Volume 2 Issue 1
Mini Review: Unresolved Issues in Innate Immune Response in Post Kala Azar Dermal Leishmaniasis (PKDL)
Ashish Kumar Singh, Neena Verma, Vidya Nand Rabi Das, Krishna Pandey, Pradeep Das and Sanjiva Bimal*
Visceral Leishmaniasis (VL) which is also known as kala azar is a neglected tropical disease caused by obligate intra-macrophage protozoan Leishmania donovani, largely affecting individuals of low socioeconomic level [1].
Cite this Article: Singh AK, Verma N, Rabi Das VN, Krishna P, Bimal S, et al. Unresolved Issues in Innate Immune Response in Post Kala Azar Dermal Leishmaniasis (PKDL). Sci J Immunol Immunother. 2017;2(1): 018-021.
Published: 10 October 2017
Raef Shams* and Ehab M. Ali
Several studies investigated the different therapeutic roles of T and B lymphocytes subsets in Rheumatoid Arthritis (RA). The disease pathogenesis implicates various cells subpopulations regarding TH1 and TH17 cells that produce pro-inflammatory cytokines as well as autoantibodies production by B cells. On the other hand, certain T and B lymphocytes negatively regulate the immune response by producing regulatory cytokines or by interaction with pathogenic subsets. Recent studies investigate that the therapeutic function of these cells is exerted by IL-10, IL-35 and TGF-β regulatory cytokines production. IL-35 showed to restrict TH1/TH17 differentiation and function, and expand the suppressive function of TReg and BReg. Furthermore, IL-35 promotes the conversion of TReg and BReg to IL-35-producers (iTr35 and IL-35+ BReg, respectively). B cell-derived IL-10 not only Suppresses IL-6 and IL-12 production by dendritic cells, but also it indirectly effects on T cell response by suppress the innate immunity. This review focuses on the current knowledge of the immune regulatory modulations of IL-10 and IL-35 to understand the potential therapeutic consequences of RA for further prospective studies.
Cite this Article: Shams R, Ali EM. IL-35- and IL-10-Dependent Immunoregulatory Lymphocytes in Rheumatoid Arthritis. Sci J Immunol Immunother. 2017;2(1): 011-017.
Published: 26 September 2017
Research Article: Calcium Propionate Alleviates DSS-Induced Colitis and Influences Lipid Profile, Interferon Gamma, Peptidoglycan Recognition Protein 3 and Calprotectin in One-Year-Old Female and Male C57BL/6 Mice
Darab Ghadimi*, Sven Olaf Frahm, Michael Ebsen, Christoph Rocken, Michael de Vrese, Knut J Heller and Wilhelm Bockelmann
Although Dextran Sodium Sulphate (DSS)-induced colitis in a murine model is frequently used to investigate the health benefits of probiotic bacteria and Short-Chain Fatty Acids (SCFAs), there has been little research attempting to verify these effects - in particular those of calcium propionate - in middle- aged mice that are at higher risk because of their reduced immuno-competence and calcium signal generation, which is known to decline with age. Since patients with ulcerative colitis exhibit reduced Ca2+ signalling and DSS-induced colitis results in colonic smooth muscle hyper contractility with increased Ca2+ sensitization, we investigated the effects of Calcium Propionate (CP) in middle-aged mice under inflammatory conditions. Sixty female and male C57BL/6 mice were divided into four groups. Control Group 1 received drink water only, Inflamed Group 2 received DSS, positive control Group 3 received DSS plus Sodium Butyrate (SB), and Group 4 received DSS plus CP for 7 days in their drinking water ad libitum. Clinical signs of inflammation were monitored daily and histology of colons was examined on day 8. Plasma samples were analysed for key biomarkers of metabolic disorders and liver inflammation. Administration of CP ameliorated DSS-induced colitis/inflation and attenuated the sum of histologic colitis scores. CP reduced plasma IFN- and calprotectin while enhancing PGlyRP3 in response to DSS treatment. Gender-specific and age-specific differences in immunological and metabolic responses of mice, following inflammation, to probiotics and enteric beneficial microbiome metabolites should be taken into account. In addition to immuno-competence, however, calcium signal generation may represent a novel mechanism by which gut microbiota regulates host metabolism.
Key words: Calcium Propionate; Colitis; Dextran; Sodium Sulphate; Ifn-?; Old Age
Cite this Article: Ghadimi D, Frahm SO, Ebsen M, Rocken C, de Vrese M, et al. Calcium Propionate Alleviates DSS-Induced Colitis and Influences Lipid Profile, Interferon Gamma, Peptidoglycan Recognition Protein 3 and Calprotectin in One-Year-Old Female and Male C57BL/6 Mice. Sci J Immunol Immunother. 2017;1(1): 001-010.
Published: 12 September 2017
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