Genetic Association of Interferon Gamma Induced Protein-10 (IP-10), CXCL-10 Gene Polymorphisms with TB Pleurisy Susceptibility in South Indian Population

Ghousunnissa Sheikh¹, Venkata Sanjeev Kumar Neela¹, Satya Sudheer Pydi¹, Naveen Chandra Suryadevara¹, Ramulu Gaddam², Suman Latha Gaddam^3,4, Sai Kumar Auzumeedi², Vijaya Lakshmi Valluri^1,3*

¹LEPRA-India, Blue Peter Public Health & Research Centre, Hyderabad, India.
²Government Chest & General Hospital, Hyderabad, India.
³Bhagwan Mahavir Medical Research Centre, Hyderabad, India.
⁴Osmania University, Hyderabad, India.

DOI: 10.4236/oji.2015.52008                

Abstract

CXCL-10 known as Interferon gamma-induced protein 10 (IP-10) or small-inducible cytokine 10 is a 8.7 kDa protein, which is secreted in response to IFN-γ by monocytes, endothelial cells and fi-broblasts. It has chemo-attraction for monocytes/macrophages, T cells, NK cells and dendritic cells in promotion of T cell adhesion to endothelial cells. In the present study, we investigated whether polymorphisms in CXCL-10 gene have any role in the manifestation of Tuberculous (TB) pleurisy. Two SNPs in CXCL-10 promoter region (﹣1447A > G and ﹣135G > A) were genotyped in patients with TB Pleurisy (n = 186), Pulmonary TB patients (n = 159) and healthy controls (n = 205) by PCR-RFLP. Disease associations were statistically analyzed by Fisher exact test. At the ﹣135G > A position, the frequencies of genotype GA and allele G were significantly high in TB pleurisy patients compared to healthy controls. While the frequencies of genotype AA and allele A were significantly low in TB pleurisy patients compared to healthy controls. The frequency of haplotype A-G with the combination of 1447A > G and ﹣135G > A was significantly high in TB pleurisy. Our results reveal that genotype GA and allele G at ﹣135G > A position were strongly associated with susceptibility to tuberculous pleurisy. The GA genotype may be a useful genetic marker for early detection of the disease in high risk individuals.

Keywords

CXCL-10, Polymorphism, Haplotype, Susceptibility, Tuberculous Pleurisy

Conflicts of Interest

The authors declare no conflicts of interest.

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