may pave the way for designing safer adenovirus-based vectors for therapy of genetic and acquired human diseases.Human adenovirus (HAdv) is remarkably efficient at infecting and replicating in human cells. These properties made HAdv-based vectors an attractive platform for developing novel therapeutics to combat genetic diseases and cancer. Unfortunately, early studies revealed that HAdv is a potent activator of the innate and adaptive arms of the immune system, and administration to animals or patients of high doses of HAdv-based vectors, especially via an intravascular route, leads to severe immunopathology, manifested by cytokine storm syndrome, disseminated intravascular coagulation, thrombocytopenia, and hepatotoxicity, which may lead to morbidity and even mortality. To harness the full potential of HAdv as a gene delivery or oncolytic virus platform, a complete understanding of the molecular and cellular components of innate Abbreviations is a founder, shareholder, and chief scientific officer of AdCure Bio, LLC, which develops Ad-based therapies for clinical use.

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Erratum for Maler et al., “Key Role of the Scavenger Receptor MARCO in Mediating Adenovirus Infection and Subsequent Innate Responses of Macrophages”

Abstract: Affiliations i and l were given incorrectly. The affiliation line should appear as shown above.

Cited by 11 publications

References 0 publications

Type I interferon, induced by adenovirus or adenoviral vector infection, regulates the cytokine response to LPS in a macrophage type-specific manner

Type I interferon, induced by adenovirus or adenoviral vector infection, regulates the cytokine response to LPS in a macrophage type-specific manner

Adenoviral strategies to overcome innate cellular responses to infection

Innate immunity to adenovirus: lessons from mice

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