scholarly journals Gene Expression Pattern in Human Monocytes as a Surrogate Marker for Systemic Inflammatory Response Syndrome (SIRS)

1999 ◽  
Vol 5 (3) ◽  
pp. 192-202 ◽  
Author(s):  
Grit Wiegand ◽  
Kathleen Selleng ◽  
Matthias Gründling ◽  
Robert S. Jack
Keyword(s):  
Gene Expression ◽  
Systemic Inflammatory Response Syndrome ◽  
Inflammatory Response ◽  
Expression Pattern ◽  
Gene Expression Pattern ◽  
Surrogate Marker ◽  
Systemic Inflammatory Response ◽  
Human Monocytes

scholarly journals African Swine Fever Virus Blocks the Host Cell Antiviral Inflammatory Response through a Direct Inhibition of PKC-θ-Mediated p300 Transactivation

2008 ◽  
Vol 83 (2) ◽  
pp. 969-980 ◽  
Author(s):  
Aitor G. Granja ◽  
Elena G. Sánchez ◽  
Prado Sabina ◽  
Manuel Fresno ◽  
Yolanda Revilla
Keyword(s):  
Gene Expression ◽  
Inflammatory Response ◽  
Viral Infection ◽  
Host Cell ◽  
Expression Pattern ◽  
African Swine Fever Virus ◽  
Gene Expression Pattern ◽  
African Swine Fever ◽  
Fever Virus ◽  
Amino Terminal

ABSTRACT During a viral infection, reprogramming of the host cell gene expression pattern is required to establish an adequate antiviral response. The transcriptional coactivators p300 and CREB binding protein (CBP) play a central role in this regulation by promoting the assembly of transcription enhancer complexes to specific promoters of immune and proinflammatory genes. Here we show that the protein A238L encoded by African swine fever virus counteracts the host cell inflammatory response through the control of p300 transactivation during the viral infection. We demonstrate that A238L inhibits the expression of the inflammatory regulators cyclooxygenase-2 (COX-2) and tumor necrosis factor alpha (TNF-α) by preventing the recruitment of p300 to the enhanceosomes formed on their promoters. Furthermore, we report that A238L inhibits p300 activity during the viral infection and that its amino-terminal transactivation domain is essential in the A238L-mediated inhibition of the inflammatory response. Importantly, we found that the residue serine 384 of p300 is required for the viral protein to accomplish its inhibitory function and that ectopically expressed PKC-θ completely reverts this inhibition, thus indicating that this signaling pathway is disrupted by A238L during the viral infection. Furthermore, we show here that A238L does not affect PKC-θ enzymatic activity, but the molecular mechanism of this viral inhibition relies on the lack of interaction between PKC-θ and p300. These findings shed new light on how viruses alter the host cell antiviral gene expression pattern through the blockade of the p300 activity, which represents a new and sophisticated viral mechanism to evade the inflammatory and immune defense responses.

TOLL LIKE RECEPTOR (TLR) PATHWAY GENE EXPRESSION: SEPSIS OR UNINFECTED SYSTEMIC INFLAMMATORY RESPONSE SYNDROME (SIRS)?

2005 ◽  
Vol 33 ◽  
pp. A163 ◽  
Author(s):  
Matthew Lissauer ◽  
Steven B Johnson ◽  
Grant Bochicchio ◽  
Carinda Field ◽  
Alan Cross ◽  
...  
Keyword(s):  
Gene Expression ◽  
Systemic Inflammatory Response Syndrome ◽  
Inflammatory Response ◽  
Systemic Inflammatory Response ◽  
Toll Like Receptor ◽  
Pathway Gene

scholarly journals Prospective evaluation of S100A12 and S100A8/A9 (calprotectin) in dogs with sepsis or the systemic inflammatory response syndrome

2019 ◽  
Vol 31 (4) ◽  
pp. 645-651 ◽  
Author(s):  
Brittany E. Thames ◽  
James W. Barr ◽  
Jan S. Suchodolski ◽  
Jörg M. Steiner ◽  
Romy M. Heilmann
Keyword(s):  
Systemic Inflammatory Response Syndrome ◽  
Inflammatory Response ◽  
Hospital Admission ◽  
Surrogate Marker ◽  
Systemic Inflammatory Response ◽  
Inflammatory Biomarkers ◽  
Healthy Controls ◽  
Prospective Evaluation ◽  
Lower Serum ◽  
Patient Groups

Pattern recognition receptors (e.g., S100A12 or S100A8/A9) hold promise as inflammatory biomarkers. We prospectively determined and compared serum S100A12 and S100A8/A9 concentrations in dogs with sepsis ( n = 11) or systemic inflammatory response syndrome (SIRS; n = 8) over a 3-d period with each other, healthy controls ( n = 50), and other clinical and clinicopathologic variables. Serum S100A12 and S100A8/A9 concentrations were significantly higher in dogs with sepsis or SIRS (all p < 0.05) at the time of hospital admission (day 1) compared to healthy controls, with no differences between patient groups. However, septic dogs had significantly lower serum S100A12 concentrations on day 2 and day 3 (both p < 0.05) compared to dogs with SIRS. Likewise, dogs with sepsis had significantly lower S100A8/A9 concentrations on day 2 ( p < 0.05). Neither serum S100A12 nor S100A8/A9 concentrations were associated with survival to discharge. Our results suggest a differential expression of the S100/calgranulins between dogs with sepsis and those with SIRS. Serum S100A12 or S100A8/A9 concentration at the time of hospital admission did not differentiate dogs with sepsis from those with SIRS, but the trend of S100/calgranulin concentrations during the following 24–48 h may be a useful surrogate marker for differentiating sepsis from SIRS.

Systemic inflammatory response syndrome after major abdominal surgery

2019 ◽  
pp. 113-116
Author(s):  
Abdullah AlSomali ◽  
Abdullah Mobarki ◽  
Mohammed Almuhanna ◽  
Abdullah Alqahtani ◽  
Ziyad Alhawali ◽  
...  
Keyword(s):  
Systemic Inflammatory Response Syndrome ◽  
Inflammatory Response ◽  
Abdominal Surgery ◽  
Systemic Inflammatory Response ◽  
Major Abdominal Surgery
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