Handicaps to host defense. Effects of hyperglycemia on C3 and Candida albicans
- PMID: 2407580
- DOI: 10.2337/diab.39.3.271
Handicaps to host defense. Effects of hyperglycemia on C3 and Candida albicans
Abstract
The hyperglycemic patient remains persistently at risk for infectious complications. Whether ascribable to diabetes mellitus, to the administration of glucocorticoids, or to the infusion of hyperalimentation fluids, hyperglycemia may impair several mechanisms of humoral host defense, including such varied neutrophil functions as adhesion, chemotaxis, and phagocytosis. In addition, binding of glucose to the biochemically active site of the third component of complement C3 inhibits the attachment of this protein to the microbial surface and thereby impairs opsonization. Last, several pathogens frequently encountered in hyperglycemic patients possess unique mechanisms of virulence that flourish in the hyperglycemic environment. Most notable in this regard is the yeast Candida albicans, which expresses a glucose-inducible protein that is structurally and functionally homologous to a complement receptor on mammalian phagocytes. This protein promotes adhesion in the yeast and subverts phagocytosis by the host. Thus, hyperglycemia serves as a central mechanism in the predisposition of hyperglycemic patients to infection.
Similar articles
-
The secreted Candida albicans protein Pra1 disrupts host defense by broadly _targeting and blocking complement C3 and C3 activation fragments.Mol Immunol. 2018 Jan;93:266-277. doi: 10.1016/j.molimm.2017.07.010. Epub 2017 Aug 30. Mol Immunol. 2018. PMID: 28860090
-
[Fungicidal and phagocytic activity against "Candida albicans" of human neutrophils in serum depleted in C3 and C4 (author's transl)].Ann Microbiol (Paris). 1975 Jan;126(1):75-81. Ann Microbiol (Paris). 1975. PMID: 1103674 French.
-
Phagocytosis of Candida albicans by polymorphonuclear leukocytes from normal and diabetic subjects.Adv Exp Med Biol. 1979;121B:33-7. doi: 10.1007/978-1-4684-8914-9_4. Adv Exp Med Biol. 1979. PMID: 121033 No abstract available.
-
[Pathogenicity of Candida albicans].Immun Infekt. 1991 Aug;19(4):108-11. Immun Infekt. 1991. PMID: 1937556 Review. German.
-
[Immunosuppressive mechanisms in diabetes mellitus].Nihon Rinsho. 2008 Dec;66(12):2233-7. Nihon Rinsho. 2008. PMID: 19069085 Review. Japanese.
Cited by
-
Hypoglycaemic and hypotensive effects of Ficus exasperata vahl. (Moraceae) leaf aqueous extract in rats.Afr J Tradit Complement Altern Med. 2011;8(3):275-83. doi: 10.4314/ajtcam.v8i3.65290. Epub 2011 Apr 2. Afr J Tradit Complement Altern Med. 2011. PMID: 22468006 Free PMC article.
-
Inpatient diabetology. The new frontier.J Gen Intern Med. 2004 May;19(5 Pt 1):466-71. doi: 10.1111/j.1525-1497.2004.30133.x. J Gen Intern Med. 2004. PMID: 15109346 Free PMC article. Review.
-
Purification and biochemical characterization of a 65-kilodalton mannoprotein (MP65), a main _target of anti-Candida cell-mediated immune responses in humans.Infect Immun. 1996 Jul;64(7):2577-84. doi: 10.1128/iai.64.7.2577-2584.1996. Infect Immun. 1996. PMID: 8698482 Free PMC article.
-
Pyogenic Liver Abscess Risk in Patients With Newly Diagnosed Type 2 Diabetes Mellitus: A Nationwide, Population-Based Cohort Study.Front Med (Lausanne). 2021 May 12;8:675345. doi: 10.3389/fmed.2021.675345. eCollection 2021. Front Med (Lausanne). 2021. PMID: 34055845 Free PMC article.
-
Hyperglycemic conditions inhibit C3-mediated immunologic control of Staphylococcus aureus.J Transl Med. 2012 Mar 5;10:35. doi: 10.1186/1479-5876-10-35. J Transl Med. 2012. PMID: 22390383 Free PMC article.
Publication types
MeSH terms
Substances
Grants and funding
LinkOut - more resources
Full Text Sources
Other Literature Sources
Medical
Miscellaneous
