Peer Review #2 of "Acute sleep fragmentation does not alter pro-inflammatory cytokine gene expression in brain or peripheral tissues of leptin-deficient mice (v0.2)"

Obesity and sleep fragmentation (SF) are often co-occurring pro-inflammatory conditions in patients with obstructive sleep apnea. Leptin is a peptide hormone produced by adipocytes that has anorexigenic effects upon appetite while regulating immunity. The role of leptin in mediating inflammatory responses to SF is incompletely understood. Male C57BL/6j (lean) and ob/ob mice (leptin-deficient mice exhibiting obese phenotype) were subjected to SF or control conditions for 24 h using an automated SF chamber. Trunk blood and tissue samples from the periphery (liver, spleen, fat, and heart) and brain (hypothalamus, prefrontal cortex, and hippocampus) were collected. Quantitative PCR was used to determine relative cytokine gene expression of pro-inflammatory (IL-1β, TNF-α) and anti-inflammatory (TGF-β1) cytokines. Enzyme-linked immunosorbent assay (ELISA) was used to determine serum corticosterone concentration. Ob/ob mice exhibited elevated cytokine gene expression in liver (TNF-α, TGF-β1), heart (TGF-β1), fat (TNF-α), and brain (hippocampus, hypothalamus, prefrontal cortex: IL-1β, TNF-α) compared with wild-type mice. Conversely, leptin deficiency decreased pro-inflammatory cytokine gene expression in heart (IL-1β, TNF-α). SF significantly increased IL-1β and TNF-α gene expression in fat and TGF-β1 expression in spleen relative to controls, but only in wild-type mice. SF increased basal serum corticosterone regardless of genotype. Taken together, these findings suggest that leptin deficiency affects cytokine gene expression differently in the brain compared to peripheral tissues with minimal interaction from acute SF.

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Effect of re-expansion after short-period lung collapse on pulmonary capillary permeability and pro-inflammatory cytokine gene expression in isolated rabbit lungs

British Journal of Anaesthesia ◽

10.1093/bja/aeh101 ◽

2004 ◽

Vol 92 (4) ◽

pp. 558-563 ◽

Cited By ~ 39

Author(s):

T Funakoshi ◽

Y Ishibe ◽

N Okazaki ◽

K Miura ◽

R Liu ◽

...

Keyword(s):

Gene Expression ◽

Inflammatory Cytokine ◽

Capillary Permeability ◽

Cytokine Gene Expression ◽

Cytokine Gene ◽

Lung Collapse ◽

Pulmonary Capillary ◽

Short Period

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

Nutrients ◽

10.3390/nu7085292 ◽

2015 ◽

Vol 7 (8) ◽

pp. 6313-6329 ◽

Cited By ~ 38

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

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

American Journal of Veterinary Research ◽

10.2460/ajvr.74.10.1333 ◽

2013 ◽

Vol 74 (10) ◽

pp. 1333-1339 ◽

Cited By ~ 3

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

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

Proceedings of the National Academy of Sciences ◽

10.1073/pnas.1820529116 ◽

2019 ◽

pp. 201820529 ◽

Cited By ~ 3

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.

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

Veterinary Pathology ◽

10.1354/vp.42-5-579 ◽

2005 ◽

Vol 42 (5) ◽

pp. 579-588 ◽

Cited By ~ 26

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.

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