scholarly journals Elevated Plasma Level of Interferon-λ1 in Chronic Spontaneous Urticaria: Upregulated Expression in CD8+and Epithelial Cells and Induction of Inflammatory Cell Accumulation

2016 ◽  
Vol 2016 ◽  
pp. 1-13 ◽  
Author(s):  
S. F. Wang ◽  
X. Q. Gao ◽  
Y. N. Xu ◽  
D. N. Li ◽  
H. Y. Wang ◽  
...  
Keyword(s):  
Mast Cells ◽  
Inflammatory Cell ◽  
Inflammatory Cells ◽  
Chronic Spontaneous Urticaria ◽  
Intercellular Adhesion Molecule ◽  
Double Labeling ◽  
Cell Accumulation ◽  
Healthy Control ◽  
Dose Dependent Increase ◽  
Dose Dependent

Interferon- (IFN-)λ1 is regarded as a potent bio-active molecule in innate immunity. However, little is known about its role in chronic spontaneous urticaria (CSU). We therefore investigated expression of IFN-λ1 in CSU, its cellular location, and its influence on inflammatory cell accumulation by using flow cytometry analysis, skin tissue dispersion, immunohistochemical stain, and a mouse peritoneal inflammation model. The results showed that level of IFN-λ1 was 2.0-fold higher in plasma of the patients with CSU than the level in healthy control (HC) subjects. Among leukocytes examined, only CD8+T cells expressed more IFN-λ1 in CSU blood. Double labeling immunohistochemical staining revealed that IFN-λ1+inflammatory cells such as mast cells, eosinophils, B cells, neutrophils, and macrophages were mainly located in dermis, whereas epidermis tissue highly expressed IFN-λ1. IFN-λ1 induced a dose-dependent increase in number of eosinophils, lymphocytes, mast cells, macrophages, and neutrophils in the peritoneum of mice at 6 h following injection, which was inhibited by pretreatment of the animals with anti-intercellular adhesion molecule- (ICAM-) 1 and/or anti-L-selectin antibodies. In conclusion, IFN-λ1 is likely to play a role in the pathogenesis of CSU. Blocking IFN-λ1 production may help to reduce the accumulation of inflammatory cells in the involved CSU skin.

scholarly journals Comparative Study on Pulmonary Toxicity in Mice Induced by Exposure to Unflavoured and Apple- and Strawberry-Flavoured Tobacco Waterpipe Smoke

2020 ◽  
Vol 2020 ◽  
pp. 1-11
Author(s):  
Abderrahim Nemmar ◽  
Suhail Al-Salam ◽  
Sumaya Beegam ◽  
Priya Yuvaraju ◽  
Badreldin H. Ali
Keyword(s):  
Pulmonary Toxicity ◽  
Nuclear Factor Kappa B ◽  
Caspase 3 ◽  
Inflammatory Cells ◽  
Airway Hyperreactivity ◽  
Histological Evaluation ◽  
Air Exposure ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
Necrosis Factor

The use of flavoured tobacco products in waterpipe smoking (WPS) has increased its attractiveness and consumption. Nonetheless, the influence of flavourings on pulmonary toxicity caused by WPS remains unclear. Here, the pulmonary toxicity induced by plain (P)-WPS, apple-flavoured (AF)-WPS, and strawberry-flavoured (SF)-WPS (30 minutes/day, 5 days/week for 1 month) was investigated in mice. Control mice were exposed to air. Exposure to P-WPS or AF-WPS or SF-WPS induced a dose-dependent increase of airway hyperreactivity to methacholine. The histological evaluation of the lungs in all the WPS groups revealed the presence focal areas of dilated alveolar spaces and foci of widening of interalveolar spaces with inflammatory cells. In the lung, the activity of neutrophil elastase and myeloperoxidase and the concentrations of tumor necrosis factor-α and glutathione were increased by the exposure to P-WPS, AF-WPS, or SF-WPS. However, the levels of interleukin-6 and catalase were only increased in the AF-WPS and SF-WPS groups, while nitric oxide activity was only increased in the SF-WPS group. DNA injury was increased in all the WPS groups, but the concentration of cleaved caspase-3 was only elevated in the SF-WPS group. The exposure to either P-WPS or AF-WPS or SF-WPS increased the expression of nuclear factor kappa-B (NF-κB) in the lung. In conclusion, the exposure to P-WPS or AF-WPS or SF-WPS induces alterations in lung function and morphology and causes oxidative stress and inflammation via mechanisms that include activation of NF-κB. Overall, the toxicity of flavoured tobacco WPS, in particular SF-WPS, was found to be greater than that of unflavoured WPS.

Persistent Acute Inflammation at the Implant-Abutment Interface

2003 ◽  
Vol 82 (3) ◽  
pp. 232-237 ◽  
Author(s):  
N. Broggini ◽  
L.M. McManus ◽  
J.S. Hermann ◽  
R.U. Medina ◽  
T.W. Oates ◽  
...  
Keyword(s):  
Bone Loss ◽  
Polymorphonuclear Leukocytes ◽  
Acute Inflammation ◽  
Inflammatory Cell ◽  
Inflammatory Cells ◽  
The Third ◽  
Initial Surgery ◽  
Cell Accumulation ◽  
Implant Abutment ◽  
Neutrophilic Polymorphonuclear Leukocytes

The inflammatory response adjacent to implants has not been well-investigated and may influence peri-implant tissue levels. The purpose of this study was to assess, histomorphometrically, (1) the timing of abutment connection and (2) the influence of a microgap. Three implant designs were placed in the mandibles of dogs. Two-piece implants were placed at the alveolar crest and abutments connected either at initial surgery (non-submerged) or three months later (submerged). The third implant was one-piece. Adjacent interstitial tissues were analyzed. Both two-piece implants resulted in a peak of inflammatory cells approximately 0.50 mm coronal to the microgap and consisted primarily of neutrophilic polymorphonuclear leukocytes. For one-piece implants, no such peak was observed. Also, significantly greater bone loss was observed for both two-piece implants compared with one-piece implants. In summary, the absence of an implant-abutment interface (microgap) at the bone crest was associated with reduced peri-implant inflammatory cell accumulation and minimal bone loss.

scholarly journals Oral Administration of Herbal Mixture Extract Inhibits 2,4-Dinitrochlorobenzene-Induced Atopic Dermatitis in BALB/c Mice

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Soon Re Kim ◽  
Han-Seok Choi ◽  
Hye Sook Seo ◽  
Jin Mo Ku ◽  
Se Hyang Hong ◽  
...  
Keyword(s):  
Mast Cells ◽  
Oral Administration ◽  
Inflammatory Cell ◽  
Ethanol Extract ◽  
Inflammatory Cells ◽  
Skin Lesions ◽  
Cell Infiltration ◽  
Mrna Levels ◽  
Beneficial Effects ◽  
Th2 Cytokine

CP001 is four traditional herbal medicine mixtures with anti-inflammatory properties. In this study, we investigated the effect of oral administration of CP001 ethanol extract on the 2,4-dinitrochlorobenzene- (DNCB-) induced AD mouse models. For that purpose, we observed the effects of oral administration of CP001 on skin inflammatory cell infiltration, skin mast cells, production of serum IgE, and expression of Th2 cytokine mRNA in the AD skin lesions of DNCB treated BALB/c mice. Histological analyses demonstrated that CP001 decreased dermis and epidermis thickening as well as dermal infiltration induced by inflammatory cells. In addition, CP001 decreased mast cell infiltration in count as well as dermal infiltration induced by inflammatory cells. In the skin lesions, mRNA expression of interleukin- (IL-) 4 and IL-13 was inhibited by CP001. CP001 also reduced the production of IgE level in mouse plasma. In addition, we investigated the effect of CP001 on the inflammatory allergic reaction using human mast cells (HMC-1). In HMC-1, cytokine production and mRNA levels of IL-4, IL-13, IL-6, and IL-8 were suppressed by CP001. Taken together, our results showed that oral administration of CP001 exerts beneficial effects in AD symptoms, suggesting that CP001 might be a useful candidate for the treatment of AD.

Regional differences in constitutive and induced ICAM-1 expression in vivo

1995 ◽  
Vol 269 (6) ◽  
pp. H1955-H1964 ◽  
Author(s):  
J. Panes ◽  
M. A. Perry ◽  
D. C. Anderson ◽  
A. Manning ◽  
B. Leone ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Regional Differences ◽  
Time Course ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1 ◽  
Fourfold Increase ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
Higher Doses

The aim of the present study was to characterize and compare the expression of intercellular adhesion molecule 1 (ICAM-1) on unstimulated and endotoxin-challenged endothelial cells in different tissues of the rat. ICAM-1 expression was measured using 125I-labeled anti-rat ICAM-1 monoclonal antibody (MAb) and an isotype-matched control MAb labeled with 131I (to correct for nonspecific accumulation of the binding MAb). Under baseline conditions, ICAM-1 MAb binding was observed in all organs. The binding of 125I-ICAM-1 MAb varied widely among organs, with the largest accumulation (per g tissue) in the lung, followed by heart (1/30th of lung activity), splanchnic organs (1/50th of lung activity), thymus (1/100th of lung activity), testes (1/300th of lung activity), and skeletal muscle (1/800th of lung activity). Endotoxin induced an increase in ICAM-1 MAb binding in all organs except the spleen. Endotoxin-induced upregulation of ICAM-1 was greatest in heart and skeletal muscle (5- to 10-fold), whereas the remaining organs exhibited a two- to fourfold increase in ICAM-1 expression. Maximal upregulation of ICAM-1 occurred at 9-12 h after endotoxin administration. A dose-dependent increase in ICAM-1 expression was elicited by 0.1-10 microgram/kg, with higher doses (up to 5 mg/kg) producing no further increment. Induction of ICAM-1 mRNA after endotoxin was observed in all tissues examined (lung, heart, intestine), peaked at 3 h, and then rapidly returned to control levels. These findings indicate that ICAM-1 is constitutively expressed on vascular endothelium in all organs of the rat and that there are significant regional differences in the magnitude and time course of endotoxin-induced ICAM-1 expression.

scholarly journals Stimulation of sulphated glycosaminoglycan and decorin production in adult dermal fibroblasts by recombinant human interleukin-4

1995 ◽  
Vol 307 (3) ◽  
pp. 673-678 ◽  
Author(s):  
Y Wegrowski ◽  
V Paltot ◽  
P Gillery ◽  
B Kalis ◽  
A Randoux ◽  
...  
Keyword(s):  
Culture Medium ◽  
Core Protein ◽  
Human Fibroblasts ◽  
Inflammatory Cells ◽  
Dermal Fibroblasts ◽  
Interleukin 4 ◽  
Proteoglycan Synthesis ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
Sulphated Glycosaminoglycan

Interleukin-4 (IL-4) is a pleiotropic cytokine expressed by inflammatory cells. Previous work from our laboratory has shown that it stimulates collagen synthesis in fibroblasts. Here we report the effects of recombinant human IL-4 on glycosaminoglycan (GAG) and proteoglycan synthesis in normal dermal fibroblasts from adult donors. IL-4 (10 and 100 units/ml) induced a dose-dependent increase of [3H]glucosamine and [35S]sulphate incorporation into total GAGs. The analysis of the different GAG fractions indicated the enhanced synthesis of dermatan/chondroitin sulphates. IL-4 had no effect on hyaluronan synthesis. The increase of sulphated GAG synthesis was correlated with an increase of proteoglycans in the culture medium. Decorin was identified as the major chondroitin/dermatan sulphate-containing proteoglycan in the culture medium of fibroblasts. Its synthesis was strongly stimulated by IL-4. Both the core-protein synthesis and mRNA expression were enhanced, indicating that the cytokine acted, at least in part, at the pre-translational level. These results indicate that IL-4 is able to modulate not only collagen, but also proteoglycan, production by human fibroblasts. Their implications in physiopathological processes such as wound healing or fibrosis is suggested.

Steroids and Asthma

PEDIATRICS ◽  
1995 ◽  
Vol 96 (2) ◽  
pp. 347-348 ◽  
Author(s):  
Gail G. Shapiro
Keyword(s):  
Single Dose ◽  
Inflammatory Cell ◽  
Inflammatory Cells ◽  
Forced Expiratory Volume ◽  
Chronic Asthma ◽  
Optimal Management ◽  
Concomitant Increase ◽  
Biopsy Specimens ◽  
Destructive Change ◽  
Cell Accumulation

It is impossible to read about asthma in the 1990s without being informed that it is an inflammatory disease and that all but the mildest cases require anti-inflammatory therapy for optimal management.1 Bronchoalveolar lavage studies document the influx of inflammatory cells and the upregulation of inflammatory cytokines in bronchial washings of patients with chronic asthma.2 Biopsy specimens confirm an inflammatory cell accumulation and the destructive change to the epithelium that one would expect from this insult.3 The pathophysiology of asthma would seem to justify the use of corticosteroids for its management. A single dose of prednisone can be shown to decrease inflammatory leukotrienes while there is a concomitant increase in forced expiratory volume in 1 second.4

Peri-implant Inflammation Defined by the Implant-Abutment Interface

2006 ◽  
Vol 85 (5) ◽  
pp. 473-478 ◽  
Author(s):  
N. Broggini ◽  
L.M. McManus ◽  
J.S. Hermann ◽  
R. Medina ◽  
R.K. Schenk ◽  
...  
Keyword(s):  
Bone Loss ◽  
Polymorphonuclear Leukocytes ◽  
Inflammatory Cell ◽  
Alveolar Bone ◽  
Inflammatory Cells ◽  
Maximum Density ◽  
Interface Position ◽  
Cell Accumulation ◽  
Implant Abutment ◽  
Neutrophilic Polymorphonuclear Leukocytes

An implant-abutment interface at the alveolar bone crest is associated with sustained peri-implant inflammation; however, whether magnitude of inflammation is proportionally dependent upon interface position remains unknown. This study compared the distribution and density of inflammatory cells surrounding implants with a supracrestal, crestal, or subcrestal implant-abutment interface. All implants developed a similar pattern of peri-implant inflammation: neutrophilic polymorphonuclear leukocytes (neutrophils) maximally accumulated at or immediately coronal to the interface. However, peri-implant neutrophil accrual increased progressively as the implant-abutment interface depth increased, i.e., subcrestal interfaces promoted a significantly greater maximum density of neutrophils than did supracrestal interfaces (10,512 ± 691 vs. 2398 ± 1077 neutrophils/mm2). Moreover, inflammatory cell accumulation below the original bone crest was significantly correlated with bone loss. Thus, the implant-abutment interface dictates the intensity and location of peri-implant inflammatory cell accumulation, a potential contributing component in the extent of implant-associated alveolar bone loss.

scholarly journals Cytofluorometric quantitation of 5-hydroxytryptamine and heparin in individual mast cell granules.

1978 ◽  
Vol 26 (1) ◽  
pp. 47-54 ◽  
Author(s):  
B Gustafsson ◽  
L Enerbäck
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
New Synthesis ◽  
5 Ht Uptake ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
Representative Samples

Cytofluorometric quantitation of 5-hydroxytryptamine (5-HT) and heparin in individual mast cell granules is described. The technique is based on micromanipulation of intact mast cells reacted with formaldehyde or stained with Berberine sulfate and the use of a cytofluorometer equipped with a sensitive peak detecting device. The quantities of 5-HT and heparin contained in mast cell granules which are of the order of 10(-16) and 10(-13) g, respectively were expressed as relative fluorescence guanta. The results of measurements on representative samples of mast cell granules indicate that all granules contain heparin as well as 5-HT, and that there are large variations in both 5-HT and heparin content within the granule populations of individual cells. A dose dependent increase in 5-HT content in both cells and individual mast cell granules occurred 24 hr after the injection of 10--50 mg L-5-hydroxytryptophan/kg intraperitoneally. There was no evidence for an increase in the heparin content of granules or cells, indicating that a new synthesis of granular macromolecules is not required for the 5-HT uptake. The results further suggest that 5-HT may be stored initially in a cytoplasmic extragranular pool and then taken up in the mast cell granules.

scholarly journals Effects of Pelargonium sidoides and Coptis Rhizoma 2 : 1 Mixed Formula (PS + CR) on Ovalbumin-Induced Asthma in Mice

2020 ◽  
Vol 2020 ◽  
pp. 1-14
Author(s):  
Byung Gu Min ◽  
Sang Mi Park ◽  
Youn Woong Choi ◽  
Sae Kwang Ku ◽  
Il Je Cho ◽  
...  
Keyword(s):  
Mast Cells ◽  
Lung Tissue ◽  
Inflammatory Cells ◽  
Tissue Homogenate ◽  
Pelargonium Sidoides ◽  
Cell Counts ◽  
Septal Thickness ◽  
Differential Cell ◽  
Lung Tissue Homogenate ◽  
Dose Dependent

Pelargonium sidoides (PS) is traditionally used to treat respiratory and gastrointestinal infections, dysmenorrhea, and hepatic disorders in South Africa. Coptis Rhizoma (CR) is used to treat gastroenteric disorders, cardiovascular diseases, and cancer in East Asia. In the present study, we intended to observe the possible beneficial antiasthma effects of PS and CR on the ovalbumin- (OVA-) induced asthma C57BL/6J mice. Asthma in mice was induced by OVA sensitization and subsequent boosting. PS + CR (300 and 1,000 mg/kg; PO) or dexamethasone (IP) was administered once a day for 16 days. The changes in the body weight and gains, lung weights and gross inspections, total and differential cell counts of leukocytes in bronchoalveolar lavage fluid (BALF), serum OVA-specific immunoglobulin E (OVA-sIgE) levels, interleukin-4 (IL-4) and IL-5 levels in BALF and lung tissue homogenate, and IL-4 and IL-5 mRNA levels in lung tissue homogenates were analyzed with lung histopathology: mean alveolar surface area (ASA), alveolar septal thickness, numbers of inflammatory cells, mast cells, and eosinophils infiltrated in the alveolar regions, respectively. Significant increases in lung weights, total and differential cell counts of leukocytes in BALF, serum OVA-sIgE levels, and IL-4 and IL-5 levels in BALF and lung tissue homogenate were observed in OVA control as compared to those of intact control. In addition, OVA control showed a significant decrease in mean ASA and increases in alveolar septal thickness, numbers of inflammatory cells, mast cells, and eosinophils infiltrated in alveolar regions. However, these allergic and inflammatory asthmatic changes were significantly inhibited by PS + CR in a dose-dependent manner. In this study, PS + CR showed dose-dependent beneficial effects on OVA-induced asthma in mice through anti-inflammatory and antiallergic activities. Therefore, it is expected that PS + CR have enough potential as a new therapeutic agent or as an ingredient of a medicinal agent for various allergic and inflammatory respiratory diseases including asthma.

scholarly journals Phorbol 12-myristate 13-acetate-induced development of functionally active mast cells in W/Wv but not Sl/Sld genetically mast cell- deficient mice

Blood ◽  
1990 ◽  
Vol 75 (8) ◽  
pp. 1637-1645
Author(s):  
JR Gordon ◽  
SJ Galli
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Normal Skin ◽  
Systemic Effect ◽  
Detectable Effect ◽  
Heparin Binding ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
Deficient Mice ◽  
Convenient Model

The normal skin and other tissues of adult genetically mast cell- deficient WBB6F1-W/Wv or WCB6F1-Sl/Sld mice contain less than 1.0% the number of mast cells present in the corresponding tissues of the congenic normal (+/+) mice. We previously reported that mature dermal mast cells developed locally in the skin of W/Wv, but not Sl/Sld, mice at sites of chronic idiopathic dermatitis. We now report that the repeated application of phorbol 12-myristate 13-acetate (PMA) to the ear skin of either W/Wv or +/+ mice induces both dermatitis and a striking and dose-dependent increase in the number of dermal mast cells. The number of dermal mast cells at sites treated for 6 weeks with 5 micrograms PMA, three times per week, was 39 +/- 7/mm2 and 305 +/- 34/mm2 for W/Wv and +/+ mice, respectively; the corresponding values for vehicle-treated skin were 1.5 +/- 1.0/mm2 and 145 +/- 8/mm2, respectively. The PMA-induced dermal mast cells in W/Wv mice appeared mature by morphology, stained with the heparin-binding fluorescent dye, berberine sulfate, and were competent to express IgE-dependent passive cutaneous anaphylaxis responses. The development of mast cells was a local, not systemic, effect of PMA treatment. PMA treatment also induced dermatitis in both WCB6F1-Sl/Sld and +/+ mice, but was associated with increased numbers of dermal mast cells only in the WCB6F1(-)+/+ mice. PMA treatment had no detectable effect on the ability of bone marrow-derived cultured mast cells to survive in the skin of Sl/Sld mice. These findings establish a convenient model system for analyzing factors associated with the development of endogenous populations of mast cells in genetically mast cell-deficient W/Wv mice.

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