Increased synthesis of anti-TBGL IgG and IgA with cavity formation in pulmonary tuberculosis

Division of Emerging Infectious Diseases, Graduate School of Medicine, Tohoku University, Sendai, Miyagi 980-8574; Fuji Research Laboratories, Kyowa Medex, Co., Ltd, Shizuoka 411-0932; Department of Respiratory Diseases, Tokyo Metropolitan Fuchu Hospital,Fuchu, Tokyo 183-8524; Japan BCG Central Laboratory, Kiyose, Tokyo 204-0022

^* To whom correspondence should be addressed. Email: hattori.t{at}rid.med.tohoku.ac.jp.

	Abstract

Tuberculous glycolipid (TBGL) antigen is a cell-wall component of Mycobacterium tuberculosis, and it has been used for the serodiagnosis of tuberculosis. We investigated correlations between the levels of anti-tuberculous glycolipid (anti-TBGL) antibodies and a variety of laboratory markers that are potentially influenced by tuberculous infection. Comparison between the patients with cavitary lesions and those without cavitary lesions was also made in order to determine the mechanism underlying the immune response to TBGL. Blood samples were obtained from 91 patients with both clinically and microbiologically confirmed active pulmonary tuberculosis (60 male and 31 female, Age 59±22 years old). 59 had cavitary lesions on chest X-rays. Positive correlations were found between anti-TBGL IgG and CRP (r=0.361, p<0.001), and between anti-TBGL IgA and soluble CD40 ligand (sCD40L) (r=0.404, p<0.005), between anti-TBGL IgG and anti-TBGL IgA (r=0.551, p<0.0000005), and between anti-TBGL IgM and serum IgM (r=0.603, p<0.00000005). The patients with cavitary lesions showed significantly higher levels of anti-TBGL IgG (p<0.005), anti-TBGL IgA (p<0.05), white blood cells (p<0.01), neutrophils (p<0.005), basophils (p<0.0005), natural killer cells (p<0.05), CRP (p<0.0005), KL-6 (sialylated carbohydrate antigen KL-6) (p<0.0005), IgA (p<0.05) and sCD40L (p<0.01). The observed positive correlations between the anti-TBGL antibody levels and inflammatory markers indicate the involvement of inflammatory cytokines and NKT cells in the immunopathogenesis of pulmonary tuberculosis.