Effects of Ultraviolet‐B Exposure on the Resistance to <i>Listeria monocytogenes</i> in the Rat

Goettsch, Wim; Garssen, Johan; Klerk, Arja de; Herremans, Tineke; Dortant, P.M.; Gruijl, Frank R. de; Loveren, Henk Van

doi:10.1111/j.1751-1097.1996.tb05672.x

Cited by 53 publications

(49 citation statements)

References 16 publications

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“…Suberythemal, distant UV exposure can inhibit specific cellular immunity to L. monocytogenes. Lymphocyte proliferation assays as well as DTH responses to Listeria particles in a rat infection model were significantly inhibited after suberythemal UV exposure (6). An increased Listeria load in the spleen and liver was observed, which indicates that the cellular immune parameters lymphocyte proliferation and DTH correlated well with impaired resistance.…”

Section: Discussionmentioning

confidence: 87%

“…In addition, UV-B exposure has been demonstrated to impair resistance to bacterial, viral, parasitic, and fungal infections. Importantly, the effects of UV are not restricted to skin-associated infections, but also to systemic (non-skin-associated) infections (3)(4)(5)(6)(7)(8)(9). Because UV-B is not able to penetrate much beyond the upper cell layers of the epidermis, UV-B-induced immunosuppression is probably mediated by these exposed cells, their products, or photoactivated factors present in the superficial layers.…”

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confidence: 99%

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Transcription-Coupled and Global Genome Repair Differentially Influence UV-B-Induced Acute Skin Effects and Systemic Immunosuppression

Garssen¹,

Steeg

Gruijl

et al. 2000

The Journal of Immunology

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Exposure to UV-B radiation impairs immune responses in mammals by inhibiting especially Th1-mediated contact hypersensitivity and delayed-type hypersensitivity. Immunomodulation is not restricted to the exposed skin, but is also observed at distant sites, indicating the existence of mediating factors such as products from exposed skin cells or photoactivated factors present in the superficial layers. DNA damage appears to play a key role, because enhanced nucleotide excision repair (NER) strongly counteracts immunosuppression. To determine the effects of the type and genomic location of UV-induced DNA damage on immunosuppression and acute skin reactions (edema and erythema) four congenic mouse strains carrying different defects in NER were compared: CSB and XPC mice lacking transcription-coupled or global genome NER, respectively, as well as XPA and TTD/XPD mice carrying complete or partial defects in both NER subpathways, respectively. The major conclusions are that 1) transcription-coupled DNA repair is the dominant determinant in protection against acute skin effects; 2) systemic immunomodulation is only affected when both NER subpathways are compromised; and 3) sunburn is not related to UV-B-induced immunosuppression.

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Section: Discussionmentioning

confidence: 87%

mentioning

confidence: 99%

Transcription-Coupled and Global Genome Repair Differentially Influence UV-B-Induced Acute Skin Effects and Systemic Immunosuppression

Garssen¹,

Steeg

Gruijl

et al. 2000

The Journal of Immunology

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“…UVR-induced immunosuppression occurs via a number of different pathways that will not be discussed in detail here. Briefly, UVR exposure can cause immunosuppression by inhibiting antigen presentation, inducing the release of immunosuppressive cytokines, reducing phagocytosis by macrophages, suppressing natural cytotoxicity activity, and inducing the stress response [41,152,153]. The mechanisms of UVR-induced immunosuppression have been studied predominantly in mammals, but given that the innate and adaptive immune system of amphibians is similar to that of mammals [151], it is likely that these immunosuppressive mechanisms also occur in amphibians.…”

Section: Uvr and Biotic Factors Infectious Diseasementioning

confidence: 99%

Drivers of amphibian declines: effects of ultraviolet radiation and interactions with other environmental factors

Alton

Franklin

2017

Clim Chang Responses

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As a consequence of anthropogenic environmental change, the world is facing a possible sixth mass extinction event. The severity of this biodiversity crisis is exemplified by the rapid collapse of hundreds of amphibian populations around the world. Amphibian declines are associated with a range of factors including habitat loss/ modification, human utilisation, exotic/invasive species, environmental acidification and contamination, infectious disease, climate change, and increased ultraviolet-B radiation (UVBR) due to stratospheric ozone depletion. However, it is recognised that these factors rarely act in isolation and that amphibian declines are likely to be the result of complex interactions between multiple anthropogenic and natural factors. Here we present a synthesis of the effects of ultraviolet radiation (UVR) in isolation and in combination with a range of naturally occurring abiotic (temperature, aquatic pH, and aquatic hypoxia) and biotic (infectious disease, conspecific density, and predation) factors on amphibians. We highlight that examining the effects of UVR in the absence of other ecologically relevant environmental factors can greatly oversimplify and underestimate the effects of UVR on amphibians. We propose that the pathways that give rise to interactive effects between multiple environmental factors are likely to be mediated by the behavioural and physiological responses of amphibians to each of the factors in isolation. A sound understanding of these pathways can therefore be gained from the continued use of multi-factorial experimental studies in both the laboratory and the field. Such an understanding will provide the foundation for a strong theoretical framework that will allow researchers to predict the combinations of abiotic and biotic conditions that are likely to influence the persistence of amphibian populations under future environmental change.

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“…In addition to locally compromising the host's defense against skin tumors, UVB-induced systemic immune suppression may influence the development and course of infectious disease. Although the evidence that this type of immune suppression occurs in humans is less compelling and still incomplete, studies with rodents have clearly demonstrated that exposure to UVB suppresses the resistance against both systemic and non-skin-associated local infections [3][4][5][6][7]. However, the mechanism by which UVB impairs the immunity to infectious disease is not known.…”

Section: Introductionmentioning

confidence: 99%

Systemic suppression of human peripheral blood phagocytic leukocytes after whole-body UVB irradiation

Leino

Saarinen

et al. 1999

Journal of Leukocyte Biology

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We examined systemic effects of wholebody UVB irradiation on human peripheral blood phagocytes. We found that 24 h after a single erythemal dose of UVB radiation two phagocyte functions, adhesion and phagocytosis, were reduced by 50%. This functional suppression was accompanied by a significant decrease in the expression of complement receptors (CR1 and CR3) and IgG Fc receptors (FcRII and FcRIII). The greatest reduction (47%) was observed in CR3, which is important for both adhesion and phagocytosis. A kinetic analysis showed that both CR1 and CR3 levels started to decrease 15 min after the UVB exposure, reaching the lowest levels at 4.5-and 24-h time points, respectively. The down-modulation of CRs after whole-body UVB exposure was not due to a defective receptor synthesis or translocation from internal stores to plasma membrane because the maximal CR levels in stimulated cells were not affected by UVB. No change in the serum soluble ICAM-1 was detected after UVB, which rules out CD11b epitope masking by sICAM-1. UVB did not release low-receptor-density myeloid progenitor cells from storage pools into circulation. Interleukin 10, a mediator of UVB-induced immunosuppression, was unable to modulate CR expression in vitro. When seven suberythemal whole-body UVB exposures were given repeatedly within 2 weeks, a significant decrease in CR expression was seen, which was greatest after three irradiations. Our data suggest that an exposure to UVB has systemic effects in humans which, possibly due to the down-modulation of preexisting cell-surface receptors, suppress some important functions of circulating phagocytic cells. J. Leukoc. Biol. 65: 573-582; 1999.

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Effects of Ultraviolet‐B Exposure on the Resistance to Listeria monocytogenes in the Rat

Cited by 53 publications

References 16 publications

Transcription-Coupled and Global Genome Repair Differentially Influence UV-B-Induced Acute Skin Effects and Systemic Immunosuppression

Transcription-Coupled and Global Genome Repair Differentially Influence UV-B-Induced Acute Skin Effects and Systemic Immunosuppression

Drivers of amphibian declines: effects of ultraviolet radiation and interactions with other environmental factors

Systemic suppression of human peripheral blood phagocytic leukocytes after whole-body UVB irradiation

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