Complement Factor B Gene Regulation: Synergistic Effects of TNF-α and IFN-γ in Macrophages

Huang, Yong; Krein, Peter M.; Muruve, Daniel A.; Winston, Brent W.

doi:10.4049/jimmunol.169.5.2627

Cited by 60 publications

(68 citation statements)

References 54 publications

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“…IFN-␥, IL-6-type cytokines, IL-1-type cytokines, hormones, LPS, and C5a have all been reported to effect complement expression both in vivo and by cultured cells (14,15,24,27,35,36,40,52). Detailed analyses of promoters and enhancers for factor B and C3 have demonstrated the intricate control by individual cytokines through specific regulatory sequences (21,22,23,50). Important future studies will be to define the mechanism by which factor B and C5 expression are modulated during LPS-induced lung injury.…”

Section: Discussionmentioning

confidence: 99%

Complement levels and activity in the normal and LPS-injured lung

Bolger

Ross

Jiang

et al. 2007

American Journal of Physiology-Lung Cellular and Molecular Phys

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Complement, a complex protein system, plays an essential role in host defense through bacterial lysis, stimulation of phagocytosis, recruitment of immune cells to infected tissue, and promotion of the inflammatory response. Although complement is most well-characterized in serum, complement activity is also present in the lung. Here we further characterize the complement system in the normal and inflamed lung. By Western blot, C5, C6, and factor I were detected in bronchoalveolar lavage (BAL) at lower levels than in serum, whereas C2 was detected at similar levels in BAL and serum. C4 binding protein (C4BP) was not detectable in BAL. Exposure to lipopolysaccharide (LPS) elevated levels of C1q, factor B, C2, C4, C5, C6, and C3 in human BAL and C3, C5, and factor B in mouse and rat BAL. Message for C1q-B, C1r, C1s, C2, C4, C3, C5, C6, factor B, and factor H, but not C9 or C4BP, was readily detectable by RT-PCR in normal mouse lung. Exposure to LPS enhanced factor B expression, decreased C5 expression, and did not affect C1q-B expression in mouse and rat lung. BAL from rats exposed to LPS had a greater ability to deposit C3b onto bacteria through complement activation than did BAL from control rats. In summary, these data demonstrate that complement levels, expression, and function are altered in acute lung injury and suggest that complement within the lung is regulated to promote opsonization of pathogens and limit potentially harmful inflammation.

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Section: Discussionmentioning

confidence: 99%

Complement levels and activity in the normal and LPS-injured lung

Bolger

Ross

Jiang

et al. 2007

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…TNF-α is a proinflammatory cytokine that activates Cfb through NF-κB (28,31). Furthermore, TNF-α expression is increased during MI (32), and increased systemic or local expression of TNF-α results in cardiomyopathy (33).…”

Section: Camkii Regulates Tnf-α Induced Cfb Expressionmentioning

confidence: 99%

Ca2+/calmodulin-dependent kinase II triggers cell membrane injury by inducing complement factor B gene expression in the mouse heart

Singh

Kapoun

Higgins³

et al. 2009

J. Clin. Invest.

154

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Myocardial Ca 2+ /calmodulin-dependent protein kinase II (CaMKII) inhibition improves cardiac function following myocardial infarction (MI), but the CaMKII-dependent pathways that participate in myocardial stress responses are incompletely understood. To address this issue, we sought to determine the transcriptional consequences of myocardial CaMKII inhibition after MI. We performed gene expression profiling in mouse hearts with cardiomyocyte-delimited transgenic expression of either a CaMKII inhibitory peptide (AC3-I) or a scrambled control peptide (AC3-C) following MI. Of the 8,600 mRNAs examined, 156 were substantially modulated by MI, and nearly half of these showed markedly altered responses to MI with CaMKII inhibition. CaMKII inhibition substantially reduced the MI-triggered upregulation of a constellation of proinflammatory genes. We studied 1 of these proinflammatory genes, complement factor B (Cfb), in detail, because complement proteins secreted by cells other than cardiomyocytes can induce sarcolemmal injury during MI. CFB protein expression in cardiomyocytes was triggered by CaMKII activation of the NF-κB pathway during both MI and exposure to bacterial endotoxin. CaMKII inhibition suppressed NF-κB activity in vitro and in vivo and reduced Cfb expression and sarcolemmal injury. The Cfb -/-mice were partially protected from the adverse consequences of MI. Our findings demonstrate what we believe is a novel target for CaMKII in myocardial injury and suggest that CaMKII is broadly important for the genetic effects of MI in cardiomyocytes.

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“…Park et al (2000) and Wu et al (2003) explains the role of NF-κB in macrophage cells that coordinate expression of the gene encoding iNOS, COX-2, TNF-α and another protein. NF-κB is required for the ability and reaction of TNF-α to stimulation of TNF-α and IFN-γ synergistically from Bf gene (Huang et al, 2002;Eckmann et al, 2008). VipAlbumin ® is a supplement from snakehead fish (Ophiocephalus striatus) with high content of albumin compare to the other kinds of fish.…”

Section: Introductionmentioning

confidence: 99%