Skip to main content
ARS Home » Research » Publications at this Location » Publication #104037

Title: BACTERIAL EVASION OF HOST-DERIVED ANTIMICROBIAL PEPTIDES ON MUCOSAL SURFACES

Author
item BROGDEN, KIM

Submitted to: Virulence Mechanisms of Bacterial Pathogens
Publication Type: Book / Chapter
Publication Acceptance Date: 8/15/1999
Publication Date: N/A
Citation: N/A

Interpretive Summary: Respiratory tract diseases are a leading cause of loss from disease in the cattle, sheep and goat industries. Annual loss in the United States is estimated to exceed one billion dollars. Losses are from mortality, reduced feed efficiency, and slaughter condemnations, as well as prevention and treatment measures. Currently, not all the factors leading to the development of pneumonia are known by scientists and veterinarians. As part of our ongoing studies to understand the disease process, the resistance mechanisms to antimicrobial peptides were reviewed. Bacteria use a number of evasive strategies to avoid killing by antimicrobial peptides. Bacteria may "hide" from the peptides in the mucosal fluid by burrowing in epithelial cells; release endotoxin to absorb peptides targeted for bacterial cells; alter the electrostatic charge on the bacterial surfaces to prevent peptide interaction; utilize peptides for attachment and colonization; or enzymatically digest peptides. On the basis of these findings, it appears that antimicrobial peptide resistance is an important factor in the disease process that may be circumvented to better control shipping fever of cattle. Corollary benefits include an increase in the profitability and international competitiveness of the U. S. cattle industry, a stronger rural economy, and a continued supply of inexpensive, wholesome beef, and beef products for the American consumer.

Technical Abstract: A variety of immune and innate mechanisms have evolved at mucosal surfaces to prevent microbial invasion and damage. Predominant among the nonimmune mechanisms is the presence of a multiple peptide-containing constitutive and inducible antimicrobial barrier in the granules of phagocytes and mucosal fluids. In spite of this barrier, microorganisms still persist and dproliferate in these environments. This is due to a number of evasive strategies microorganisms have developed to avoid killing by antimicrobial peptides. Bacteria may "hide" from the peptides in the mucosal fluid by burrowing in epithelial cells; release endotoxin to absorb peptides targeted for bacterial cells; alter the electrostatic charge on the bacterial surfaces and membranes to prevent peptide interaction; utilize peptides for attachment and colonization; or enzymatically digest peptides. For the first time, identification of these resistance mechanisms, gives us sinsight on how microorganisms initially interact with the innate immune system and become primary pathogens or enter into commensal, latency, or carrier states in susceptible hosts.