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Acute phase induction of mouse serum amyloid P component. Correlation with other parameters of inflammation
1Division of Immunology, Children's Hospital, Boston, MA.
Abstract:
Hepatic mRNA levels of the mouse major acute phase proteins serum amyloid P component (SAP) and serum amyloid A component (SAA) were monitored at timed intervals after i.p. injection of thioglycollate or s.c. injection of azocasein. Both mRNA increased dramatically in response to either inflammatory stimulus. The increase in SAA mRNA levels accompanied an abrupt change in mRNA size from 650 to 750 bases. Peak SAA mRNA concentrations were observed 18 h after either stimulus; by 72 h concentrations had returned to preinflammatory levels. Peak SAP mRNA concentrations were observed 8 h after thioglycollate and 12 to 18 h after azocasein injection; by 36 h concentrations were close to preinflammatory levels. All mRNA species studied (SAP, SAA and the complement components C3, C5 and factor B) were induced more rapidly by the thioglycollate stimulus and reached higher peak concentrations. SAP mRNA levels were correlated with other parameters of inflammation: infiltration of peritoneal exudate cells (PEC) into the peritoneum after thioglycollate injection, and serum concentrations of SAP after azocasein injection. Serum SAP concentrations rose 20-fold in response to the latter stimulus by 36 h, i.e., 18 to 24 h after the peak SAP mRNA levels. The highest numbers of PEC were present 24 h after the thioglycollate stimulus, i.e. 16 h after the maximum SAP mRNA concentration, indicating the continuation of an active local inflammation many hours after one aspect of the systemic response has ceased.
Insights
Inflammatory stimuli significantly increase mouse hepatic mRNA for serum amyloid P component (SAP) and serum amyloid A component (SAA). These acute phase proteins show distinct temporal responses and mRNA size changes, indicating dynamic inflammation.
Area of Science:
- Molecular Biology
- Immunology
- Biochemistry
Background:
- Acute phase proteins, such as serum amyloid P component (SAP) and serum amyloid A component (SAA), are key indicators of inflammation.
- Understanding the transcriptional regulation of these proteins is crucial for comprehending the inflammatory response.
Purpose of the Study:
- To investigate the hepatic mRNA expression patterns of SAP and SAA in response to inflammatory stimuli.
- To compare the kinetics and magnitude of mRNA induction by different inflammatory agents.
- To correlate mRNA levels with other markers of inflammation, such as peritoneal exudate cells and serum protein concentrations.
Main Methods:
- Mice were subjected to intraperitoneal injection of thioglycollate or subcutaneous injection of azocasein to induce inflammation.
- Hepatic mRNA levels of SAP and SAA were quantified at various time points using molecular techniques.
- mRNA size and serum protein concentrations were also analyzed, alongside peritoneal exudate cell counts.
Main Results:
- Both thioglycollate and azocasein significantly upregulated hepatic mRNA for SAP and SAA.
- SAA mRNA exhibited a size shift and peaked at 18 hours, returning to baseline by 72 hours.
- Thioglycollate induced a faster and higher peak in mRNA levels for SAP, SAA, and complement components (C3, C5, factor B) compared to azocasein.
Conclusions:
- Hepatic mRNA levels of SAP and SAA are sensitive and dynamic markers of acute inflammation in mice.
- The thioglycollate stimulus elicits a more rapid and pronounced transcriptional response than azocasein.
- SAP mRNA levels correlate with both local (peritoneal exudate cells) and systemic (serum SAP) inflammatory markers.