TY - JOUR
T1 - Delayed role of tumor necrosis factor-α in overcoming the effects of pertussis toxin
AU - Wolfe, Daniel N.
AU - Mann, Paul B.
AU - Buboltz, Anne M.
AU - Harvill, Eric T.
N1 - Funding Information:
Received 7 December 2006; accepted 20 April 2007; electronically published 12 September 2007. Potential conflicts of interest: none reported. Financial support: US Department of Agriculture (grant 2002-35204-11684 to E.T.H.); National Institutes of Health (grant AI 053075 to E.T.H.). a Present affiliation: Department of Clinical Support Services, Army Medical Department Center and School, Fort Sam Houston, Texas. Reprints or correspondence: Eric Harvill, Dept. of Veterinary and Biomedical Sciences, Pennsylvania State University, 115 Henning Bldg., University Park, PA 16802 ([email protected]).
PY - 2007
Y1 - 2007
N2 - Bordetella pertussis causes whooping cough, an endemic respiratory disease that is increasing in prevalence despite vaccination efforts. Although host immunity is modulated by virulence factors of this pathogen, it is unclear what host factors are required to overcome their effects. Here, we investigate an apparent relationship between the effects of pertussis toxin and tumor necrosis factor (TNF)-α. B. pertussis grew efficiently and caused moderate pathology in wild-type mice, whereas TNF-α-/- mice had higher numbers of bacteria and leukocytes in lungs, experienced more airway resistance, and died of the infection. Interestingly, an isogenic B. pertussis strain lacking pertussis toxin did not induce these effects in TNF-α -/- mice and behaved similarly in wild-type and TNF-α-deficient hosts. Together, these results indicate that TNF-α is essential for the host to overcome the effects of pertussis toxin, allowing both control of B. pertussis numbers and regulation of the inflammation induced by infection.
AB - Bordetella pertussis causes whooping cough, an endemic respiratory disease that is increasing in prevalence despite vaccination efforts. Although host immunity is modulated by virulence factors of this pathogen, it is unclear what host factors are required to overcome their effects. Here, we investigate an apparent relationship between the effects of pertussis toxin and tumor necrosis factor (TNF)-α. B. pertussis grew efficiently and caused moderate pathology in wild-type mice, whereas TNF-α-/- mice had higher numbers of bacteria and leukocytes in lungs, experienced more airway resistance, and died of the infection. Interestingly, an isogenic B. pertussis strain lacking pertussis toxin did not induce these effects in TNF-α -/- mice and behaved similarly in wild-type and TNF-α-deficient hosts. Together, these results indicate that TNF-α is essential for the host to overcome the effects of pertussis toxin, allowing both control of B. pertussis numbers and regulation of the inflammation induced by infection.
UR - http://www.scopus.com/inward/record.url?scp=35348850099&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=35348850099&partnerID=8YFLogxK
U2 - 10.1086/521303
DO - 10.1086/521303
M3 - Article
C2 - 17955442
AN - SCOPUS:35348850099
SN - 0022-1899
VL - 196
SP - 1228
EP - 1236
JO - Journal of Infectious Diseases
JF - Journal of Infectious Diseases
IS - 8
ER -
