**5. C - reactive protein concentrations in cerebral spinal fluid in grampositive and gram-negative bacterial meningitis**

C-Reactive Protein 97

http://www.jci.org/articles/view/18921/files/pdf?disposition=attachment.

[5] Peter J. Kennelly; Murray, Robert F.; Victor W. Rodwell; Kathleen M. Botham (2009).

[6] Matthew R. Pincus; McPherson, Richard A.; Henry, John Bernard (2007). *Henry's clinical diagnosis and management by laboratory methods*. Saunders Elsevier. ISBN 1-4160-0287-1. [7] John J. Ratey MD; Gary A. Noskin MEd MD; MD, Ralph Braun; Edward N. Hanley Jr MD; Iain B. McInnes; Shaun Ruddy MD (2008). *Kelley's Textbook of Rheumatology: 2- Volume Set, Expert Consult: Online and Print (Textbook of Rheumatology (Kelley's)(2 Vol))*.

[10] Thompson, D; Pepys, MB; Wood, SP (February 1999). "The physiological structure of human C-reactive protein and its complex with phosphocholine". Structure 7 (2): 169–

[11] Dhillon, B; Yan, H; Szmitko, PE; Verma, S (May 2005). "Adipokines: molecular links between obesity and atheroslcerosis". Am J Physiol Heart Circ Physiol 288 (5): H2031–

[13] A C-reactive protein promoter polymorphism is associated with type 2 diabetes mellitus in Pima Indians. (PubMed id 12618085)1, 4, 5 Wolford J.K....Hanson R.L. *(2003)*

[15] A C-reactive protein promoter polymorphism is associated with type 2 diabetes mellitus in Pima Indians. (PubMed id 12618085)1, 4, 5 Wolford J.K....Hanson R.L. *(2003)* [16] Mantovani A, Garlanda C, Doni A, Bottazzi B (January 2008). "Pentraxins in innate immunity: from C-reactive protein to the long pentraxin PTX3". J. Clin. Immunol. 28 (1):

[17] Clyne B, Olshaker JS (1999). "The C-reactive protein". J Emerg Med 17 (6): 1019–25.

[23] Pepys, MB; Hirschfield, GM (June 2003). "C-reactive protein: a critical update" (PDF). *J Clin Invest* 111 (12): 1805–12. doi:10.1172/JCI18921. PMC 161431. PMID 12813013.

[24] Clyne B, Olshaker JS (1999). "The C-reactive protein". *J Emerg Med* 17 (6): 1019–25.

[20] http://www.proz.com/kudoz/english\_to\_spanish/medical\_general/1100998-

http://www.jci.org/articles/view/18921/files/pdf?disposition=attachment.

*Harper's illustrated biochemistry*. McGraw-Hill Medical. ISBN 0-07-162591-7.

[4] http://en.wikipedia.org/wiki/C-reactive\_protein

Philadelphia: Saunders. ISBN 1-4160-3285-1.

[9] http://www.genecards.org/cgi-bin/carddisp.pl?gene=CRP

77. doi:10.1016/S0969-2126(99)80023-9. PMID 10368284.

41. doi:10.1152/ajpheart.01058.2004. PMID 15653761. http://ajpheart.physiology.org/content/288/5/H2031.full.pdf. [12] http://www.genecards.org/cgi-bin/carddisp.pl?gene=CRP

[14] http://www.genecards.org/cgi-bin/carddisp.pl?gene=CRP

1–13. doi:10.1007/s10875-007-9126-7. PMID 17828584

doi:10.1016/S0736-4679(99)00135-3. PMID 10595891

doi:10.1016/S0736-4679(99)00135-3. PMID 10595891.

[18] NCBI Entrez Protein #CAA39671 [19] http://en.wikipedia.org/wiki/ELISA

immunoturbidimetric\_method.html [21] http://en.wikipedia.org/wiki/Immunodiffusion [22] http://en.wikipedia.org/wiki/C-reactive\_protein

[8] http://www.jbc.org/content/279/47/48487

Several reports have shown an ability of CRP to discriminate between patients with bacterial meningitis and patients with aseptic (viral) meningitis. Although a recent Metaanalysis suggested that a negative CRP test in either cerebrospinal fluid (CSF) or serum can be used with a very high probability to rule out bacterial meningitis, a more recent report suggested that serum concentrations are a better screening tool for this differential diagnosis.

The substantial increase in CSF CRP, as well as the trend of an increased CSF/blood ratio of CRP, suggests that infection with gram-negative bacteria enhances permeability of CRP through the blood-brain barrier. It is possible that these findings reflect the ability of the endotoxin lipopolysaccharide-s, present in gram-negative but not in gram-positive bacteria, to affect the permeability of the blood-brain barrier [57][58]. CSF nitric oxide (NO) may be involved in this mechanism because its concentration in CSF is higher in gram-negative meningitis. This possibility is supported by the higher potency of gram-negative bacteria to promote macrophage NO production [59], the enhanced production of NO in the CSF of septic meningitis [60], and the role of NO in permeability changes of the blood-brain barrier in LPS-induced experimental meningitis [61].

Another interesting potential explanation for the present observation is that lipopolysaccharide-s produced by gram-negative bacteria could induce local CRP synthesis in the central nervous system. CRP can be produced in neurons [62], and lipopolysaccharide-s can induce CRP in extrahepatic sites [63]. This may also explain the increase, albeit nonsignificant, in serum CRP in the gram-negative cases. There is currently no single test to diagnose the etiology of meningitis promptly and accurately. Given its high sensitivity and easy measurability, CRP may be a useful supplement for rapid diagnosis and categorization of bacterial meningitis.
