Sulfur mustard (SM) is a strong toxic agent that causes acute and chronic health effects on a myriad of organs following exposure. Although the primary targets of inhaled mustard gas are the epithelia of the upper respiratory tract, the lower respiratory tract is the focus of the current study, and upper tract complications remain obscure. To our knowledge there is no study addressing the secretory IgA (S-IgA), C5a, alpha 1 antitrypsin (A1AT) in the saliva of SM-exposed victims. In this study, as many as 500 volunteers, including 372 SM-exposed cases and 128 control volunteers were recruited. A 3 ml sample of saliva was collected from each volunteer, and the level of secretory IgA, C5a, and alpha 1 antitrypsin in the samples were compared between the two groups. The SM-exposed group showed a significantly higher amount of salivary alpha 1 antitrypsin and secretary IgA compared to the control group (p<.006 and p<.018 respectively). The two groups showed no significant difference (p=0.192) in the level of C5a. The results also showed that the level of salivary A1AT is more than that of IgA in severely injured cases. The findings presented here provide valuable insight for both researchers and practitioners dealing with victims of the chemical warfare agent, sulfur mustard. This research indicates that certain branches of the inflammatory processes mandate serious attention in therapeutic interventions.
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http://dx.doi.org/10.1016/j.intimp.2012.12.021 | DOI Listing |
Ecotoxicol Environ Saf
December 2024
Department of Clinical Laboratory, The First Affiliated Hospital, and College of Clinical Medicine of Henan University of Science and Technology, Luoyang, China. Electronic address:
Background: Podophyllotoxin (PPT), a highly active compound extracted from the rhizome of Dysosma versipellis (DV), has been used as an effective anti-cancer drug clinically since the 1950s. It possesses various biological activities, including antiviral and antitumor effects. However, its clinical application is severely limited due to its hepatotoxicity, and the underlying mechanisms remain unclear.
View Article and Find Full Text PDFNan Fang Yi Ke Da Xue Xue Bao
November 2024
Xi'an TANK Medicinal Biology Institute, Xi'an 710032, China.
Objective: To explore the therapeutic mechanism of maggot for psoriasis-like lesions in mice from the perspective of immune stress and complement activation regulation.
Methods: Thirty-six male C57BL/6 mice were randomly divided into control group, model group, maggot (1.25%, 2.
J Clin Med
November 2024
Department of Periodontics, School of Dentistry, University of Granada, 18071 Granada, Spain.
: This review synthesizes the role of () and () in modulating immune responses through citrullination and assesses its impact on periodontitis and systemic conditions. A systematic review was conducted on preclinical and clinical studies focusing on and -induced citrullination and its effects on immune responses, particularly inflammatory pathways, and systemic diseases. The search included PubMed, Scopus, Google Scholar, Web of Science, and gray literature.
View Article and Find Full Text PDFInt J Mol Sci
November 2024
Division of Human Genetics, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA.
Fabry disease is a rare X-linked lysosomal storage disorder caused by mutations in the galactosidase alpha () gene, resulting in the accumulation of globotriaosylceramide (Gb3) and its deacetylated form, globotriaosylsphingosine (Lyso-Gb3) in various tissues and fluids throughout the body. This pathological accumulation triggers a cascade of processes involving immune dysregulation and complement system activation. Elevated levels of complement 3a (C3a), C5a, and their precursor C3 are observed in the plasma, serum, and tissues of patients with Fabry disease, correlating with significant endothelial cell abnormalities and vascular dysfunction.
View Article and Find Full Text PDFPharmaceutics
September 2024
Department of Medicine, Rush University Medical Center, Chicago, IL 60612, USA.
A major reason for the failure of the immune system to detect tumor antigens (TAs) is the insufficient uptake, processing, and presentation of TAs by antigen-presenting cells (APCs). The immunogenicity of TAs in the individual patient can be markedly increased by the in situ targeting of tumor cells for robust uptake by APCs, without the need to identify and characterize the TAs. This is feasible by the intra-tumoral injection of α-gal micelles comprised of glycolipids presenting the carbohydrate-antigen "α-gal epitope" (Galα1-3Galβ1-4GlcNAc-R).
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