Cryptosporidiosis and the pathogenesis of AIDS-cholangiopathy

Xian Ming Chen, Nicholas F La Russo

Research output: Contribution to journalArticle

41 Citations (Scopus)

Abstract

Cryptosporidium, an intracellular parasite that infects the gastrointestinal epithelium and other mucosal surfaces, causes self-limited diarrhea in immunocompetent subjects and potentially life-threatening syndromes in immunocompromised individuals, primarily those with acquired immunodeficiency syndrome (AIDS). Cryptosporidium is also the single most common identifiable pathogen in the biliary tract in patients with AIDS-cholangiopathy, an important biliary disorder caused by opportunistic infection of the billary epithelium and resulting in significant morbidity and mortality in AIDS patients. The organism stimulates periductal inflammation in the biliary tree, induces biliary epithelial cell apoptosis, and thus contributes to the pathogenesis of AIDS-cholangiopathy. Currently, there is no fully effective medical therapy for both of the diseases. A better understanding of the parasitology of Cryptosporidium and the pathophysiology of biliary cryptosporidiosis should aid not only our understanding of the pathogenesis of AIDS-cholangiopathy but also the development of effective therapies and control of this ubiquitous, highly infectious threat.

Original languageEnglish (US)
Pages (from-to)277-289
Number of pages13
JournalSeminars in Liver Disease
Volume22
Issue number3
DOIs
StatePublished - Aug 2002

Fingerprint

Cryptosporidiosis
Acquired Immunodeficiency Syndrome
Cryptosporidium
Biliary Tract
Epithelium
Parasitology
Opportunistic Infections
Diarrhea
Parasites
Epithelial Cells
Apoptosis
Inflammation
Morbidity
Mortality
Therapeutics

Keywords

  • AIDS-cholangiopathy
  • Bile ducts
  • Cryptosporidium
  • HIV
  • Pathogenesis

ASJC Scopus subject areas

  • Hepatology

Cite this

Cryptosporidiosis and the pathogenesis of AIDS-cholangiopathy. / Chen, Xian Ming; La Russo, Nicholas F.

In: Seminars in Liver Disease, Vol. 22, No. 3, 08.2002, p. 277-289.

Research output: Contribution to journalArticle

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