Microbes and their products - Physiological effects upon mammalian mucosa

Virinchipuram Viswanathan, Rachna Sharma, Gail Hecht

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

A dynamic array of interactions occurs between pathogens and host mucosal surfaces. The signature molecules unique to microbial pathogens allow the mammalian immune system to recognize them as non-self. This recognition, mediated by the toll-like receptor proteins, results in innate immune responses targeted against the invading organism. Pathogens also elaborate a variety of proteins that actively engage host signaling pathways and subvert them to facilitate their growth and dispersal. These interactions, developed over a long evolutionary period, have been specialized to exquisite detail. These proteins and toxins are either secreted into the medium or directly delivered into host cells by specialized secretion systems. An array of host function alterations is mediated by microbial pathogens including inflammatory responses, secretory responses, alteration of host cytoskeleton, disruption of epithelial tight junctions and apoptosis. The signaling axes involved in these interactions are potential targets for therapeutic strategies against infectious microbes.

Original languageEnglish (US)
Pages (from-to)727-762
Number of pages36
JournalAdvanced Drug Delivery Reviews
Volume56
Issue number6
DOIs
StatePublished - Apr 19 2004
Externally publishedYes

Fingerprint

Mucous Membrane
Proteins
Tight Junctions
Toll-Like Receptors
Cytoskeleton
Innate Immunity
Immune System
Apoptosis
Growth
Therapeutics

Keywords

  • Host response
  • Host-pathogen relationship
  • Pathogen
  • Secretion
  • Tight junction
  • Toll receptor

ASJC Scopus subject areas

  • Pharmaceutical Science

Cite this

Microbes and their products - Physiological effects upon mammalian mucosa. / Viswanathan, Virinchipuram; Sharma, Rachna; Hecht, Gail.

In: Advanced Drug Delivery Reviews, Vol. 56, No. 6, 19.04.2004, p. 727-762.

Research output: Contribution to journalArticle

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