Effect of combined radiation injury on cell death and inflammation in skin

Jadhav, Sachin Suresh; Meeks, Christopher J.; Mordwinkin, Nicholas M.; Espinoza, Theresa; Louie, Stan G.; diZerega, Gere S.; Rodgers, Kathleen E.

doi:10.1007/s10495-015-1116-2

Cited by 12 publications

(7 citation statements)

References 52 publications

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“…Whether the expression of death receptors and the concentrations of their ligands are sufficient to induce apoptosis remains an open question (see the section on death-receptor-linked apoptosis). While caspase 9 immunoreactivity has not been analysed in vivo after thermal stress, an intrinsic pathway has not been excluded, as Bax was identified on the mRNA level in murine skin after thermal trauma [ 50 ]. However, the precise involvement of mitochondria or the endoplasmic reticulum (ER) in thermally induced regulated cell death has not been analysed in human skin.…”

Section: Apoptosis Of Keratinocytes In Vitromentioning

confidence: 99%

Burn Injury: Mechanisms of Keratinocyte Cell Death

Rennekampff¹,

Alharbi

2021

Medical Sciences

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Cutaneous burn injury is associated with epidermal loss in the zone of coagulation zone and delayed tissue loss in the zone of stasis. Thus, thermal stress can trigger both necrosis and regulated cell death (RCD) or apoptosis. Experimental in vitro and in vivo work has clearly demonstrated apoptotic events of thermally injured keratinocytes that are accompanied by morphological and biochemical markers of regulated cell death. However, in vivo data for the different pathways of regulated cell death are sparse. In vitro experiments with heat-stressed human keratinocytes have demonstrated death receptor involvement (extrinsic apoptosis), calcium influx, and disruption of mitochondrial membrane potential (intrinsic apoptosis) in regulated cell death. In addition, caspase-independent pathways have been suggested in regulated cell death. Keratinocyte heat stress leads to reduced proliferation, possibly as a result of reduced keratinocyte adhesion (anoikis) or oncogene involvement. Understanding the underlying mechanisms of RCD and the skin’s responses to thermal stress may lead to improved strategies for treating cutaneous burn trauma.

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Section: Apoptosis Of Keratinocytes In Vitromentioning

confidence: 99%

Burn Injury: Mechanisms of Keratinocyte Cell Death

Rennekampff¹,

Alharbi

2021

Medical Sciences

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“…Ionizing radiation produces large amounts of free radicals and ROS which can be toxic to many tissues, including the skin . Additionally, the ROS generated by radiation is known to be a contributing factor to immune reactions and local inflammation via its promotion of the secretion of certain cytokines, including TNF‐α, IL‐1β, IL‐6, and other proinflammation factors .…”

Section: Discussionmentioning

confidence: 69%

Ionizing radiation promotes CCL27 secretion from keratinocytes through the cross talk between TNF‐α and ROS

Zhang

Zhu

Wang

et al. 2016

J Biochem & Molecular Tox

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The skin-associated chemokine CCL27 and its receptor CCR10 mediate the immune response of skin-homing T cells. The CCL27 secreted from keratinocytes was reportedly involved in inflammatory skin diseases such as atopic dermatitis, contact dermatitis, and psoriasis. However, whether ionizing radiation increases the levels of CCL27 secretion still remains unclear. In HaCaT cells, a human keratinocyte cell line, CCL27 secretion was markedly increased after X-ray irradiation. We further found that irradiation boosted the generation of reactive oxygen species (ROS), which was concomitant with the release of tumor necrosis factor-alpha (TNF-α). Moreover, alteration of ROS in irradiated HaCaT cells correlated with TNF-α secretion, indicating a positive loop of TNF-α secretion and ROS generation. This positive loop regulated the secretion of CCL27 from irradiated cells. We therefore concluded that the cross talk between TNF-α and ROS after keratinocytes was exposed to radiation, triggered CCL27 secretion for subsequent inflammation response.

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Section: Resultsmentioning

confidence: 99%

“…Combined radiation lesions are a multicomponent pathological process progressing with simultaneous or sequential exposure of the body to ionizing radiation and damage effects of radiation-free etiology [25]. e following mechanical, thermal, chemical, and biological factors are distinguished as damaging factors of a nonradiation nature [26]. CRL has a number of features, of which the most characteristic is the presence of signs of two or more pathologies, because of which a specific clinical picture of radiation and traumatic symptoms is formed [27].…”

Section: Resultsmentioning

confidence: 99%

Development of an Optimal Model of Combined Radiation and Biological Lesions

Gaynutdinov¹,

Vagin²,

Kurbangaleev³

et al. 2022

Veterinary Medicine International

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Since the search for the effective medication in combined lesions includes the selection of an optimal experimental model for such injuries, there is actually a study aimed at developing an optimal model of combined radiation-biology (Pasteurella) lesions. The pathogen Pasteurella multocida (as one of the most frequent pathogenic agents involved in both isolated and combined radiation-biology lesions of agricultural animals) was used as a model of a biological agent to reproduce experimental biological research. We employed the “Chinchilla” rabbits of 2.5–3.0 kg body weight as a biological model for doing combined radiation Pasteurella lesion. When determining the optimal model of combined radiation-biology (Pasteurella) lesion, we consider that in the joint action of various pathological agents on the organism, there is a synergistic effect of explosion agents, previously specifying minimal doses of external γ-radiation and pasteurellosis pathogen that in the joint action of nonfatal doses would be lethal. The first stage of the experiments determined the minimal doses of gamma rays and pasteurellosis pathogen that in joint action causes combined radiation-biology pathology. We examined 66 rabbits divided into 11 groups of 6 animals each to determine minimal doses of infectious agent-pasteurellosis pathogen. The animals of the first 9 groups were given subcutaneously Pasteurella species at doses 1·109, 1·108, 1·107, 1·106, 1·105, 1·104, 1·103, 1·102, and 1·101 of microbial cells per animal of 0.3 ml suspension in volume; the 10th group of animals were given saline solution; the 11th served as a biological control group. In determining the minimal doses of gamma rays, we conducted experimental tests on 36 rabbits, which have been exposed to external γ-radiation in the “PUMA” system with a 137Cs radiation source of the exposure dose of 5.38 R/min at doses 2.0, 4.0, 6.0, 8.0, 10, and 12 Gy. To specify the optimal model of radiation-pasteurellosis lesion, we used the rabbits subjected to a combined radiation-biology effect using minimal doses of gamma rays and pasteurellosis agent, leading to a lethal effect during their complex action. The researches revealed that 50% of the death of rabbits infected with pasteurellosis occurs using Pasteurella at a dose of 3.7·104 microbial cells per kilogram (LD50 = 3.7∙104 m.c./kg), and 50% of radiation death in rabbits occurs when irradiated their gamma rays at a dose of 8.0 Gy (LD50 = 8.0 Gy). The combined effect of nonlethal doses of the studied agents in the indicated doses on rabbits led to the aggravation of the course of radiation and pasteurellosis infection, causing the death of animals from combined radiation-pasteurellosis pathology. The model combined radiation-pasteurellosis disease ran its course rapidly, and the animals died 3 to 6 days after the onset. The autopsy of the animals that died from acute radiation-pasteurellosis pathogen had found swelling of the subcutaneous tissue in the pharynx and intermaxillary space of the neck, hyperemia, lymphoid nodular hyperplasia, numerous hemorrhages on the serous and mucous membranes and in the tissues of the parenchymal organs, serous or serous-fibrinous exudate, and in the chest and abdominal regions, pulmonary edema. The research stated that gamma radiation of rabbits at a dose of 8.0 Gy conducted before exposure with Pasteurella at LD50 (3.7·104 m.c./kg) declined the course of the pasteurellosis process, facilitated its generalization, and fastened the death of animals. Combined radiation-pasteurellosis infection ran its course rapidly, and the animals died within 3 to 6 days after the onset of the disease. The autopsy showed the pathologicoanatomic factors of the acute pasteurellosis: swelling of the subcutaneous tissue, purulent-catarrhal bronchopneumonitis, and pulmonary edema.

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Effect of combined radiation injury on cell death and inflammation in skin

Cited by 12 publications

References 52 publications

Burn Injury: Mechanisms of Keratinocyte Cell Death

Burn Injury: Mechanisms of Keratinocyte Cell Death

Ionizing radiation promotes CCL27 secretion from keratinocytes through the cross talk between TNF‐α and ROS

Development of an Optimal Model of Combined Radiation and Biological Lesions

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