Prior administration of probiotic bacteria reduced mucosal inflammation and damage in DSS-induced colitis. DSS colitis was associated with significant changes in the fecal anaerobic bacterial flora and these changes were modulated by administration of probiotic bacteria.

Assessment of disease activity in Takayasu arteritis (TA) is challenging. We aimed to study utility of serum amyloid A (SAA) to assess disease activity and its association with SAA gene polymorphisms, if any, in our TA patients. Serum of 99 consecutive adult TA patients and 40 healthy controls were assayed for SAA. Depending on the ITAS2010 and ITAS-CRP score, patients were designated as having active disease if ITAS2010 ≥ 2 or ITAS-CRP ≥ 3 and stable disease if ITAS2010 = 0 or ITAS-CRP is ≤1. Clinical ITAS of 0 with raised inflammatory markers scoring a ITAS-CRP of 2 was considered as indeterminate for disease activity assessment. Repeat SAA levels for active group was measured after 6 months from baseline. SAA levels between active and stable disease as well as serial levels were compared. DNA of 40 patients and controls were genotyped for SAA polymorphisms (rs12218, rs2468844) and the allele frequencies were compared. At baseline, SAA levels were higher in patients as compared to controls (137.4 vs 100.8 ng/ml, p = 0.001) and higher in patients with active disease (166.4 ng/ml) than those with stable disease (98.2 ng/ml), p = 0.001. SAA decreased during follow-up in treatment responders (189.9 ng/ml at baseline vs 119.0 ng/ml at follow-up, p = 0.008); in contrast, there was no significant change among non-responders during follow-up. Allelic frequencies of SAA gene polymorphisms did not differ between cases and controls. SAA may be a reliable biomarker to assess disease activity and treatment response in TA.

Epithelial cells participate in the innate immune response to pathogenic bacteria by elaborating chemokines. This study examined the effect of Vibrio cholerae and Lactobacillus rhamnosus GG on inflammatory chemokine gene expression in the HT29 human intestinal epithelial cell line. HT29 cells were exposed to V. cholerae 0139, Lactobacillus or both for 2 h and cultured further thereafter for 4 h. RNA was extracted from the cells and expression of genes for chemokines and related molecules was quantitated by real time PCR using a pathway‐focused PCR array. TLR4 was silenced using shRNA and output of interleukin‐8 (IL‐8) into the media quantitated with and without V. cholerae exposure. NFκB and p38 MAP kinase activation were determined by immunoblotting for IκBα and phosphorylated p38. Vibrio cholerae significantly upregulated gene expression for the neutrophil chemoattractant CXCL chemokines, IL‐8, CXCL and CXCL in HT29 cells, while downregulating the expression of macrophage‐attracting C‐C chemokines. TLR4 silencing did not reduce IL‐8 output from HT29 cells in response to V. cholerae. IκBα degradation was noted in the HT29 cells soon after exposure to V. cholerae and this recovered over time after removal of bacteria. p38 MAP kinase activation was not noted. Vibrio cholerae upregulated the expression of neutrophil attractant chemokines, most prominently IL‐8, in HT29 cells, but downregulated macrophage‐attracting chemokines. Probiotic lactobacilli modulated the IL‐8, but not the other chemokine gene changes, in response to V. cholerae.

Cytokine gene expression patterns in intestinal mucosa and PBMC of intestinal TB were remarkably similar to Crohn's disease, and demonstrated innate immune activation and T-helper 1 polarisation.

Acetylcholine type 3 receptor (M3R) is recognized as an autoantigen in primary Sjögren's syndrome (pSS). Assay of anti-M3R antibody levels in serum is fraught with low sensitivity for diagnosis of pSS. Salivary assay is more likely to improve the diagnostic accuracy. Patients with pSS classified either by the American European Consensus Group (AECG) or American college of Rheumatology (ACR) criteria, attending rheumatology clinic between October 2014 and July 2015 were included. Hospital staff and lupus patients constituted healthy and disease controls, respectively. Evaluation of pSS included clinical evaluation, laboratory tests, ESSDAI and ESSPRI scoring. Unstimulated saliva was collected by the spitting method. Salivary IgG antibody against M3R (anti-M3R) was quantified by indirect ELISA. In this study, 43 patients with pSS, 34 with lupus and 42 healthy controls were recruited. The frequency of anti-M3R antibody levels was 55.81, 17.64 and 7 % for pSS, lupus and healthy controls, respectively. Area under the Receiver Operator Characteristic was 0.7791 (95 % CI,, 0.67-0.87). Sensitivity and specificity of the assay for diagnosis of pSS were 44.19 and 88.16 %, respectively. Salivary anti-M3R IgG antibody positivity was associated with lower age, shorter disease duration and higher globulin levels in our cohort. Salivary anti-M3R IgG antibody assay has high specificity in pSS; younger patients and those with hyperglobulinemia more frequently tested positive for this antibody.