This is the authors' abstract. We don't add key points for this paper.
Dear Editor, C-reactive protein (CRP) is one of the most commonly used diagnostic biomarkers in the clinical setting for diagnosing and monitoring of inflammatory and infectious diseases. However, in neonates several questions remain, regarding the interpretation of an increased serum CRP concentration during the first days of life in otherwise healthy newborns, especially in preterms (1). Pentraxins are endogenous substances that neutralize or eliminate a variety of pathogenic agents in concert with the complement system and macrophages. These complex biological responses to tissue injury, necrosis, infections, or immune-related diseases are part of the natural innate defence system (2). The pentraxin family consists of proteins with cyclic multimeric structures. The well-known acute-phase protein CRP belongs to the short members of the family, while pentraxin 3 (PTX3) belongs to the long counterparts. PTX3 is released from macrophages and endothelial cells among a great variety of other cell types in which the protein is synthesized and stored. On stimuli from primary inflammatory signal proteins, as interleukin-1 (IL-1), tumour necrosis factor-alpha (TNF-a), and microbial lipopolysaccharides (LPS) as well as toll-receptor-mediated signals, PTX3 will be synthesized, and the serum concentration will increase up to 100-fold in 6-8 hours. Interleukin-6 (IL-6) is a weak inducer for PTX3 (3,4). PTX3 synthesis is thus produced close to the site of inflammation and is not dependent on cytokine production or liver function.
Answers are grounded in this paper and cite their sources.
No takes yet. Share an insight, caveat, or question.
Lannergård et al. (2014) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: