• Journal of Life Science
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• v.27 no.4
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• pp.482-499
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• 2017

Allergic diseases have increased over the past several decade worldwide including developing countries. Allergic inflammatory responses are caused by Th (T helper)2 immune responses, triggered by allergen ingestion by antigen presenting cells such as dendritic cells (DCs). Intestinal microorganisms control the metabolism and physiological functions of the host, contribute to early immune system maturation during the early life, and homeostasis and epithelial integrity during life. Bifidobacteria have strain-specific immunostimulatory properties in the Th1/Th2 balance, inhibit TSLP (thymic stromal lymphopoietin) and IgE expression, and promote Flg (Filaggrin) and FoxP3 (Treg) expression to alleviate allergies. In addition, unmethylated CpG motif ODN (oligodeoxynucleotides) is recognized by TLR (toll-like receptors)9 of B cells and plasmacytoid dendritic cells (pDCs) to induce innate and adaptive immune responses, while the butyrate produced by Clostridium butyricum activates the GPR (G-protein coupled receptors)109a signaling pathway to induce the expression of anti-inflammatory gene of pDCs, and directly stimulates the proliferation of thymically derived regulatory T (tTreg) cells through the activation of GPR43 or inhibits the activity of HADC (histone deacetylase) to differentiate naive $CD4^+$ T cells into pTreg cells through the histone H3 acetylation of Foxp3 gene intronic enhancer.

• Tuberculosis and Respiratory Diseases
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• v.66 no.3
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• pp.205-210
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• 2009

Background: CXCL10 and CXCL11, which are family of CXCR3 ligands, are expressed by lymphocytes and even by bronchial epithelial cells if the cellular immunity is activated. This study evaluated the potential utility of CXCL10 and CXCL11 in the serum for active pulmonary tuberculosis in comparison with lung cancer, which activates the cellular immunity, and benign lung diseases. Methods: Patients who newly visited Pusan National University Hospital from January 2007 to December 2007 and were suspected of having lung cancer or tuberculosis were enrolled prospectively. The patients were classified pathologically and clinically into three groups, 47 with lung cancer, 18 with active pulmonary tuberculosis and 38 control patients with benign pulmonary disease. ELISA was used to determine the levels of CXCL10 and CXCL11 were determined in the serum. Results: The level of CXCL10 and CXCL11 were significantly higher in the active pulmonary tuberculosis group than in the lung cancer and benign lung disease groups (p<0.001, Kruskal-Wallis). The level of CXCL11 was significantly higher in the lung cancer group than in the benign pulmonary disease group, but there was no significant difference in level of CXCL10 between the three groups (p<0.001, p=0.655, respectively, Mann-Whitney U). The level of CXCL10 in patients with stage III+IV lung cancer was significantly higher than those with stage I+II, but there was no significant difference in the level of CXCL11 between the groups (p<0.001, p=0.07, respectively, Mann-Whitney U). There was no significant difference in the level of CXCL10 and CXCL11 between those with the presence and absence of lung cancer metastasis. There was a significant correlation between the level of CXCL10 and CXCL11 (r=0.223, p<0.001). Conclusion: CXCL10 and CXCL11 may be a potential useful markers for active pulmonary tuberculosis if used alongside other diagnostic methods.