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Increased Synthesis of Anti-Tuberculous Glycolipid Immunoglobulin G (IgG) and IgA with Cavity Formation in Patients with Pulmonary Tuberculosis

Division of Emerging Infectious Diseases, Graduate School of Medicine, Tohoku University, Sendai, Miyagi 980-8574,¹ Fuji Research Laboratories, Kyowa Medex, Co., Ltd., Shizuoka 411-0932,² Department of Respiratory Diseases, Tokyo Metropolitan Fuchu Hospital, Fuchu, Tokyo 183-8524,³ Japan BCG Central Laboratory, Kiyose, Tokyo 204-0022, Japan⁴

Received 23 August 2007/ Returned for modification 24 September 2007/ Accepted 19 December 2007

Tuberculous glycolipid (TBGL) antigen is a cell wall component of Mycobacterium tuberculosis and has been used for the serodiagnosis of tuberculosis. We investigated correlations between the levels of anti-TBGL antibodies and a variety of laboratory markers that are potentially influenced by tuberculous infection. Comparisons between patients with cavitary lesions and those without cavitary lesions were 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; mean age, 59 ± 22 years old). Fifty-nine patients had cavitary lesions on chest X-rays. Positive correlations were found between anti-TBGL immunoglobulin G (IgG) and C-reactive protein (CRP) (r = 0.361; P < 0.001), 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.

Published ahead of print on 9 January 2008.

^¶ Present address: Jichi Medical University Hospital, 3311-1 Yakushiji, Shimotsuke-shi, Tochigi 329-0498, Japan.