The Effect of Endotoxin on Gene Expression and Total Amount of Surfactant Protein A.

Moon, Doo Seop; Sohn, Jang Won; Yang, Seok Chul; Yoon, Ho Joo; Shin, Dong Ho; Park, Sung Soo

doi:2000.49.6.703

Tuberc Respir Dis > Volume 49(6); 2000 > Article

Original Article

Tuberculosis and Respiratory Diseases 2000;49(6):703-714.
DOI: https://doi.org/10.4046/trd.2000.49.6.703 Published online December 1, 2000.

The Effect of Endotoxin on Gene Expression and Total Amount of Surfactant Protein A.

Doo Seop Moon, Jang Won Sohn, Seok Chul Yang, Ho Joo Yoon, Dong Ho Shin, Sung Soo Park

Abstract

BACKGROUND
Surfactant protein A (SP-A) is important in the regulation of surfactant secretion, synthesis and recycling. SP-A has important roles in regulating surfactant metabolism as well as in determining surfactant's physical properties. Since systemic sepsis is one of the common causes of acute respiratory distress syndrome (ARDS) and abnormalities in surfactant function have been described in ARDS, the authors investigated the effects of endotoxemia on the accumulation of mRNA encoding SP-A and SP-A protein content. METHODS: Adult rats were given various doses of intraperitoneal endotoxin from Salmonella enteritidis and sacrificed at different times. SP-A mRNA was measured by filter hybridization method. Lung SP-A protein content was determined by double sandwich ELISA assay using a polyclonal antiserum raised in rabbits against purified rat SP-A. RESULTS: 1) The accumulation of SP-A mFNA in the endotoxin treated group 24 hours after 2mg/kg and 5mg/kg endotosin treatments was significantly increased 50.9% and 27.3%, respectively, compared to the control group (P<0.001, P<0.025). 2) The accumulation of SP-A mRNA 24 hours in the 5mg/kg endotoxin treated group was significantly increased by 26.5% compared to the control group (P<0.01). 3) Total amount of lung SP-A was not altered at 24 hours by various doses of treatment. Total lung Sp-A content 144 hours after endotoxin administration was significantly decreased by 51.4% compared to the control group (P<0.01) CONCLUSIONS: The specific regulation of SP-A by various time course in vivo is evident. The late decline in SP-A protein content was unexpected and suggests that SP-A may be differentially regulated during lung inflammation. The functional significance of these alterations remains to be clarified.

Key Words: Gene expression, Surfactant protein A, Endotoxemia

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