Die Kennzeichnungspflicht von Influencer-Beiträgen auf Instagram : die Folgen der Werbeerkennung auf das Markenvertrauen

Der Einsatz von Influencer auf Instagram ist bei vielen Unternehmen ein Bestandteil des Marketing-Mix geworden, was für die Marke aber auch negative Folgen haben kann. Influencer sind gesetzlich verpflichtet, Werbung in ihren Posts durch Kennzeichnung offenzulegen, wenn sie im Auftrag eines Unternehmens agieren. Diese Pflicht wurde jedoch lange ignoriert. Gerichte und Aufsichtsbehörden wurden deshalb vermehrt aktiv und verurteilten widerrechtliche Handlungen, um Follower zu schützen. Ohne Werbekennzeichnung ist es für diese schwierig zu erkennen, ob eine kommerzielle Absicht hinter dem Post besteht. Es existieren Empfehlungen, wie Influencer-Beiträge zu kennzeichnen sind. Auch Instagram stellt mittlerweile ein Tool zur Offenlegung von Beziehungen zu Marken zur Verfügung. Der Einsatz einer Werbeoffenlegung kann aber negative Folgen für das Vertrauen in die Marke als wichtigster Faktor der Kunden-Marken-Beziehung haben, wenn Follower erkennen, dass sie einem Überzeugungsversuch ausgesetzt sind. Unternehmen und ihre Influencer sollten wissen, welche Kennzeichnung geeignet ist, den Werbecharakter zu vermitteln, um damit gesetzeskonform handeln zu können. Gleichzeitig benötigen Unternehmen die Gewissheit, ob sie dadurch ihrer Marke schaden. In der Masterarbeit wurde deshalb untersucht, ob die bestehenden Möglichkeiten der Werbeoffenlegung zur Werbeerkennung geeignet sind und dadurch das Markenvertrauen beeinflusst wird. Dazu wurde die Theorie des Überzeugungswissensmodells hinzugezogen. Die Zusammenhänge wurden mittels Experiments analysiert. Bei einer Experimentalgruppe wurde beim Instagram-Post #Werbung im Text platziert. Bei der zweiten das Instagram-Tool verwendet, bei dem die Kennzeichnung Bezahlte Partnerschaft mit unterhalb des Benutzernamens erfolgt. In der Kontrollgruppe wurde zum Vergleich keine Kennzeichnung gesetzt. Mit dem Kruskal-Wallis-Test wurde der Einfluss der Kennzeichnung auf die Werbeerkennung untersucht. Für deren Einfluss auf das Markenvertrauen wiederum wurde die lineare Regression verwendet. Der indirekte Einfluss der Werbeoffenlegung auf das Markenvertrauen wurde durch eine Mediatoranalyse festgehalten

Physiological bases of low FODMAP diets

PòsterJun

Molecular insights of p47phox phosphorylation dynamics in the regulation of NADPH oxidase activation and superoxide production

Phagocyte superoxide production by a multicomponent NADPH oxidase is important in host defense against microbial invasion. However inappropriate NADPH oxidase activation causes inflammation. Endothelial cells express NADPH oxidase and endothelial oxidative stress due to prolonged NADPH oxidase activation predisposes many diseases. Discovering the mechanism of NADPH oxidase activation is essential for developing novel treatment of these diseases. The p47phox is a key regulatory subunit of NADPH oxidase; however, due to the lack of full protein structural information, the mechanistic insight of p47phox phosphorylation in NADPH oxidase activation remains incomplete. Based on crystal structures of three functional domains, we generated a computational structural model of the full p47phox protein. Using a combination of in silico phosphorylation, molecular dynamics simulation and protein/protein docking, we discovered that the C-terminal tail of p47phox is critical for stabilizing its autoinhibited structure. Ser-379 phosphorylation disrupts H-bonds that link the C-terminal tail to the autoinhibitory region (AIR) and the tandem Src homology 3 (SH3) domains, allowing the AIR to undergo phosphorylation to expose the SH3 pocket for p22phox binding. These findings were confirmed by site-directed mutagenesis and gene transfection of p47phox_/_ coronary microvascular cells. Compared with wild-type p47phoxcDNAtransfected cells, the single mutation of S379A completely blocked p47phox membrane translocation, binding to p22phox and endothelial O2 . production in response to acute stimulation of PKC. p47phox C-terminal tail plays a key role in stabilizing intramolecular interactions at rest. Ser-379 phosphorylation is a molecular switch which initiates p47phox conformational changes and NADPH oxidase-dependent superoxide production by cells

Bilirubin decreases NOS2 expression via inhibition of NAD(P)H oxidase: implications for protection against endotoxic shock in rats.

We investigated a possible beneficial role for bilirubin, one of the products of heme degradation by the cytoprotective enzyme heme oxygenase-1 in counteracting Escherichia coli endotoxin-mediated toxicity. Homozygous jaundice Gunn rats, which display high plasma bilirubin levels due to deficiency of glucuronyl transferase activity, and Sprague-Dawley rats subjected to sustained exogenous bilirubin administration were more resistant to endotoxin (LPS)-induced hypotension and death compared with nonhyperbilirubinemic rats. LPS-stimulated production of nitric oxide (NO) was significantly decreased in hyperbilirubinemic rats compared with normal animals; this effect was associated with reduction of inducible NO synthase (NOS2) expression in renal, myocardial, and aortic tissues. Furthermore, NOS2 protein expression and activity were reduced in murine macrophages stimulated with LPS and preincubated with bilirubin at concentrations similar to that found in the serum of hyperbilirubinemic animals. This effect was secondary to inhibition of NAD(P)H oxidase since 1) inhibition of NAD(P)H oxidase attenuated NOS2 induction by LPS, 2) bilirubin decreased NAD(P)H oxidase activity in vivo and in vitro, and 3) down-regulation of NOS2 by bilirubin was reversed by addition of NAD(P)H. These findings indicate that bilirubin can act as an effective agent to reduce mortality and counteract hypotension elicited by endotoxin through mechanisms involving a decreased NOS2 induction secondary to inhibition of NAD(P)H oxidase

Punicic Acid a Conjugated Linolenic Acid Inhibits TNFα-Induced Neutrophil Hyperactivation and Protects from Experimental Colon Inflammation in Rats

BACKGROUND:Neutrophils play a major role in inflammation by releasing large amounts of ROS produced by NADPH-oxidase and myeloperoxidase (MPO). The proinflammatory cytokine TNFalpha primes ROS production through phosphorylation of the NADPH-oxidase subunit p47phox on Ser345. Conventional anti-inflammatory therapies remain partially successful and may have side effects. Therefore, regulation of neutrophil activation by natural dietary components represents an alternative therapeutic strategy in inflammatory diseases such as inflammatory bowel diseases. The aim of this study was to assess the effect of punicic acid, a conjugated linolenic fatty acid from pomegranate seed oil on TNFalpha-induced neutrophil hyperactivation in vitro and on colon inflammation in vivo. METHODOLOGY AND PRINCIPAL FINDINGS:We analyzed the effect of punicic acid on TNFalpha-induced neutrophil upregulation of ROS production in vitro and on TNBS-induced rat colon inflammation. Results show that punicic acid inhibited TNFalpha-induced priming of ROS production in vitro while preserving formyl-methionyl-leucyl-phenylalanine (fMLP)-induced response. This effect was mediated by the inhibition of Ser345-p47phox phosphorylation and upstream kinase p38MAPK. Punicic acid also inhibited fMLP- and TNFalpha+fMLP-induced MPO extracellular release from neutrophils. In vivo experiments showed that punicic acid and pomegranate seed oil intake decreased neutrophil-activation and ROS/MPO-mediated tissue damage as measured by F2-isoprostane release and protected rats from TNBS-induced colon inflammation. CONCLUSIONS/SIGNIFICANCE:These data show that punicic acid exerts a potent anti-inflammatory effect through inhibition of TNFalpha-induced priming of NADPH oxidase by targeting the p38MAPKinase/Ser345-p47phox-axis and MPO release. This natural dietary compound may provide a novel alternative therapeutic strategy in inflammatory diseases such as inflammatory bowel diseases