TY - JOUR
T1 - Mycobactenum tuberculosis binding to human surfactant proteins A and D, fibronectin, and small airway epithelial cells under shear conditions
AU - Hall-Stoodley, Luanne
AU - Watts, Gayle
AU - Crowther, Joy E.
AU - Balagopal, Ashwin
AU - Torrelles, Jordi B.
AU - Robison-Cox, James
AU - Bargatze, Robert F.
AU - Harmsen, Allen G.
AU - Crouch, Erika C.
AU - Schlesinger, Larry S.
PY - 2006/6
Y1 - 2006/6
N2 - A crucial step in infection is the initial attachment of a pathogen to host cells or tissue. Mycobacterium tuberculosis has evolved multiple strategies for establishing an infection within the host. The pulmonary microenvironment contains a complex milieu of pattern recognition molecules of the innate immune system that play a role in the primary response to inhaled pathogens. Encounters of M. tuberculosis with these recognition molecules likely influence the outcome of the bacillus-host interaction. Here we use a novel fluid shear assay to investigate the binding of M. tuberculosis to innate immune molecules that are produced by pulmonary epithelial cells and are thought to play a role in the lung innate immune response. Virulent and attenuated M. tuberculosis strains bound best to immobilized human fibronectin (FN) and surfactant protein A (SP-A) under this condition. Binding under fluid shear conditions was more consistent and significant compared to binding under static conditions. Soluble FN significantly increased the adherence of both virulent and attenuated M. tuberculosis strains to human primary small airway epithelial cells (SAEC) under fluid shear conditions. In contrast, SP-A and SP-D effects on bacterial adherence to SAEC differed between the two strains. The use of a fluid shear model to simulate physiological conditions within the lung and select for high-affinity binding interactions should prove useful for studies that investigate interactions between M. tuberculosis and host innate immune determinants.
AB - A crucial step in infection is the initial attachment of a pathogen to host cells or tissue. Mycobacterium tuberculosis has evolved multiple strategies for establishing an infection within the host. The pulmonary microenvironment contains a complex milieu of pattern recognition molecules of the innate immune system that play a role in the primary response to inhaled pathogens. Encounters of M. tuberculosis with these recognition molecules likely influence the outcome of the bacillus-host interaction. Here we use a novel fluid shear assay to investigate the binding of M. tuberculosis to innate immune molecules that are produced by pulmonary epithelial cells and are thought to play a role in the lung innate immune response. Virulent and attenuated M. tuberculosis strains bound best to immobilized human fibronectin (FN) and surfactant protein A (SP-A) under this condition. Binding under fluid shear conditions was more consistent and significant compared to binding under static conditions. Soluble FN significantly increased the adherence of both virulent and attenuated M. tuberculosis strains to human primary small airway epithelial cells (SAEC) under fluid shear conditions. In contrast, SP-A and SP-D effects on bacterial adherence to SAEC differed between the two strains. The use of a fluid shear model to simulate physiological conditions within the lung and select for high-affinity binding interactions should prove useful for studies that investigate interactions between M. tuberculosis and host innate immune determinants.
UR - http://www.scopus.com/inward/record.url?scp=33646923702&partnerID=8YFLogxK
U2 - 10.1128/IAI.01644-05
DO - 10.1128/IAI.01644-05
M3 - Article
C2 - 16714591
AN - SCOPUS:33646923702
VL - 74
SP - 3587
EP - 3596
JO - Infection and Immunity
JF - Infection and Immunity
SN - 0019-9567
IS - 6
ER -