ABSTRACT
BACKGROUND: Bacterial extract consisting of immuno-stimulating components derived from 18 Escherichia coli (E. coli) strains has been used for the prophylaxis of recurrent cystitis. Catechin, extract of green tea, has antimicrobial effect against uropathogens. To evaluate the anti-inflammatory effect of E. coli extract and green tea, we measured the cytokine levels from bladder tissue after oral administration and analyzed bladder inflammation by histopathologic examination in a model of lipopolysaccharide (LPS)-induced cystitis in mice. MATERIALS AND METHODS: After 10-day administration of E. coli extract or catechin, cytokine [interleukin-6 (IL-6), IL-10, monocyte chemoattractant protein-1 (MCP-1), interferon-gamma (IFN-gamma), Tumor necrosis factor-alpha (TNF-alpha), IL-12p70] levels in the bladder of female BALB/c mice were measured using cytometric bead array. Bladder macrophage inflammatory protein-2 (MIP-2) level was also measured using sandwich enzyme immunoassay. After immunization with E. coli extract and catechin E. coli LPS was instilled into the bladders. Twenty-four hours later, mice were sacrificed and inflammation of the bladder were quantified using the bladder inflammatory index (BII). RESULTS: Significant increases of IL-6 and IFN-gamma in bladder tissue were observed after treatment with E. coli extract and catechin. IL-12p70 level was only elevated in bladder tissue of the catechin group. Bladder instilled with LPS showed high inflammation scores for edema, leukocyte infiltration, and hemorrhage in saline treated control mice. In contrast, E. coli extract and catechin treated mice exhibited mild inflammation with significant reduction of BII scores compared to controls. CONCLUSION: These results demonstrate that immunization using oral E. coli extract and green tea provides protection from inflammatory responses in a mouse model of LPS-induced cystitis.
Subject(s)
Animals , Female , Humans , Mice , Administration, Oral , Catechin , Chemokine CCL2 , Cystitis , Edema , Escherichia coli , Escherichia , Hemorrhage , Immunization , Immunoenzyme Techniques , Inflammation , Interferon-gamma , Interleukin-10 , Interleukin-6 , Leukocytes , Macrophages , Tea , Tumor Necrosis Factor-alpha , Urinary BladderABSTRACT
BACKGROUND: Bacterial extract consisting of immuno-stimulating components derived from 18 Escherichia coli (E. coli) strains has been used for the prophylaxis of recurrent cystitis. Catechin, extract of green tea, has antimicrobial effect against uropathogens. To evaluate the anti-inflammatory effect of E. coli extract and green tea, we measured the cytokine levels from bladder tissue after oral administration and analyzed bladder inflammation by histopathologic examination in a model of lipopolysaccharide (LPS)-induced cystitis in mice. MATERIALS AND METHODS: After 10-day administration of E. coli extract or catechin, cytokine [interleukin-6 (IL-6), IL-10, monocyte chemoattractant protein-1 (MCP-1), interferon-gamma (IFN-gamma), Tumor necrosis factor-alpha (TNF-alpha), IL-12p70] levels in the bladder of female BALB/c mice were measured using cytometric bead array. Bladder macrophage inflammatory protein-2 (MIP-2) level was also measured using sandwich enzyme immunoassay. After immunization with E. coli extract and catechin E. coli LPS was instilled into the bladders. Twenty-four hours later, mice were sacrificed and inflammation of the bladder were quantified using the bladder inflammatory index (BII). RESULTS: Significant increases of IL-6 and IFN-gamma in bladder tissue were observed after treatment with E. coli extract and catechin. IL-12p70 level was only elevated in bladder tissue of the catechin group. Bladder instilled with LPS showed high inflammation scores for edema, leukocyte infiltration, and hemorrhage in saline treated control mice. In contrast, E. coli extract and catechin treated mice exhibited mild inflammation with significant reduction of BII scores compared to controls. CONCLUSION: These results demonstrate that immunization using oral E. coli extract and green tea provides protection from inflammatory responses in a mouse model of LPS-induced cystitis.