scholarly journals Lymph flow directs rapid neutrophil positioning in the lymph node in infection

2020 ◽  
Author(s):  
Jingna Xue ◽  
Yujia Lin ◽  
Darellynn Oo ◽  
Jianbo Zhang ◽  
Flavia Jesus ◽  
...  
Keyword(s):  
Secondary Infection ◽  
Neutrophil Migration ◽  
Skin Inflammation ◽  
Lymph Flow ◽  
High Endothelial Venules ◽  
Chemokine Production ◽  
Systemic Spread ◽  
Inflammatory Chemokines ◽  
Flow Through ◽  
Frequent Infection

AbstractSoon after Staphylococcus aureus (S. aureus) skin infection, neutrophils infiltrate the LN via the high endothelial venules (HEVs) to restrain and kill the invading microbes to prevent systemic spread of microbes. In this study, we found that rapid neutrophil migration depends on lymph flow, through which inflammatory chemokines/cytokines produced in the infected tissue are transported to the LN. Without lymph flow, bacteria accumulation in the LN was insufficient to stimulate chemokine production or neutrophil migration. Oxazolone (OX)-induced skin inflammation impaired lymphatic function, and reduced chemokines in the LN after a secondary infection with S. aureus. Due to LN reconstruction and impaired conduit-mediated lymph flow, neutrophil preferentially transmigrated in HEVs located in the medullary sinus, where the HEVs remained exposed to lymph-borne chemokines. Altered neutrophil migration resulted in persistent infection in the LN. Our studies showed that lymph flow directed chemokine dispersal in the LN and ensured rapid neutrophil migration for timely immune protection in infection. The impaired lymph flow and neutrophil migration may contribute to the frequent infection in skin inflammation, such as atopic dermatitis.

scholarly journals 2,4-Dimethoxy-6-Methylbenzene-1,3-diol, a Benzenoid From Antrodia cinnamomea, Mitigates Psoriasiform Inflammation by Suppressing MAPK/NF-κB Phosphorylation and GDAP1L1/Drp1 Translocation

2021 ◽  
Vol 12 ◽  
Author(s):  
Shih-Yi Chuang ◽  
Chi-Yuan Chen ◽  
Shih-Chun Yang ◽  
Ahmed Alalaiwe ◽  
Chih-Hung Lin ◽  
...  
Keyword(s):  
Cell Model ◽  
Mitochondrial Fission ◽  
Neutrophil Migration ◽  
Chemokine Production ◽  
Antrodia Cinnamomea ◽  
Effective Treatment Modality ◽  
Mitogen Activated Protein ◽  
Anti Inflammatory ◽  
Novel Target

Antrodia cinnamomea exhibits anti-inflammatory, antioxidant, and immunomodulatory activities. We aimed to explore the antipsoriatic potential of 2,4-dimethoxy-6-methylbenzene-1,3-diol (DMD) derived from A. cinnamomea. The macrophages activated by imiquimod (IMQ) were used as the cell model for examining the anti-inflammatory effect of DMD in vitro. A significantly high inhibition of IL-23 and IL-6 by DMD was observed in THP-1 macrophages and bone marrow-derived mouse macrophages. The conditioned medium of DMD-treated macrophages could reduce neutrophil migration and keratinocyte overproliferation. DMD could downregulate cytokine/chemokine by suppressing the phosphorylation of mitogen-activated protein kinases (MAPKs) and NF-κB. We also observed inhibition of GDAP1L1/Drp1 translocation from the cytoplasm to mitochondria by DMD intervention. Thus, mitochondrial fission could be a novel target for treating psoriatic inflammation. A psoriasiform mouse model treated by IMQ showed reduced scaling, erythema, and skin thickening after topical application of DMD. Compared to the IMQ stimulation only, the active compound decreased epidermal thickness by about 2-fold. DMD diminished the number of infiltrating macrophages and neutrophils and their related cytokine/chemokine production in the lesional skin. Immunostaining of the IMQ-treated skin demonstrated the inhibition of GDAP1LI and phosphorylated Drp1 by DMD. The present study provides insight regarding the potential use of DMD as an effective treatment modality for psoriatic inflammation.

scholarly journals Estimation of Pressure Drop Required for Lymph Flow through Initial Collecting Lymphatics

2015 ◽  
Vol 29 (S1) ◽  
Author(s):  
Scott Stewart ◽  
David Sloas ◽  
Walter Murfee
Keyword(s):  
Pressure Drop ◽  
Lymph Flow ◽  
Flow Through

scholarly journals Bacterial skin colonization and infections in patients with atopic dermatitis

2012 ◽  
Vol 87 (5) ◽  
pp. 729-734 ◽  
Author(s):  
Vanessa Petry ◽  
Giancarlo Resende Bessa ◽  
Claudia Schermann Poziomczyck ◽  
Caio Fernando de Oliveira ◽  
Magda Blessmann Weber ◽  
...  
Keyword(s):  
Atopic Dermatitis ◽  
Bacterial Resistance ◽  
Antimicrobial Agents ◽  
Secondary Infection ◽  
Skin Barrier ◽  
Skin Inflammation ◽  
Skin Surface ◽  
Number Of Children ◽  
Chronic Skin ◽  
Systemic Antibiotics

Atopic Dermatitis is a chronic inflammatory skin disease that affects a large number of children and adults. The disease results from an interaction between genetic predisposition, host environment, skin barrier defects, and immunological factors. A major aggravating factor associated with Atopic Dermatitis is the presence of microorganisms on the patient's skin surface. Staphylococcus aureus and Streptococcus pyogenes, for instance, can exacerbate chronic skin inflammation. As a result, antimicrobials have often been prescribed to control the acute phase of the disease. However, increased bacterial resistance to antimicrobial agents has made it difficult for dermatologists to prescribe appropriate medication. In the presence of disseminated dermatitis with secondary infection, systemic antibiotics need to be prescribed; however, treatment should be individualized, in an attempt to find the most effective antibiotic with fewer side effects. Also, the medication should be used for as short as possible in order to minimize bacterial resistance.

A note on the mechanisms of lymph flow through the terminal lymphatics

1975 ◽  
Vol 10 (2) ◽  
pp. 214-216 ◽  
Author(s):  
Narender P. Reddy ◽  
Thomas A. Krouskop ◽  
Paul H. Newell
Keyword(s):  
Lymph Flow ◽  
Flow Through

scholarly journals Effects of dapagliflozin on human epicardial adipose tissue: modulation of insulin resistance, inflammatory chemokine production, and differentiation ability

2017 ◽  
Vol 114 (2) ◽  
pp. 336-346 ◽  
Author(s):  
Esther Díaz-Rodríguez ◽  
Rosa M Agra ◽  
Ángel L Fernández ◽  
Belén Adrio ◽  
Tomás García-Caballero ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Cardiovascular Disease ◽  
Wound Healing ◽  
Endothelial Cells ◽  
Adipose Tissue ◽  
Glucose Uptake ◽  
Epicardial Adipose Tissue ◽  
Diabetic Patients ◽  
Chemokine Production ◽  
Inflammatory Chemokines

AbstractAimsIn patients with cardiovascular disease, epicardial adipose tissue (EAT) is characterized by insulin resistance, high pro-inflammatory chemokines, and low differentiation ability. As dapagliflozin reduces body fat and cardiovascular events in diabetic patients, we would like to know its effect on EAT and subcutaneous adipose tissue (SAT).Methods and resultsAdipose samples were obtained from 52 patients undergoing heart surgery. Sodium-glucose cotransporter 2 (SGLT2) expression was determined by real-time polymerase chain reaction (n = 20), western blot, and immunohistochemistry. Fat explants (n = 21) were treated with dapagliflozin and/or insulin and glucose transporters expression measured. Glucose, free fatty acid, and adipokine levels (by array) were measured in the EAT secretomes, which were then tested on human coronary endothelial cells using wound healing assays. Glucose uptake was also measured using the fluorescent glucose analogue (6NBDG) in differentiated stromal vascular cells (SVCs) from the fat pads (n = 11). Finally, dapagliflozin-induced adipocyte differentiation was assessed from the levels of fat droplets (AdipoRed staining) and of perilipin. SGLT2 was expressed in EAT. Dapagliflozin increased glucose uptake (20.95 ± 4.4 mg/dL vs. 12.97 ± 4.1 mg/dL; P < 0.001) and glucose transporter type 4 (2.09 ± 0.3 fold change; P < 0.01) in EAT. Moreover, dapagliflozin reduced the secretion levels of chemokines and benefited wound healing in endothelial cells (0.21 ± 0.05 vs. 0.38 ± 0.08 open wound; P < 0.05). Finally, chronic treatment with dapagliflozin improved the differentiation of SVC, confirmed by AdipoRed staining [539 ± 142 arbitrary units (a.u.) vs. 473 ± 136 a.u.; P < 0.01] and perilipin expression levels (121 ± 10 vs. 84 ± 11 a.u.).ConclusionsDapagliflozin increased glucose uptake, reduced the secretion of pro-inflammatory chemokines (with a beneficial effect on the healing of human coronary artery endothelial cells), and improved the differentiation of EAT cells. These results suggest a new protective pathway for this drug on EAT from patients with cardiovascular disease.

scholarly journals Estimation of the Pressure Drop Required for Lymph Flow through Initial Lymphatic Networks

2016 ◽  
Vol 14 (2) ◽  
pp. 62-69 ◽  
Author(s):  
David C. Sloas ◽  
Scott A. Stewart ◽  
Richard S. Sweat ◽  
Travis M. Doggett ◽  
Natascha G. Alves ◽  
...  
Keyword(s):  
Pressure Drop ◽  
Lymph Flow ◽  
Flow Through

Antibodies go with the lymphatic flow

2019 ◽  
Vol 11 (517) ◽  
pp. eaaz7147
Author(s):  
Heather D. Hickman
Keyword(s):  
Antibody Production ◽  
Lymph Flow ◽  
Peyer's Patches ◽  
Peyer’S Patches ◽  
Lymphatic Flow ◽  
Mucosal Antibody ◽  
Flow Through

Lymph flow through Peyer’s patches enhances mucosal antibody production.

Lymphatic regulation of hematocrit during hypoxia in the toad Bufo woodhousei

1995 ◽  
Vol 269 (4) ◽  
pp. R814-R821 ◽  
Author(s):  
G. M. Malvin ◽  
S. Macias ◽  
M. Sanchez ◽  
R. Dasalla ◽  
A. Park ◽  
...  
Keyword(s):  
Plasma Volume ◽  
Lymph Flow ◽  
Cholinergic Nerves ◽  
Arterial Blood ◽  
Rate Of Increase ◽  
Lymph Heart ◽  
Flow Through ◽  
Bufo Woodhousei ◽  
Induced Changes ◽  
Toad Bufo

Hypoxia rapidly increases hematocrit (Hct) in anuran amphibians by reducing plasma volume, but the mechanism(s) mediating this response is unknown. We tested the hypothesis that, during hypoxia, plasma volume is reduced by impaired lymph heart (LH) function, decreasing lymph flow into the circulation. In Bufo woodhousei, we measured the effects of hypoxia on Hct, lymph heart rate (LHR), LH pressure, the movement of dye from the dorsal lymph sac to the arterial blood, and flow through an open LH cannula. We also tested whether splenic contraction or cholinergic nerves contribute to the hypoxia-induced changes. Graded hypoxia between 21 and 4% O2 produced graded increases in Hct (P < 0.0001) and decreases in LHR (P = 0.01). Hypoxia reduced the rate of increase in arterial Evans blue concentration after injection into the dorsal lymph sac (P = 0.041) and decreased flow through an open LH cannula (P < 0.012). Hypoxia increased Hct and reduced LHR similarly in control, splenectomized, and sham-splenectomized toads. Atropine had no significant effect on Hct and LHR. These results indicate that the LHs play a regulatory role in hypoxia-induced hemoconcentration.

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