Markers and mediators of inflammatory response in infection and sepsis

Lobo, Suzana Margareth; Lobo, Francisco

doi:10.1590/s0103-507x2007000200012

Cited by 8 publications

(10 citation statements)

References 46 publications

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“…Some studies also include IL-1β, IL-6, IL-8, MCP-1, and G-CSF, as cytokines positively correlated with the progression to MODS. In terms of predicting fatality, IL-1β, IL-6, IL-8, MCP-1, and G-CSF are more strongly related to the possibility of early death (<48 h), while IL-8 and MCP-1 are more predictive of later fatality [14,23].…”

Section: The Cytokines As Biomarkers In Sepsismentioning

confidence: 99%

“…These molecules are released by different cells when affected by different types of stress and by necrotic factors, and are able to activate immune system receptors in a manner similar to the activation induced by bacterial patterns. Examples include the release of large quantities of fibrinogen, hyaluronic acid, and the high-mobility group box-1 protein (HMGB-1) during the inflammatory process, molecules that are capable of amplifying the pro-inflammatory response event more ( Figure 1) [9,14,21].…”

Section: The Pro-inflammatory Response and Its Mediatorsmentioning

confidence: 99%

“…Thus, they are able to carry out different functions, connecting various immune response pathways (Table 2) [14,22]. This inflammatory response, however, must be strictly controlled: it requires protection from the causative microorganism, but at the same time, an exaggerated activation of NLR induces caspase-1 activity, which leads to intense processing of pro-inflammatory cytokines such as IL-1 and IL-18, resulting in promotion of significant damage to the organism [23,24].…”

Section: The Pro-inflammatory Response and Its Mediatorsmentioning

confidence: 99%

“…These events are responsible, in part, for the microvascular alterations present in septic shock. However, the complement system also modulates responses associated to TLR4 binding and cytokine release, such as macrophage migration inhibitory factor (MIF) and HMGB (High-Mobility Group Box 1 Protein) [14] (Figure 2 …”

Section: The Pro-inflammatory Response and Its Mediatorsmentioning

confidence: 99%

“…It is increasingly recognized that the inflammatory response and unregulated production of cytokines play fundamental roles in the development of organs dysfunction. The emphasis on the possibility of using the cytokines in medical practice is due precisely to the central role they play in the pathogenesis of sepsis [14].…”

Section: Interaction With Trl2 and Trl4mentioning

confidence: 99%

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Pro-Inflammatory Cytokines in Sepsis: Biological Studies and Prospects From In Silico Research

Gomes¹,

Miguel²

2015

Biol syst Open Access

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Section: The Cytokines As Biomarkers In Sepsismentioning

confidence: 99%

Section: The Pro-inflammatory Response and Its Mediatorsmentioning

confidence: 99%

Section: The Pro-inflammatory Response and Its Mediatorsmentioning

confidence: 99%

Section: The Pro-inflammatory Response and Its Mediatorsmentioning

confidence: 99%

Section: Interaction With Trl2 and Trl4mentioning

confidence: 99%

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Pro-Inflammatory Cytokines in Sepsis: Biological Studies and Prospects From In Silico Research

Gomes¹,

Miguel²

2015

Biol syst Open Access

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Zerumin A attenuates the inflammatory responses in LPS‐stimulated H9c2 cardiomyoblasts

Shyni

Somappa

et al. 2021

J Biochem & Molecular Tox

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Zerumin A (ZA) is one of the potential components of Curcuma amada rhizomes, and it has been shown to possess a variety of pharmacological activities. This study deals with the beneficial activity of ZA in lipopolysaccharide (LPS)-stimulated inflammation in H9c2 cardiomyoblasts. Herein, H9c2 cells were preincubated with ZA for 1 h and stimulated with LPS for 24 h. The cells were analyzed for the expression of various pro-inflammatory mediators and signaling molecules. Results showed that the cell viability was significantly improved and reactive oxygen species production was alleviated remarkably with ZA pretreatment. We also found that ZA pretreatment significantly suppressed the upregulation of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2) protein levels, and nitric oxide (NO) release in LPS-stimulated cells. In addition, ZA significantly ameliorated LPS-elicited overexpression of pro-inflammatory chemokines and cytokines such as monocyte chemoattractant protein-1 (MCP-1), tumor necrosis factor α (TNF-α), interferon-γ (IFN-γ), and interleukin-1 (IL-1) in H9c2 cells, and it upregulated the synthesis of the anti-inflammatory cytokine interleukin-10 (IL-10). Moreover, pretreatment with ZA and the mitogen-activated protein kinases (MAPK) pathway inhibitors also reduced the phosphorylation of extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinases (JNK), and p38. ZA significantly inhibited IKB-a phosphorylation and nuclear factor (NF)-KB p65 subunit translocation into nuclei. Overall data demonstrated that ZA protects cardiomyocytes against LPS injury by inhibiting NF-KB p65 activation via the MAPK signaling pathway in vitro. These findings suggest that ZA may be a promising agent for a detailed study for the prevention or treatment of myocardial dysfunction in sepsis.

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