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Toxicants and Their Effects on Innate Immune Function and Inflammatory Response

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Toxicology".

Deadline for manuscript submissions: 20 November 2025 | Viewed by 531

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Department of Biological Sciences, Sam Houston State University, Huntsville, TX, USA
Interests: aging; endocrinology; comparative physiology; animal models; cell biology
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Special Issue Information

Dear Colleagues,

Toxicants such as pesticides and plasticizing agents have become ubiquitous in both terrestrial and aquatic environments. Although the effects of these man-made substances on reproductive and metabolic functions have been studied thoroughly, how they may impact other aspects of physiological functions are not as well known. For example, innate immune function serves as a critical line of defense against pathogens in both invertebrates and vertebrates, and there is mounting evidence that exposure to various toxicants may significantly impair innate immune function in multiple species. In addition, within vertebrates, the inflammatory response is an important component of an innate immune response, and it is also an important mediator of the effects of tissue injury. As with innate immune function, in general, there are data suggesting that the inflammatory response is significantly altered by exposure to various toxicants. The purpose of this Special Issue is to highlight the impact of environmental pollutants on innate immune function and the inflammatory response in both invertebrate and vertebrate animal models.

Dr. James M. Harper
Guest Editor

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Keywords

  • ecotoxicology
  • innate immunity
  • inflammation
  • pesticides
  • plasticizers
  • pattern-recognition receptors

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Published Papers (1 paper)

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Research

23 pages, 2440 KiB  
Article
LRP1 Shedding in Ricin-Induced Lung Injury: A Cell-Specific Response to Toxin Exposure
by Anita Sapoznikov, Yentl Evgy, Moshe Aftalion and Reut Falach
Int. J. Mol. Sci. 2025, 26(12), 5448; https://doi.org/10.3390/ijms26125448 - 6 Jun 2025
Abstract
Ricin is a highly potent toxin that causes severe lung injury upon inhalation by initiating a complex cascade of cellular responses that ultimately leads to cell death. The low-density lipoprotein receptor-related protein 1 (LRP1) is a multifunctional receptor involved in various physiological processes, [...] Read more.
Ricin is a highly potent toxin that causes severe lung injury upon inhalation by initiating a complex cascade of cellular responses that ultimately leads to cell death. The low-density lipoprotein receptor-related protein 1 (LRP1) is a multifunctional receptor involved in various physiological processes, including ricin-mediated toxicity. This study explores the role of LRP1 shedding in the development of ricin-induced lung injury. Analysis of bronchoalveolar lavage fluid (BALF) from ricin-intoxicated mice and swine showed a significant increase in soluble LRP1 (sLRP1) levels, whereas serum LRP1 levels remained largely unchanged, suggesting the lungs are the primary source of sLRP1 release. In vitro assays demonstrated the formation of ricin-sLRP1 complexes, indicating that sLRP1 in BALF retained ricin-binding capability. Flow cytometric analysis of lung cells revealed a reduction in both the percentage and total number of LRP1-expressing cells following ricin exposure. Further investigation of specific lung cell populations showed that alveolar epithelial type II (AT-II) cells, despite experiencing significant injury, exhibited minimal LRP1 shedding. No shedding of LRP1 occurred in neutrophils. In contrast, fibroblasts, which were resistant to ricin-induced cell death, exhibited increased shedding of LRP1 and a corresponding decrease in membrane-bound LRP1 expression. This shedding of the LRP1 ectodomain was mediated by metalloproteinases. Immunohistochemical staining further confirmed decreased LRP1 expression in fibroblasts from ricin-exposed mice. Macrophages also showed substantial LRP1 shedding, despite undergoing significant depletion. These findings highlight the complex cell-specific nature of LRP1 shedding in response to ricin intoxication and suggests the potential role of LRP1 in modulation of cellular susceptibility and resistance to ricin-induced lung injury. Full article
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