ABSTRACT
I. Introduction 330
II. Clues from the Biophysical Characteristics of SP-B and SP-C 331
III. Clues from the Channel Activities of
Amyloid-Forming Peptides 332
IV. Clues from the Channel Activities of SAPLIPs 334
V. Observed Cation Channel Insertion by SP-B/C in Planar Lipid Bilayers 335
A. Electrophysiology of Planar Lipid Bilayers 336
B. Channel Activity Inserted by Commercial Surfactant
Containing SP-B and SP-C 337
C. Channel Activity Inserted by Extracted SP-B and SP-C 338
VI. Observed Neutrophil Depolarization and G Protein-Mediated
Calcium Mobilization by Surfactant with SP-B/C 342 A. Surfactant with SP-B/C Depolarize Neutrophils 342 B. Surfactant with SP-B/C Induces Transient Ca2þ Activity 343 C. Pertussis Toxin Inhibits Surfactant-Induced
Ca2þ Changes 345 VII. Observed Inhibition of Neutrophil Activation by Surfactant
with SP-B/C 345
VIII. Conclusions 350
References 350
I. Introduction
Reduction of surface tension created by alveolar air-liquid interfaces is a
primary function of pulmonary surfactant (PS). Of the four apoproteins associ-
ated with PS, SP-B, and SP-C are necessary and sufficient for reduction of alveo-
lar surface tension (1). This occurs through the transformation, stabilization, and
recycling of the phospholipid surface film. Although the other two apoproteins,
SP-A and SP-D, support surface film homeostasis, they are not necessary for
normal gas exchange (2), and their primary functions appear related to host
defense and anti-inflammation (3).
