scholarly journals Dermal Mast Cells Determine Susceptibility to Ultraviolet B–induced Systemic Suppression of Contact Hypersensitivity Responses in Mice

1998 ◽  
Vol 187 (12) ◽  
pp. 2045-2053 ◽  
Author(s):  
Prue H. Hart ◽  
Michele A. Grimbaldeston ◽  
Georgina J. Swift ◽  
Aleksandra Jaksic ◽  
Frances P. Noonan ◽  
...  
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Ultraviolet B ◽  
Contact Hypersensitivity ◽  
Delayed Type Hypersensitivity ◽  
Parental Origin ◽  
Uvb Radiation ◽  
Uvb Irradiation ◽  
Systemic Immunosuppression ◽  
Different Strains

Different strains of mice have varying susceptibilities to ultraviolet radiation (UV) of wavelength 280–320 nm (UVB) for 50% suppression of systemic contact hypersensitivity (CHS) responses. Prevalence of histamine-staining dermal mast cells in different strains of mice (C57BL/ 6J, DBA/2, BALB/c) correlated directly with their susceptibility to UVB-induced systemic immunosuppression. BALB/c mice carrying Uvs1, a major locus for susceptibility to UV-induced immunosuppression, contained greater numbers of dermal mast cells than BALB/c mice of the same parental origin. Strains of mice that were differentiated on their susceptibility to UVB-induced downregulation of systemic CHS responses were similar in their susceptibility to histamine-induced immunomodulation. Histamine, but not UVB irradiation, decreased systemic CHS responses in mast cell–depleted mice (W  f/W  f). Reconstitution of the dorsal skin of W  f/W  f mice with bone marrow–derived mast cell precursors from nonmutant mice rendered the mice susceptible to UVB irradiation for systemic suppression of CHS responses. UVB irradiation did not suppress delayed type hypersensitivity responses to allogeneic spleen cells in W  f/W  f mice. In contrast, UV irradiation suppressed CHS responses in W  f/W  f mice when hapten was applied to the irradiated site. This study demonstrates that dermal mast cells are necessary for the induction of systemic suppression of CHS responses by UVB radiation, and suggests that mast cell– derived histamine is one component of this UVB-induced systemic immunosuppression.

scholarly journals Protective Effect of Bixin Isolated from Bixa orellana L. Seeds on UVB-Induced Inflammation and Immunosuppression of the Skin

2018 ◽  
Vol 18 (1) ◽  
pp. 107-111 ◽  
Author(s):  
Atina Hussaana ◽  
Suparmi ◽  
Hani Afnita Murti
Keyword(s):  
Medical Science ◽  
Skinfold Thickness ◽  
Ultraviolet B ◽  
Contact Hypersensitivity ◽  
Control Group ◽  
Uvb Radiation ◽  
Bixa Orellana ◽  
Uvb Irradiation ◽  
Significant Difference ◽  
Inflammatory Edema

Background: DNA damage caused by excessive ultraviolet B (UVB) radiation on the skin triggers the response to inflammatory and immunosuppression. The bixin from Bixa orellana L. has been proven to be able to inhibit cyclo-oxygenase. Objective: to verify whether the bixin lotion has the effect to offer protection against inflammation and immunosuppression due to acute UVB irradiation in shaved BALB /c mice. Methods: Protection against inflammation and immunosuppression, respectively were studied in 4 groups of mice. Each group was treated respectively with topical application of base lotion as a control; bixin lotion doses of 0.5 mg; 2.5 mg and 125 mg, for 10 days prior to and during the UVB irradiation. The Inflammation was induced by UVB irradiation, 360 mJ/cm2 once a day for 3 consecutive days, whereas the immunosuppression was induced by UVB irradiation, 360 mJ/cm2 once a day for 5 consecutive days. The inflammatory response was measured as an increase in middorsal skinfold thickness at the peak response. The immune response was measured as the contact hypersensitivity (CHS) response to oxasolon sensitization. Results: The results indicated that in concentration range used, bixin lotion significantly decreased the middorsal skinfold thickness at 72 hours after UVB radiation (p <0.05) compared to the control, but there was no significant difference between couples of the dose of bixin. Bixin lotion was also capable to restore the suppression of CHS from 34.22% in the control group to 11.4%; 0.5% and 0% at doses of 0.5; 2.5 and 125 mg respectively (p <0.05). Conclusion: Bixin lotion has the potential to reduce the inflammatory edema reaction and the suppression of CHS of mice induced by UVB radiation. Bangladesh Journal of Medical Science Vol.18(1) 2019 p.107-111

scholarly journals UVB irradiation of human platelet concentrates does not prevent HLA alloimmunization in recipients

Blood ◽  
1994 ◽  
Vol 84 (10) ◽  
pp. 3524-3531
Author(s):  
MA Grijzenhout ◽  
MI Aarts-Riemens ◽  
FR de Gruijl ◽  
H van Weelden ◽  
HC van Prooijen
Keyword(s):  
Cell Death ◽  
Hla Antigens ◽  
Ultraviolet B ◽  
Control Group ◽  
Unexpected Finding ◽  
Uvb Radiation ◽  
Platelet Concentrates ◽  
Uvb Irradiation ◽  
Hla Class I Antigens ◽  
Delayed Cell Death

Exposure of platelet concentrates (PCs) to ultraviolet B radiation (UVB) has been advocated as an alternative method for prevention of the onset of HLA sensitization in recipients. In this study, pooled PCs were irradiated in a Haemonetics UV irradiator (Haemonetics Corp, Braintree, MA) at a dose that did not induce platelet activation. The effect of UVB irradiation on prevention of primary HLA sensitization was evaluated in a prospective controlled clinical study performed in cardiac patients undergoing cardiopulmonary bypass. Patients were treated with filtered red blood cells and a single transfusion of either standard (control group) or UVB-irradiated (UVB group) pooled platelets prepared from 12 donors. Five of 39 patients in the control group and 6 of 62 patients in the UVB group developed allo-antibodies against HLA antigens, which is not significantly different (P = .62). This unexpected finding prompted us to check the efficacy of UVB irradiation. We determined UVB-specific DNA damage in cells by measuring the fluorescence from a labeled specific monoclonal antibody against thymine dimers. With this novel flow cytometer technique, we estimated in UVB-irradiated leukocytes in saline that a mean fluorescence intensity (MFI) of 47 +/- 2 arbitrary units (n = 6) correlated with abolition of alloreactivity in mixed lymphocyte cultures and delayed cell death (within 72 hours). MFI in leukocytes suspended in plasma and exposed to the clinical dose of UVB was sixfold higher (310 +/- 41 arbitrary units) and resulted in early cell death (within 24 hours). We hypothesize that this high level of UVB radiation induces fragmentation of the leukocytes. As a consequence, the poor results of UVB irradiation may be explained by the onset of HLA- alloimmunization induced by soluble donor HLA class I antigens processed and presented by host antigen-presenting cells.

scholarly journals Effect of Lactobacillus reuteri Administration on Wrinkle Formation and Type I Procollagen Levels in UVB-Exposed Male Balb/c Mice (Mus musculus)

2020 ◽  
Vol 4 (3) ◽  
pp. 113
Author(s):  
Ivanna Valentina ◽  
Achadiyani Achadiyani ◽  
Sunarjati Sudigdo Adi ◽  
Ronny Lesmana ◽  
Reni Farenia
Keyword(s):  
Oxidative Stress ◽  
Lactobacillus Reuteri ◽  
Ultraviolet B ◽  
Type I ◽  
Uvb Radiation ◽  
Dorsal Skin ◽  
Uvb Irradiation ◽  
Type I Procollagen ◽  
Group 3 ◽  
Group 1

Background: Chronic Ultraviolet B (UVB) exposure causes oxidative stress that may induce damages to the collagen matrix and thus plays a role in the wrinkle formation. Lactobacillus reuteri is a probiotic that may exerts antioxidant effects, thus helping to reduce damages caused by UVB-induced oxidative stress in the skin.Materials and Methods: Twenty-eight male Balb/c mice were divided equally into control group, UVB radiation only group, oral L. reuteri supplementation only group, and UVB radiation with oral L. reuteri supplementation group. UVB irradiation was given 3 times a week (100 seconds/exposure, within 3 cm distance) for 10 weeks, with a total dose of 166 mJ/cm2. Oral L. reuteri supplementation (0.2 mL, 108 CFU) was provided every morning after meal via orogastric feeding tube for 10 weeks. Wrinkle formation on the dorsal skin of the mice was evaluated in accordance with the Bissett method and type I procollagen levels was evaluated by western blotting.Results: In comparison with the group receiving only UVB irradiation, the group receiving probiotic and UVB irradiation showed significantly lower wrinkle scores (Group 1 vs. Group 3, 2.50±0.55 vs. 1.00±0,00; p<0.05) and significantly higher type I procollagen levels (Group 1 vs. Group 3, 0.88±0.36 vs. 1.92±0.46; p<0.05).Conclusion: Results of the current study showed that L. reuteri supplementation may reduce wrinkle formation and increase type I procollagen production in UVB-exposed dorsal skin of male Balb/c mice.Keywords: Lactobacillus reuteri, type I procollagen, photoaging, wrinkles, ultraviolet B

scholarly journals UVB irradiation of human platelet concentrates does not prevent HLA alloimmunization in recipients

Blood ◽  
1994 ◽  
Vol 84 (10) ◽  
pp. 3524-3531 ◽  
Author(s):  
MA Grijzenhout ◽  
MI Aarts-Riemens ◽  
FR de Gruijl ◽  
H van Weelden ◽  
HC van Prooijen
Keyword(s):  
Cell Death ◽  
Hla Antigens ◽  
Ultraviolet B ◽  
Control Group ◽  
Unexpected Finding ◽  
Uvb Radiation ◽  
Platelet Concentrates ◽  
Uvb Irradiation ◽  
Hla Class I Antigens ◽  
Delayed Cell Death

Abstract Exposure of platelet concentrates (PCs) to ultraviolet B radiation (UVB) has been advocated as an alternative method for prevention of the onset of HLA sensitization in recipients. In this study, pooled PCs were irradiated in a Haemonetics UV irradiator (Haemonetics Corp, Braintree, MA) at a dose that did not induce platelet activation. The effect of UVB irradiation on prevention of primary HLA sensitization was evaluated in a prospective controlled clinical study performed in cardiac patients undergoing cardiopulmonary bypass. Patients were treated with filtered red blood cells and a single transfusion of either standard (control group) or UVB-irradiated (UVB group) pooled platelets prepared from 12 donors. Five of 39 patients in the control group and 6 of 62 patients in the UVB group developed allo-antibodies against HLA antigens, which is not significantly different (P = .62). This unexpected finding prompted us to check the efficacy of UVB irradiation. We determined UVB-specific DNA damage in cells by measuring the fluorescence from a labeled specific monoclonal antibody against thymine dimers. With this novel flow cytometer technique, we estimated in UVB-irradiated leukocytes in saline that a mean fluorescence intensity (MFI) of 47 +/- 2 arbitrary units (n = 6) correlated with abolition of alloreactivity in mixed lymphocyte cultures and delayed cell death (within 72 hours). MFI in leukocytes suspended in plasma and exposed to the clinical dose of UVB was sixfold higher (310 +/- 41 arbitrary units) and resulted in early cell death (within 24 hours). We hypothesize that this high level of UVB radiation induces fragmentation of the leukocytes. As a consequence, the poor results of UVB irradiation may be explained by the onset of HLA- alloimmunization induced by soluble donor HLA class I antigens processed and presented by host antigen-presenting cells.

scholarly journals Mast Cells Control Neutrophil Recruitment during T Cell–Mediated Delayed-Type Hypersensitivity Reactions through Tumor Necrosis Factor and Macrophage Inflammatory Protein 2

2000 ◽  
Vol 192 (10) ◽  
pp. 1441-1452 ◽  
Author(s):  
Tilo Biedermann ◽  
Manfred Kneilling ◽  
Reinhard Mailhammer ◽  
Konrad Maier ◽  
Christian A. Sander ◽  
...  
Keyword(s):  
Mast Cell ◽  
T Cell ◽  
Mast Cells ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Delayed Type Hypersensitivity ◽  
Hypersensitivity Reactions ◽  
Inflammatory Protein ◽  
Macrophage Inflammatory Protein ◽  
Necrosis Factor

Polymorphonuclear leukocytes (PMNs) characterize the pathology of T cell–mediated autoimmune diseases and delayed-type hypersensitivity reactions (DTHRs) in the skin, joints, and gut, but are absent in T cell–mediated autoimmune diseases of the brain or pancreas. All of these reactions are mediated by interferon γ–producing type 1 T cells and produce a similar pattern of cytokines. Thus, the cells and mediators responsible for the PMN recruitment into skin, joints, or gut during DTHRs remain unknown. Analyzing hapten-induced DTHRs of the skin, we found that mast cells determine the T cell–dependent PMN recruitment through two mediators, tumor necrosis factor (TNF) and the CXC chemokine macrophage inflammatory protein 2 (MIP-2), the functional analogue of human interleukin 8. Extractable MIP-2 protein was abundant during DTHRs in and around mast cells of wild-type (WT) mice but absent in mast cell–deficient WBB6F1-KitW/KitW-v (KitW/KitW-v) mice. T cell–dependent PMN recruitment was reduced &gt;60% by anti–MIP-2 antibodies and &gt;80% in mast cell–deficient KitW/KitW-v mice. Mast cells from WT mice efficiently restored DTHRs and MIP-2–dependent PMN recruitment in KitW/KitW-v mice, whereas mast cells from TNF−/− mice did not. Thus, mast cell–derived TNF and MIP-2 ultimately determine the pattern of infiltrating cells during T cell–mediated DTHRs.

scholarly journals UVB Irradiation Induced Cell Damage and Early Onset of Junbb Expression in Zebrafish

Animals ◽  
2020 ◽  
Vol 10 (6) ◽  
pp. 1096
Author(s):  
Rui-Yi Chen ◽  
Chun-Ju Lin ◽  
Sung-Tzu Liang ◽  
Omar Villalobos ◽  
Oliver B. Villaflores ◽  
...  
Keyword(s):  
Early Onset ◽  
Cultured Cells ◽  
Cell Damage ◽  
Biological Response ◽  
Ultraviolet B ◽  
Gene Profiling ◽  
Molecular Response ◽  
Uvb Radiation ◽  
Zebrafish Model ◽  
Uvb Irradiation

Ultraviolet B (UVB) radiation has drawn more attention over these past few decades since it causes severe DNA damage and induces inflammatory response. Serial gene profiling and high throughput data in UVB-associated phenomenon in human cultured cells or full rack of human skin have been investigated. However, results using different tissue models lead to ambiguity in UVB-induced pathways. In order to systematically understand the UVB-associated reactions, the zebrafish model was used, and whole organism gene profiling was performed to identify a novel biomarker which can be used to generate a new mechanistic approach for further screening on a UVB-related system biology. In this study, detailed morphological assays were performed to address biological response after receiving UVB irradiation at morphological, cellular, and molecular levels. Microarray screening and whole genome profiling revealed that there is an early onset expression of junbb in zebrafish embryos after UVB irradiation. Also, the identified novel biomarker junbb is more sensitive to UVB response than mmps which have been used in mouse models. Moreover, cellular and molecular response chronology after UVB irradiation in zebrafish provide a solid and fundamental mechanism for use in a UV radiation-associated study in the future.

scholarly journals An early component of delayed-type hypersensitivity mediated by T cells and mast cells.

1983 ◽  
Vol 157 (5) ◽  
pp. 1604-1617 ◽  
Author(s):  
H van Loveren ◽  
R Meade ◽  
P W Askenase
Keyword(s):  
T Cells ◽  
Mast Cell ◽  
T Cell ◽  
Mast Cells ◽  
Mast Cell Activation ◽  
Delayed Type Hypersensitivity ◽  
Antigen Binding ◽  
Hypersensitivity Reactions ◽  
Early Component ◽  
Binding Factor

In four different systems it was shown that murine delayed-type hypersensitivity (DTH) responses at 18-48 h were preceded by early 2-h responses. CBA mice immunized with picryl chloride, BDF1 mice immunized with oxazolone, BALB/c mice immunized with dinitrofluorobenzene, and C57BL/6 mice immunized with L5178Y lymphoma cells, and challenged with the appropriate specific antigen, all gave rise to expected 18-48 h delayed-in-time hypersensitivity reactions, but all of these responses were preceded by early hypersensitivity reactions that peaked at 2 h. These early 2-h reactions are transferable with T cells or with a T cell-derived, antigen-binding factor and are antigen-specific. The early and late components of DTH reactions are mast cell dependent since neither are elicited in mast cell deficient W/Wv or Sl/Sld mice. The T cell activity mediating the early component of DTH is demonstrable as early as 24 h after immunization, while the classical late component of DTH is not demonstrable until days 3-4. The difference in onset after immunization of the early and late components of DTH, and the different kinetics of these components in recipients of cell transfers that were challenged immediately or 24 h after transfer, led to the hypothesis that immunization for DTH leads to rapid induction in lymphoid organs of a certain population of T cells to produce an antigen-binding factor. This factor sensitizes peripheral tissues, probably mast cells, and local challenge with appropriate antigen leads to mast cell activation and release of the vasoactive amine serotonin, resulting in increased permeability of the local vasculature. This allows other circulating antigen-specific T cells, which are induced later after immunization, to enter the tissues and interact with antigen, resulting in production of chemoattractant lymphokines that recruit accessory leukocytes such as monocytes and polymorphs to enter the tissues via gaps between endothelial cells. These inflammatory cells, that are recruited to the site via two different T cell activities, constitute the characteristic infiltrate of DTH responses. Identification of an early 2-h component of DTH that is T cell- and mast cell-dependent provides evidence that the tissue-sensitizing, antigen-binding, T cell factor probably functions in vivo in the early phases of DTH responses.

scholarly journals Zinc transporter Znt5/Slc30a5 is required for the mast cell–mediated delayed-type allergic reaction but not the immediate-type reaction

2009 ◽  
Vol 206 (6) ◽  
pp. 1351-1364 ◽  
Author(s):  
Keigo Nishida ◽  
Aiko Hasegawa ◽  
Susumu Nakae ◽  
Keisuke Oboki ◽  
Hirohisa Saito ◽  
...  
Keyword(s):  
Mast Cell ◽  
Plasma Membrane ◽  
Mast Cells ◽  
Cell Activation ◽  
Nuclear Translocation ◽  
Nuclear Factor Κb ◽  
Allergic Response ◽  
Contact Hypersensitivity ◽  
Mast Cell Activation ◽  
Zn Homeostasis

Zinc (Zn) is an essential nutrient and its deficiency causes immunodeficiency. However, it remains unknown how Zn homeostasis is regulated in mast cells and if Zn transporters are involved in allergic reactions. We show that Znt5/Slc30a5 is required for contact hypersensitivity and mast cell–mediated delayed-type allergic response but not for immediate passive cutaneous anaphylaxis. In mast cells from Znt5−/− mice, Fcε receptor I (FcεRI)–induced cytokine production was diminished, but degranulation was intact. Znt5 was involved in FcεRI-induced translocation of protein kinase C (PKC) to the plasma membrane and the nuclear translocation of nuclear factor κB. In addition, the Zn finger–like motif of PKC was required for its plasma membrane translocation and binding to diacylglycerol. Thus, Znt5 is selectively required for the mast cell–mediated delayed-type allergic response, and it is a novel player in mast cell activation.

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