Immunology of cryptosporidiosis

Guoku Hu, Yaoyu Feng, Steven P. O’Hara, Xian-Ming Chen

Research output: Chapter in Book/Report/Conference proceedingChapter

6 Citations (Scopus)

Abstract

Cryptosporidium spp. infect the gastrointestinal epithelium of vertebrate hosts. Intestinal species typically cause self-limiting diarrhea in immunocompetent individuals, suggesting an efficient host immune defense to eliminate the infection. Both innate and adaptive immunity are involved in host anti-parasite defense. Because of the “minimally invasive” nature of Cryptosporidium infection, mucosal epithelial cells are critical to the host’s anti-Cryptosporidium immunity. Epithelial cells not only provide the first and rapid defense against Cryptosporidium infection, but also mobilize immune effector cells to the infection site to activate adaptive immunity. Attachment to the apical cell surface by Cryptosporidium, as well as molecules inserted into host cells after attachment, can activate host cell signal pathways and thereby alter cell function. Pathogen recognition receptors (e.g., Toll-like receptors) in epithelial cells recognize Cryptosporidium and initiate downstream signaling pathways (e.g., NF-kappaB) which trigger a series of antimicrobial responses and activate adaptive immunity. Non-coding RNAs are critical regulators of mucosal immunity to infection, while release of exosomes from epithelial cells may be a relatively unexplored, important component of mucosal anti-parasite defense. Conversely, it appears that Cryptosporidium has also developed strategies of immune evasion to escape host immunity, at least at the early stage of infection. Immune responses contribute to the pathophysiologic features of cryptosporidiosis. A better understanding the immunology of cryptosporidiosis will provide a framework for the potential development of novel therapeutic strategies.

Original languageEnglish
Title of host publicationCryptosporidium: Parasite and Disease
PublisherSpringer-Verlag Wien
Pages423-454
Number of pages32
ISBN (Electronic)9783709115626
ISBN (Print)9783709115619
DOIs
StatePublished - Jan 1 2014

Fingerprint

Cryptosporidiosis
Cryptosporidium
Allergy and Immunology
Adaptive Immunity
Infection
Epithelial Cells
Immunity
Parasites
Exosomes
Immune Evasion
Mucosal Immunity
Untranslated RNA
NF-kappa B
Toll-Like Receptors
Innate Immunity
Vertebrates
Diarrhea
Signal Transduction
Epithelium

All Science Journal Classification (ASJC) codes

  • Medicine(all)
  • Immunology and Microbiology(all)

Cite this

Hu, G., Feng, Y., O’Hara, S. P., & Chen, X-M. (2014). Immunology of cryptosporidiosis. In Cryptosporidium: Parasite and Disease (pp. 423-454). Springer-Verlag Wien. https://doi.org/10.1007/978-3-7091-1562-6_10

Immunology of cryptosporidiosis. / Hu, Guoku; Feng, Yaoyu; O’Hara, Steven P.; Chen, Xian-Ming.

Cryptosporidium: Parasite and Disease. Springer-Verlag Wien, 2014. p. 423-454.

Research output: Chapter in Book/Report/Conference proceedingChapter

Hu, G, Feng, Y, O’Hara, SP & Chen, X-M 2014, Immunology of cryptosporidiosis. in Cryptosporidium: Parasite and Disease. Springer-Verlag Wien, pp. 423-454. https://doi.org/10.1007/978-3-7091-1562-6_10
Hu G, Feng Y, O’Hara SP, Chen X-M. Immunology of cryptosporidiosis. In Cryptosporidium: Parasite and Disease. Springer-Verlag Wien. 2014. p. 423-454 https://doi.org/10.1007/978-3-7091-1562-6_10
Hu, Guoku ; Feng, Yaoyu ; O’Hara, Steven P. ; Chen, Xian-Ming. / Immunology of cryptosporidiosis. Cryptosporidium: Parasite and Disease. Springer-Verlag Wien, 2014. pp. 423-454
@inbook{dc5987a4c4084421a95da0110268a2d1,
title = "Immunology of cryptosporidiosis",
abstract = "Cryptosporidium spp. infect the gastrointestinal epithelium of vertebrate hosts. Intestinal species typically cause self-limiting diarrhea in immunocompetent individuals, suggesting an efficient host immune defense to eliminate the infection. Both innate and adaptive immunity are involved in host anti-parasite defense. Because of the “minimally invasive” nature of Cryptosporidium infection, mucosal epithelial cells are critical to the host’s anti-Cryptosporidium immunity. Epithelial cells not only provide the first and rapid defense against Cryptosporidium infection, but also mobilize immune effector cells to the infection site to activate adaptive immunity. Attachment to the apical cell surface by Cryptosporidium, as well as molecules inserted into host cells after attachment, can activate host cell signal pathways and thereby alter cell function. Pathogen recognition receptors (e.g., Toll-like receptors) in epithelial cells recognize Cryptosporidium and initiate downstream signaling pathways (e.g., NF-kappaB) which trigger a series of antimicrobial responses and activate adaptive immunity. Non-coding RNAs are critical regulators of mucosal immunity to infection, while release of exosomes from epithelial cells may be a relatively unexplored, important component of mucosal anti-parasite defense. Conversely, it appears that Cryptosporidium has also developed strategies of immune evasion to escape host immunity, at least at the early stage of infection. Immune responses contribute to the pathophysiologic features of cryptosporidiosis. A better understanding the immunology of cryptosporidiosis will provide a framework for the potential development of novel therapeutic strategies.",
author = "Guoku Hu and Yaoyu Feng and O’Hara, {Steven P.} and Xian-Ming Chen",
year = "2014",
month = "1",
day = "1",
doi = "10.1007/978-3-7091-1562-6_10",
language = "English",
isbn = "9783709115619",
pages = "423--454",
booktitle = "Cryptosporidium: Parasite and Disease",
publisher = "Springer-Verlag Wien",

}

TY - CHAP

T1 - Immunology of cryptosporidiosis

AU - Hu, Guoku

AU - Feng, Yaoyu

AU - O’Hara, Steven P.

AU - Chen, Xian-Ming

PY - 2014/1/1

Y1 - 2014/1/1

N2 - Cryptosporidium spp. infect the gastrointestinal epithelium of vertebrate hosts. Intestinal species typically cause self-limiting diarrhea in immunocompetent individuals, suggesting an efficient host immune defense to eliminate the infection. Both innate and adaptive immunity are involved in host anti-parasite defense. Because of the “minimally invasive” nature of Cryptosporidium infection, mucosal epithelial cells are critical to the host’s anti-Cryptosporidium immunity. Epithelial cells not only provide the first and rapid defense against Cryptosporidium infection, but also mobilize immune effector cells to the infection site to activate adaptive immunity. Attachment to the apical cell surface by Cryptosporidium, as well as molecules inserted into host cells after attachment, can activate host cell signal pathways and thereby alter cell function. Pathogen recognition receptors (e.g., Toll-like receptors) in epithelial cells recognize Cryptosporidium and initiate downstream signaling pathways (e.g., NF-kappaB) which trigger a series of antimicrobial responses and activate adaptive immunity. Non-coding RNAs are critical regulators of mucosal immunity to infection, while release of exosomes from epithelial cells may be a relatively unexplored, important component of mucosal anti-parasite defense. Conversely, it appears that Cryptosporidium has also developed strategies of immune evasion to escape host immunity, at least at the early stage of infection. Immune responses contribute to the pathophysiologic features of cryptosporidiosis. A better understanding the immunology of cryptosporidiosis will provide a framework for the potential development of novel therapeutic strategies.

AB - Cryptosporidium spp. infect the gastrointestinal epithelium of vertebrate hosts. Intestinal species typically cause self-limiting diarrhea in immunocompetent individuals, suggesting an efficient host immune defense to eliminate the infection. Both innate and adaptive immunity are involved in host anti-parasite defense. Because of the “minimally invasive” nature of Cryptosporidium infection, mucosal epithelial cells are critical to the host’s anti-Cryptosporidium immunity. Epithelial cells not only provide the first and rapid defense against Cryptosporidium infection, but also mobilize immune effector cells to the infection site to activate adaptive immunity. Attachment to the apical cell surface by Cryptosporidium, as well as molecules inserted into host cells after attachment, can activate host cell signal pathways and thereby alter cell function. Pathogen recognition receptors (e.g., Toll-like receptors) in epithelial cells recognize Cryptosporidium and initiate downstream signaling pathways (e.g., NF-kappaB) which trigger a series of antimicrobial responses and activate adaptive immunity. Non-coding RNAs are critical regulators of mucosal immunity to infection, while release of exosomes from epithelial cells may be a relatively unexplored, important component of mucosal anti-parasite defense. Conversely, it appears that Cryptosporidium has also developed strategies of immune evasion to escape host immunity, at least at the early stage of infection. Immune responses contribute to the pathophysiologic features of cryptosporidiosis. A better understanding the immunology of cryptosporidiosis will provide a framework for the potential development of novel therapeutic strategies.

UR - http://www.scopus.com/inward/record.url?scp=84929656185&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84929656185&partnerID=8YFLogxK

U2 - 10.1007/978-3-7091-1562-6_10

DO - 10.1007/978-3-7091-1562-6_10

M3 - Chapter

SN - 9783709115619

SP - 423

EP - 454

BT - Cryptosporidium: Parasite and Disease

PB - Springer-Verlag Wien

ER -