scholarly journals The release of prostaglandin D2 from human skin in vivo and in vitro during immediate allergic reactions

1988 ◽  
Vol 94 (3) ◽  
pp. 773-780 ◽  
Author(s):  
R.M. Barr ◽  
O. Koro ◽  
D.M. Francis ◽  
A. Kobza Black ◽  
T. Numata ◽  
...  
2020 ◽  
pp. 40-50
Author(s):  
A. Nikitina

Analysis of literature data presented in search engines — Elibrary, PubMed, Cochrane — concerning the risk of developing type I allergic reactions in patients with blood diseases is presented. It is shown that the most common cause of type I allergic reactions is drugs included in the treatment regimens of this category of patients. The article presents statistics on the increase in the number of drug allergies leading to cases of anaphylactic shock in patients with blood diseases. Modern methods for the diagnosis of type I allergic reactions in vivo and in vitro are considered.


2005 ◽  
Vol 201 (3) ◽  
pp. 385-396 ◽  
Author(s):  
Stefan Kraft ◽  
Tony Fleming ◽  
James M. Billingsley ◽  
Shih-Yao Lin ◽  
Marie-Hélène Jouvin ◽  
...  

High-affinity IgE receptor (FcεRI) cross-linking on mast cells (MCs) induces secretion of preformed allergy mediators (degranulation) and synthesis of lipid mediators and cytokines. Degranulation produces many symptoms of immediate-type allergic reactions and is modulated by adhesion to surfaces coated with specific extracellular matrix (ECM) proteins. The signals involved in this modulation are mostly unknown and their contribution to allergic reactions in vivo is unclear. Here we report the generation of monoclonal antibodies that potently suppress FcεRI-induced degranulation, but not leukotriene synthesis. We identified the antibody target as the tetraspanin CD63. Tetraspanins are membrane molecules that form multimolecular complexes with a broad array of molecules including ECM protein-binding β integrins. We found that anti-CD63 inhibits MC adhesion to fibronectin and vitronectin. Furthermore, anti-CD63 inhibits FcεRI-mediated degranulation in cells adherent to those ECM proteins but not in nonadherent cells. Thus the inhibition of degranulation by anti-CD63 correlates with its effect on adhesion. In support of a mechanistic linkage between the two types of inhibition, anti-CD63 had no effect on FcεRI-induced global tyrosine phosphorylation and calcium mobilization but impaired the Gab2–PI3K pathway that is known to be essential for both degranulation and adhesion. Finally, we showed that these antibodies inhibited FcεRI-mediated allergic reactions in vivo. These properties raise the possibility that anti-CD63 could be used as therapeutic agents in MC-dependent diseases.


1989 ◽  
Vol 8 (5) ◽  
pp. 853-859 ◽  
Author(s):  
Ronald C. Wester ◽  
Howard I. Maibach

Contaminants exist in ground and surface water. Human skin has the capacity to bind and then absorb these contaminants into the body during swimming and bathing. Powdered human stratum corneum will bind both lipid-soluble (alachlor, polychlorinated biphenyls [PCBs], benzene) and water-soluble (nitroaniline) chemicals. In vitro (human skin) and in vivo (Rhesus monkey) studies show that these chemicals readily distribute into skin, and then some of the chemical is absorbed into the body. Linearity in binding and absorption exists for nitroaniline over a 10-fold concentration range. Multiple exposure to benzene is at least cumulative. Binding and absorption can be significant for exposures as short as 30 min, and will increase with time. Absorption with water dilution increased for alachlor, but not for dinoseb. Soap reversed the partitioning of alachlor between human stratum corneum and water. The PCBs could be removed from skin by soap and water (70% efficiency) for up to 3 h and then decontamination potential decreased, due to continuing skin absorption. The model in vitro and in vivo systems used should permit easy estimation of this area of extensive human exposure effect on risk assessment.


2017 ◽  
Vol 309 (4) ◽  
pp. 275-283 ◽  
Author(s):  
Wen-Hwa Li ◽  
Heng-Kuan Wong ◽  
José Serrano ◽  
Manpreet Randhawa ◽  
Simarna Kaur ◽  
...  
Keyword(s):  

2021 ◽  
Vol 12 ◽  
Author(s):  
Misun Kim ◽  
Hyein Jo ◽  
Yoojung Kwon ◽  
Myeong Seon Jeong ◽  
Hyun Suk Jung ◽  
...  

In a previous study, we have demonstrated that p62, a selective receptor of autophagy, can regulate allergic inflammation. In the present study, microRNA array analysis showed that miR-154-5p was increased by antigen (DNP-HSA) in a p62-dependent manner in rat basophilic leukemia cells (RBL2H3). NF-kB directly increased the expression of miR-154-5p. miR-154-5p mediated in vivo allergic reactions, including passive cutaneous anaphylaxis and passive systemic anaphylaxis. Cytokine array analysis showed that antigen stimulation increased the expression of MCP1 in RBL2H3 cells in an miR-154-5p-dependent manner. Reactive oxygen species (ROS)-ERK-NF-kB signaling increased the expression of MCP1 in antigen-stimulated RBL2H3 cells. Recombinant MCP1 protein induced molecular features of allergic reactions both in vitro and in vivo. Anaphylaxis-promoted tumorigenic potential has been known to be accompanied by cellular interactions involving mast cells, and macrophages, and cancer cells. Our experiments employing culture medium, co-cultures, and recombinant MCP1 protein showed that miR-154 and MCP1 mediated these cellular interactions. MiR-154-5p and MCP1 were found to be present in exosomes of RBL2H3 cells. Exosomes from PSA-activated BALB/C mouse induced molecular features of passive cutaneous anaphylaxis in an miR-154-5p-dependent manner. Exosomes from antigen-stimulated RBL2H3 cells enhanced both tumorigenic and metastatic potentials of B16F1 melanoma cells in an miR-154-5p-dependent manner. Exosomes regulated both ROS level and ROS mediated cellular interactions during allergic inflammation. Our results indicate that the miR-154-5p-MCP1 axis might serve as a valuable target for the development of anti-allergy therapeutics.


2016 ◽  
Vol 32 (3) ◽  
pp. 723-738 ◽  
Author(s):  
Chi-Chuan Li ◽  
Fu-Shun Yu ◽  
Ming-Jen Fan ◽  
Ya-Yin Chen ◽  
Jin-Cherng Lien ◽  
...  

Pharmaceutics ◽  
2019 ◽  
Vol 11 (7) ◽  
pp. 310 ◽  
Author(s):  
Stella Zsikó ◽  
Kendra Cutcher ◽  
Anita Kovács ◽  
Mária Budai-Szűcs ◽  
Attila Gácsi ◽  
...  

The aim of this research was to investigate the stability of a lidocaine-loaded nanostructured lipid carrier dispersion at different temperatures, formulate a nanostructured lipid carrier gel, and test the penetration profile of lidocaine from the nanostructured lipid carrier gel using different skin penetration modeling methods. The formulations were characterized by laser diffraction, rheological measurements and microscopic examinations. Various in vitro methods were used to study drug release, diffusion and penetration. Two types of vertical Franz diffusion cells with three different membranes, including cellulose, Strat-M®, and heat separated human epidermis were used and compared to the Skin-parallel artificial membrane permeability assay (PAMPA) method. Results indicated that the nanostructured lipid carrier dispersion had to be gelified as soon as possible for proper stability. Both the Skin-PAMPA model and Strat-M® membranes correlated favorably with heat separated human epidermis in this research, with the Strat-M® membranes sharing the most similar drug permeability profile to an ex vivo human skin model. Our experimental findings suggest that even when the best available in vitro experiment is selected for modeling human skin penetration to study nanostructured lipid carrier gel systems, relevant in vitro/in vivo correlation should be made to calculate the drug release/permeation in vivo. Future investigations in this field are still needed to demonstrate the influence of membranes and equipment from other classes on other drug candidates.


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