CRP - what I wish I’d been taught! This (large!) protein comes as a pentamer of units 23 k-daltons. It has equivalents in almost all species and is found on chromosome 1. It’s the arch enemy of bacteria ESPECIALLY encapsulated bacteria

Because of some neat functions. Firstly it is produced in myriad locations but especially hepatocytes. It is produced and kept in the endoplasmic reticulum until needed. A small basal turnover occurs. Usually less than 1, 40% basal turnover is hereditary.

IL-6, the matriarch of inflammatory cytokines, is its inducer and then it all gets chucked out. Can go nothing to clinically detectable in hours. Peaks in 48. It does a billion things BUT

Has an anti bacterial role in that it is a pattern recognition molecules for polysaccharides on bacterial membranes/walls. Indeed it is named for being very fond of the C polysaccharide of streptococcus. Mice pre-treated with CRP injection have strep survival advantage.

Pattern recognition molecules are the innate immune system - no memory or antigen-learning required. Just bish bash bosh before the pathogen takes hold. CRP opsonises strep and haemophilus in particular, and activates classic complement.

It also activates macrophages, acts as a chemo attractant, interacts with other immune cells, a hundred inflammatory things, and generally rages for a few days until settling (half life is 19 hours)

Liver failure affects CRP response. Bacterial infection is it’s thing (most sources suggest viral infection can increase it to about 40 or so but above this be suspicious) although it is a feature of inflammation in general...

Note pancreatitis and the surgical stress response. Lower but chronically raised levels are features of ageing, pregnancy, inflam diseases like rheumatoid, heart disease, and actually even schizophrenia (now apparently a neuro-immunological disease process!)

Structurally CRP is related to amyloid. V conserved. Binding is calcium dependent. Crab CRP does things our complement does like punch holes in membranes. Glycosylation sites on CRP affect function and may be relevant to diabetes control.

Essentially CRP is not your enemy, intact human CRP hugely protective in encapsulated bacteria infection in mice. If trigger is treated it should exponentially disappear after 48 hours - sustained plateau day 3 post op is suspicious. Rise after a fall is suspicious.