scholarly journals Effect of Indigofera oblongifolia on the Hepatic Oxidative Status and Expression of Inflammatory and Apoptotic Genes during Blood-Stage Murine Malaria

2019 ◽  
Vol 2019 ◽  
pp. 1-7 ◽  
Author(s):  
Mohamed A. Dkhil ◽  
Esam M. Al-Shaebi ◽  
Saleh Al-Quraishy
Keyword(s):  
Potential Role ◽  
Interleukin 1 ◽  
B Cell Lymphoma ◽  
Disease Spread ◽  
Hepatic Inflammation ◽  
Stress Markers ◽  
Apoptotic Genes ◽  
Indigofera Oblongifolia ◽  
Necrosis Factor

Malaria is a dangerous disease spread across several countries. Recent studies have focused on medicinal plants to discover alternative agents to the currently used drugs for malaria treatment. Here, we investigated the potential role of Indigofera oblongifolia leaf extract (IE) on hepatic inflammation in mice with Plasmodium chabaudi-infected erythrocytes. Female C57BL/6 mice were divided into three groups. The first group served as a control noninfected group, while the second and third groups were intraperitoneally injected with 106 erythrocytes parasitized by P. chabaudi. Mice from the third group were treated daily with a dose of 100 mg/kg of IE for 7 days. IE significantly reduced the number of leukocytes and apoptotic cells. The numbers of CD68-positive cells decreased in the livers of mice from the treatment group. Moreover, IE raised the hepatic antioxidant levels (glutathione and catalase) and reduced the levels of hepatic oxidative stress markers (malondialdehyde, nitric oxide, and reactive oxygen species). IE regulated some functions of the genes related to immune responses, including apoptotic genes (B-cell lymphoma-2, Bax, and caspase-3) and cytokine genes (interleukin-1β (IL-1β), IL-6, interferon-γ, and tumor necrosis factor-α). Therefore, IE exerts significant effects against malaria and protects the liver from injury caused by P. chabaudi via antioxidant and anti-inflammatory ways.

scholarly journals Salvadora persica protects mouse intestine from eimeriosis

2019 ◽  
Vol 28 (4) ◽  
pp. 605-612 ◽  
Author(s):  
Saleh Al-Quraishy ◽  
Felwa Abdullah Thagfan ◽  
Esam Mohamed Al-Shaebi ◽  
Mahmood Qasem ◽  
Rewaida Abdel-Gaber ◽  
...  
Keyword(s):  
B Cell Lymphoma ◽  
Interferon Γ ◽  
Salvadora Persica ◽  
Leaf Extracts ◽  
Therapeutic Value ◽  
Mouse Intestine ◽  
Apoptotic Genes ◽  
Factor Α ◽  
Necrosis Factor

Abstract Eimeriosis is a global poultry health problem. In the current study, we investigated the role of Salvadora persica leaf extracts (SE) against murine eimeriosis induced by Eimeria papillata. The infection induced an oocyst output of 6242 ± 731 oocysts/g feces. After treatment with 300 mg⁄kg SE, the oocysts expelled in feces decreased by approximately 3-fold. In addition, the total number of E. papillata in the parasitic stage decreased in the jejunum of mice after treatment with SE. In addition, SE significantly reduced the number of apoptotic cells by approximately 2-fold in the infected jejunum. SE ameliorated the changes in glutathione, malondialdehyde, and catalase due to E. papillata infection. Finally, SE regulated the cytokine genes, interleukin (IL)-1β, IL-6, interferon-γ, and tumor necrosis factor-α, and the apoptotic genes, B-cell lymphoma-2, Bax, and Caspase-3. SE protects the jejunum from E. papillata induced injury and may have potential therapeutic value as a food additive during eimeriosis.

scholarly journals Interleukin 10 (IL-10) upregulates IL-1 receptor antagonist production from lipopolysaccharide-stimulated human polymorphonuclear leukocytes by delaying mRNA degradation.

1994 ◽  
Vol 179 (5) ◽  
pp. 1695-1699 ◽  
Author(s):  
M A Cassatella ◽  
L Meda ◽  
S Gasperini ◽  
F Calzetti ◽  
S Bonora
Keyword(s):  
Receptor Antagonist ◽  
Polymorphonuclear Leukocytes ◽  
Potential Role ◽  
Inflammatory Responses ◽  
Interleukin 1 ◽  
Interleukin 10 ◽  
Mrna Stabilization ◽  
Human Polymorphonuclear Leukocytes ◽  
Necrosis Factor

Polymorphonuclear leukocytes (PMN) have been identified as cells capable of producing a number of pro- and antiinflammatory cytokines in response to specific agonists. Previously, we showed that tumor necrosis factor (TNF), interleukin-1 beta (IL-1 beta), and IL-8, are produced by PMN after stimulation with agonists, such as lipopolysaccharide (LPS). In this study, we demonstrate that LPS is also a potent stimulus for the mRNA expression and release of the IL-1 receptor antagonist (IL-1ra). In addition, we show that the release of IL-1ra from LPS-stimulated PMN is markedly potentiated in the presence of IL-10 (from two to threefold after 18 h of stimulation). Moreover, we observed that this upregulation of IL-1ra production by IL-10 in LPS-stimulated PMN took place through IL-1ra mRNA stabilization. Indeed, the half-life of IL-1ra mRNA was prolonged in PMN stimulated in the presence of IL-10 and LPS, as compared with cells stimulated with LPS alone. That IL-10 selectively upregulates IL-1ra production in LPS-activated PMN, while it inhibits the production of IL-1 beta, TNF, and IL-8 under the same conditions, suggests that IL-10 may be an important physiologic regulator of cytokine production from PMN, and emphasizes the potential role of IL-10 in inflammatory responses.

Potential role of interleukin-1 in reproduction of a squamate reptile (Chalcides chalcides)

Placenta ◽  
1996 ◽  
Vol 17 (5-6) ◽  
pp. A48
Author(s):  
L. Paulesu ◽  
R. Romagnoli ◽  
G. Ghiarar
Keyword(s):  
Potential Role ◽  
Interleukin 1 ◽  
Squamate Reptile

scholarly journals Thymic stromal lymphopoietin is released by human epithelial cells in response to microbes, trauma, or inflammation and potently activates mast cells

2007 ◽  
Vol 204 (2) ◽  
pp. 253-258 ◽  
Author(s):  
Zoulfia Allakhverdi ◽  
Michael R. Comeau ◽  
Heidi K. Jessup ◽  
Bo-Rin Park Yoon ◽  
Avery Brewer ◽  
...  
Keyword(s):  
Mast Cells ◽  
Epithelial Cell ◽  
Epithelial Cells ◽  
Immunoglobulin E ◽  
Interleukin 1 ◽  
Allergic Inflammation ◽  
Thymic Stromal Lymphopoietin ◽  
Microbial Products ◽  
Necrosis Factor

Compelling evidence suggests that the epithelial cell–derived cytokine thymic stromal lymphopoietin (TSLP) may initiate asthma or atopic dermatitis through a dendritic cell–mediated T helper (Th)2 response. Here, we describe how TSLP might initiate and aggravate allergic inflammation in the absence of T lymphocytes and immunoglobulin E antibodies via the innate immune system. We show that TSLP, synergistically with interleukin 1 and tumor necrosis factor, stimulates the production of high levels of Th2 cytokines by human mast cells (MCs). We next report that TSLP is released by primary epithelial cells in response to certain microbial products, physical injury, or inflammatory cytokines. Direct epithelial cell–mediated, TSLP-dependent activation of MCs may play a central role in “intrinsic” forms of atopic diseases and explain the aggravating role of infection and scratching in these diseases.

Insights from vaccinia virus into Toll-like receptor signalling proteins and their regulation by ubiquitin: role of IRAK-2

2008 ◽  
Vol 36 (3) ◽  
pp. 449-452 ◽  
Author(s):  
Andrew G. Bowie
Keyword(s):  
Vaccinia Virus ◽  
Interleukin 1 ◽  
Nuclear Factor Κb ◽  
Tumour Necrosis Factor Receptor ◽  
Relative Role ◽  
Toll Like Receptor ◽  
Turn On ◽  
Receptor Signalling ◽  
Necrosis Factor

TLRs (Toll-like receptors) are an important class of pathogen-sensing proteins, which signal the presence of a pathogen by activating transcription factors, such as NF-κB (nuclear factor κB). The TLR pathway to NF-κB activation involves multiple phosphorylation and ubiquitination events. Notably, TRAF-6 [TNF (tumour necrosis factor)-receptor-associated factor-6] Lys63 polyubiquitination is a critical step in the formation of signalling complexes, which turn on NF-κB. Here, the relative role of different IRAKs [IL-1 (interleukin 1)-receptor-associated kinases] in NF-κB activation is discussed. Further, I demonstrate how understanding one molecular mechanism whereby vaccinia virus inhibits NF-κB activation has led to a revealing of a key role for IRAK-2 in TRAF-6-mediated NF-κB activation.

The potential role of tumour necrosis factor a in asthma

1993 ◽  
Vol 23 (4) ◽  
pp. 247-250 ◽  
Author(s):  
J. C. KIPS ◽  
J. H. TAVERNIER ◽  
G. F. JOOS ◽  
R. A. PELEMAN ◽  
R. A. PAUWELS
Keyword(s):  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Potential Role ◽  
Necrosis Factor
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