Serum Amyloid P Component and Systemic Fungal Infection: Does It Protect the Host or Is It a Trojan Horse?
Open accessAbstract
It is a striking observation that tissue of patients invaded by the deep mycoses often lacks evidence of an inflammatory response. This lack of host response is often attributed to neutropenia secondary to chemotherapy. However, systematic studies do not support this simplistic explanation. However, invasive fungal lesions are characterized by abundant fungal functional amyloid, which in turn is bound by serum amyloid P component (SAP). We postulate that SAP is important in the local immune response in invasive fungal infections. The interaction between fungal functional amyloid, SAP, and the immune response in deep mycoses is discussed.
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CPHPC efficiently binds to SAP, leading to the dissociation of SAP from bound amyloids and subsequent depletion of SAP levels in the body.
“This compound efficiently binds to SAP, leading to the dissociation of SAP from bound amyloids and subsequent depletion of SAP levels in the body24,62–68.”
From Serum amyloid P secreted by bone marrow adipocytes drives skeletal amyloidosis (2025) · cites this paper as [65]
The SERUM AMYLOID P COMPONENT section (page unavailable) says that depleting SAP in plasma leads to its dissociation from amyloid deposits. It does not mention CPHPC or establish that the compound binds SAP; it also describes depletion as preceding dissociation, rather than following it. (LLM, conf=0.86)
Experimental — accuracy not yet measuredCPHPC (miridesap) at a concentration of 5 mg ml−1 in drinking water is an established dose for SAP depletion from the body.
“To examine the effects of CPHPC on age-associated bone changes, male and female mice aged 18 months were treated with CPHPC (miridesap) at a concentration of 5 mg ml−1 in drinking water, which is an established dose for SAP depletion from the body62–65,67,68,84.”
From Serum amyloid P secreted by bone marrow adipocytes drives skeletal amyloidosis (2025) · cites this paper as [65]
The SERUM AMYLOID P COMPONENT section says that depleting plasma SAP is an effective treatment for amyloidoses. It does not mention CPHPC (miridesap), administration in drinking water, or a 5 mg ml−1 dose, so it does not establish the specific dosing claim. (LLM, conf=0.83)
Experimental — accuracy not yet measured
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Cites
Human Serum Amyloid P Component is a Single Uncomplexed Pentamer in Whole Serum
Hutchinson, W. L., Hohenester, E., & Pepys, M. B. (2000) · Molecular Medicine · doi:10.1007/bf03401789 · Cited by 66 · cited 1× · see citing works
“Each protomer of SAP is a 25 kDa domain with a β-jelly roll fold, and the pentamer has a total Mr of 127 310 [8].”
BackgroundGilchrist, K. B., Garcia, M. C., Sobonya, R., Lipke, P. N., & Klotz, S. A. (2012) · Journal of Infectious Diseases · doi:10.1093/infdis/jis464 · Cited by 41 · see citing works
Self-citation
Flagged first, then by citations
Research works printed but not linked: 19
- [1]Pepys MB Amyloidosis. Annu Rev Med 2006; 57: 223– 41. 16409147
- [2]Fowler DM, Koulov AV, Alory-Jost C et al Functional amyloid formation within mammalian tissue. PLoS Biol 2006; 4: e6. 16300414 PMC1288039
- [3]Otzen D Functional amyloid: turning swords into plowshares. Prion 2010; 4: 256– 64. 20935497 PMC3268958
- [4]Ramsook CB, Tan C, Garcia MC et al Yeast cell adhesion molecules have functional amyloid-forming sequences. Eukaryot Cell 2010; 9: 393– 404. 20038605 PMC2837979
- [5]Lipke PN, Ramsook CB, Garcia-Sherman MC et al Between amyloids and aggregation lies a connection with strength and adhesion. New J Sci 2014; 2014: 815102. PMC3981074 24729913
- [6]Pepys MB, Dash AC, Markham R et al Comparative clinical study of protein SAP (amyloid P component) and C-reactive protein in serum. Clin Exp Immunol 1978; 32: 119– 24. 668189 PMC1541304
- [7]Pepys MB, Booth S, Tennent GA et al Binding of pentraxins to different nuclear structures: C-reactive protein binds to small nuclear ribonucleoprotein particles, serum amyloid P component binds to chromatin and nucleoli. Clin Exp Immunol 1994; 97: 152– 7. 8033412 PMC1534802
- [9]Vilahur G, Badimon L Biological actions of pentraxins. Vascul Pharmacol 2015; 73: 38– 44. 25962566
- [10]Al-Shawi R, Tennent GA, Millar DJ et al Pharmacological removal of serum amyloid P component from intracerebral plaques and cerebrovascular Aβ amyloid deposits in vivo. Open Biol 2016; 6: 150202. 26842068 PMC4772805
- [11]Richards DB, Cookson LM, Berges AC et al Therapeutic clearance of amyloid by antibodies to serum amyloid P component. N Engl J Med 2015 17; 373: 1106– 14. 26176329
- [13]Garcia-Sherman MC, Lysak N, Filonenko A et al Peptide detection of fungal functional amyloids in infected tissue. PLoS One 2014; 9: e86067. 24465872 PMC3897640
- [14]Noursadeghi M, Bickerstaff MC, Gallimore JR et al Role of serum amyloid P component in bacterial infection: protection of the host or protection of the pathogen. Proc Natl Acad Sci U S A 2000; 97: 14584– 89. 11121061 PMC18962
- [15]Cox N, Pilling D, Gomer R Serum amyloid P: a systemic regulator of the innate immune response. J Leukoc Biol 2014; 96: 739– 43. 24804675 PMC6607997
- [16]Garcia-Sherman MC, Lundberg T, Sobonya RE et al A unique biofilm in human deep mycoses: fungal amyloid is bound by host serum amyloid P component. NPJ Biofilms Microbiomes 2015; 1: pii: 15009. PMC4563996 26366292
- [17]Stergiopoulou T, Meletiadis J, Roilides E et al Host-dependent patterns of tissue injury in invasive pulmonary aspergillosis. Am J Clin Pathol 2007; 127: 349– 55. 17276936
- [18]Ben-Ami R, Luna M, Lewis R et al A clinicopathological study of pulmonary mucormycosis in cancer patients: extensive angioinvasion but limited inflammatory response. J Infect 2009; 59: 134– 8. 19576639 PMC7006840
- [19]Shaukat A, Bakri F, Young P et al Invasive filamentous fungal infection in allogeneic hematopoietic stem cell transplant recipients after recovery from neutropenia: clinical, radiologic, and pathologic characteristics. Mycopathologica 2005; 159: 181– 8. 15770441
- [20]Tennent GA, Lovat L, Pepys MB Serum amyloid P component prevents proteolysis of amyloid fibers. Proc Natl Acad Sci U S A 1995; 92: 4299– 303. 7753801 PMC41931
- [21]Pepys MB Invasive candidiasis: new insights presaging new therapeutic approaches? J Infect Dis 2012; 206: 1339– 41. 22927458
Cited by
Sorted by citations
Serum amyloid P secreted by bone marrow adipocytes drives skeletal amyloidosis
Kumar, S., Song, K., Wang, J., Baghel, M. S., Zeng, Y., Shen, K., Zheng, J., Crane, J., Demehri, S., Gao, P., et al. (2025) · Nature Aging · doi:10.1038/s43587-025-00924-z · Cited by 16 · see citing works
The Paradoxical Effects of Serum Amyloid-P Component on Disseminated Candidiasis
Klotz, S. A., & Lipke, P. N. (2022) · Pathogens · doi:10.3390/pathogens11111304 · Cited by 5 · see citing works
“This finding led us to hypothesize that SAP’s presence in deep seated fungal infections was deleterious to the host, likely dampening the host immune response [12,14,15].”
BackgroundSelf-citation
- Authors
- Klotz, S. A., Sobonya, R. E., Lipke, P. N., & Garcia-Sherman, M. C.
- Affiliations
- Division of Infectious Diseases
- University of Arizona (US)
- City University of New York (US)
- Department of Biology, City University of New York at Brooklyn
- Corresponding author
- Klotz, Stephen A.
- Venue
- Open Forum Infectious Diseases
- Publisher
- Oxford University Press (OUP)
- Published
- 2016
- Volume
- 3
- Issue
- 3
- Pages
- ofw166-ofw166
- ISSN
- 2328-8957 (ISSN-L)
- PMC
- PMC5047411
- OpenAlex
- W2485334616
- Cited by
- 22
- References
- 2
- Citations by year
- 2025: 3 · 2023: 3 · 2022: 4 · 2021: 3 · 2020: 1 · 2019: 2 · 2018: 3 · 2017: 3
- FWCI
- 2.46
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Open Forum Infectious Diseases (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- UA Campus Repository (The University of Arizona) (acceptedVersion, cc-by-nc-nd)
- HighWire Press Open Archive (submittedVersion)
- Funders
- National Institute of General Medical Sciences (R01GM098616)
- Topics
- Health Sciences › Medicine › Infectious Diseases › Antifungal resistance and susceptibility
- Health Sciences › Medicine › Epidemiology › Fungal Infections and Studies
- Life Sciences › Immunology and Microbiology › Immunology › Biomarkers in Disease Mechanisms
- Keywords
- serum amyloid P component, invasive fungal infections, systemic fungal infection, host immune response, neutropenia, chemotherapy, inflammation, host-fungus interactions
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