scholarly journals IL‐22 directly induces keratinocyte hyperplasia, up‐regulates anti‐microbial peptide and pro‐inflammatory cytokine gene expression in mouse skin

2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
Lee Napierata ◽  
Spencer Liang ◽  
Larry Mason ◽  
Jie Cai ◽  
Mary Collins ◽  
...  
Keyword(s):  
Gene Expression ◽  
Inflammatory Cytokine ◽  
Mouse Skin ◽  
Cytokine Gene Expression ◽  
Cytokine Gene

scholarly journals Rice Bran Protein Hydrolysates Improve Insulin Resistance and Decrease Pro-inflammatory Cytokine Gene Expression in Rats Fed a High Carbohydrate-High Fat Diet

Nutrients ◽  
2015 ◽  
Vol 7 (8) ◽  
pp. 6313-6329 ◽  
Author(s):  
Kampeebhorn Boonloh ◽  
Veerapol Kukongviriyapan ◽  
Bunkerd Kongyingyoes ◽  
Upa Kukongviriyapan ◽  
Supawan Thawornchinsombut ◽  
...  
Keyword(s):  
Gene Expression ◽  
Insulin Resistance ◽  
Rice Bran ◽  
High Fat Diet ◽  
Inflammatory Cytokine ◽  
Cytokine Gene Expression ◽  
Cytokine Gene ◽  
High Fat ◽  
High Carbohydrate ◽  
Improve Insulin Resistance

Evaluation of antioxidant capacity and inflammatory cytokine gene expression in horses fed silibinin complexed with phospholipid

2013 ◽  
Vol 74 (10) ◽  
pp. 1333-1339 ◽  
Author(s):  
Eileen S. Hackett ◽  
Khursheed R. Mama ◽  
David C. Twedt ◽  
Daniel L. Gustafson
Keyword(s):  
Gene Expression ◽  
Antioxidant Capacity ◽  
Inflammatory Cytokine ◽  
Cytokine Gene Expression ◽  
Cytokine Gene

scholarly journals Caspase-8 promotes c-Rel–dependent inflammatory cytokine expression and resistance againstToxoplasma gondii

2019 ◽  
pp. 201820529 ◽  
Author(s):  
Alexandra A. DeLaney ◽  
Corbett T. Berry ◽  
David A. Christian ◽  
Andrew Hart ◽  
Elisabet Bjanes ◽  
...  
Keyword(s):  
Gene Expression ◽  
Enzymatic Activity ◽  
Inflammatory Cytokine ◽  
Cytokine Expression ◽  
Cytokine Gene Expression ◽  
Caspase 8 ◽  
Cytokine Gene ◽  
Inflammatory Gene Expression ◽  
Inflammatory Gene ◽  
Monocyte Recruitment

Caspase-8 is a key integrator of cell survival and cell death decisions during infection and inflammation. Following engagement of tumor necrosis factor superfamily receptors or certain Toll-like receptors (TLRs), caspase-8 initiates cell-extrinsic apoptosis while inhibiting RIPK3-dependent programmed necrosis. In addition, caspase-8 has an important, albeit less well understood, role in cell-intrinsic inflammatory gene expression. Macrophages lacking caspase-8 or the adaptor FADD have defective inflammatory cytokine expression and inflammasome priming in response to bacterial infection or TLR stimulation. How caspase-8 regulates cytokine gene expression, and whether caspase-8–mediated gene regulation has a physiological role during infection, remain poorly defined. Here we demonstrate that both caspase-8 enzymatic activity and scaffolding functions contribute to inflammatory cytokine gene expression. Caspase-8 enzymatic activity was necessary for maximal expression ofIl1bandIl12b, but caspase-8 deficient cells exhibited a further decrease in expression of these genes. Furthermore, the ability of TLR stimuli to induce optimal IκB kinase phosphorylation and nuclear translocation of the nuclear factor kappa light chain enhancer of activated B cells family member c-Rel required caspase activity. Interestingly, overexpression of c-Rel was sufficient to restore expression of IL-12 and IL-1β in caspase-8–deficient cells. Moreover,Ripk3−/−Casp8−/−mice were unable to control infection by the intracellular parasiteToxoplasma gondii, which corresponded to defects in monocyte recruitment to the peritoneal cavity, and exogenous IL-12 restored monocyte recruitment and protection of caspase-8–deficient mice during acute toxoplasmosis. These findings provide insight into how caspase-8 controls inflammatory gene expression and identify a critical role for caspase-8 in host defense against eukaryotic pathogens.

Inflammatory Cytokine Gene Expression in Different Types of Granulomatous Lesions during Asymptomatic Stages of Bovine Paratuberculosis

2005 ◽  
Vol 42 (5) ◽  
pp. 579-588 ◽  
Author(s):  
S. Tanaka ◽  
M. Sato ◽  
T. Onitsuka ◽  
H. Kamata ◽  
Y. Yokomizo
Keyword(s):  
Gene Expression ◽  
Inflammatory Cytokine ◽  
Clinical Signs ◽  
Interleukin 4 ◽  
Cytokine Gene Expression ◽  
Enzyme Linked Immunosorbent Assay ◽  
Cytokine Gene ◽  
Gm Csf ◽  
Granulomatous Lesions

The granulomatous lesions in bovine paratuberculosis have been classified into two types, i.e., the lepromatous type and the tuberculoid type. To clarify the immunopathologic mechanisms at the site of infection, we compared inflammatory cytokine gene expression between the two types of lesions. Samples were obtained from noninfected control cows ( n =5) and naturally infected cows ( n =7) that were diagnosed by enzyme-linked immunosorbent assay (ELISA) and fecal culture test. Although none of the infected cows showed clinical signs, tuberculoid lesions were observed in five cows (tuberculoid group) and lepromatous lesions in two cows (lepromatous group). Among the cytokines examined by reverse transcription-polymerase chain reaction (RT-PCR), Th2-type cytokines interleukin-4 (IL-4) and IL-10, and Th1-type cytokine IL-2 were expressed more significantly in the lepromatous group than in the tuberculoid ( P < 0.01) and noninfected groups ( P < 0.05). No statistical differences were observed in the expression of interferon-gamma, IL-1 beta, TNF-alpha, and GM-CSF among lepromatous, tuberculoid, and noninfected groups. Expression of proinflammatory cytokine IL-12 mRNA, however, did not differ among the three groups; IL-18 was expressed at lower levels in the lepromatous group than in the tuberculoid group and the noninfected group ( P < 0.0001). Moreover, the number of cells in which IL-18 mRNAs were detected by in situ hybridization was markedly decreased in the lepromatous group. These results indicate that the formation of lepromatous-type lesions or tuberculoid-type lesions may be influenced by alterations in Th1/Th2-type cytokine production and that IL-18 may play an important role in a Th1-to-Th2 switch in paratuberculosis.

Inflammatory cytokine gene expression in the urinary sediment of patients with lupus nephritis

2003 ◽  
Vol 48 (5) ◽  
pp. 1326-1331 ◽  
Author(s):  
Rebecca Wing-Yan Chan ◽  
Lai-Shan Tam ◽  
Edmund Kwok-Ming Li ◽  
Fernand Mac-Moune Lai ◽  
Kai-Ming Chow ◽  
...  
Keyword(s):  
Gene Expression ◽  
Lupus Nephritis ◽  
Inflammatory Cytokine ◽  
Cytokine Gene Expression ◽  
Cytokine Gene ◽  
Urinary Sediment
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