Enhancement of the innate immune response of bladder epithelial cells by Astragalus polysaccharides through upregulation of TLR4 expression

Yin, Xiaolin; Chen, Lei; Liu, Ying; Yang, Jun; Ma, Cuiqing; Yao, Zhigang; Yang, Lijuan; Wei, Lin; Li, Mingyuan

doi:10.1016/j.bbrc.2010.05.090

Cited by 54 publications

(28 citation statements)

References 29 publications

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“…The urothelium, via secretion of prostaglandins and other active mediators, is involved in the contractile function of the bladder (1,8,38), specifically exerting an inhibitory effect on contraction, much like the endothelium of blood vessels. We observed TLR4 expression in the urothelium, confirming results that urothelial TLR4 is expressed and functional (32,33,39). Activation of urothelial TLR4 by bacterial LPS during urinary tract infections, which are more frequent in patients with diabetes, may be a factor confounding manifestations of DBD.…”

Section: Discussionsupporting

confidence: 88%

Toll-Like Receptor 4 Activation Contributes to Diabetic Bladder Dysfunction in a Murine Model of Type 1 Diabetes

et al. 2016

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Diabetic bladder dysfunction (DBD) is a common urological complication of diabetes. Innate immune system activation via Toll-like receptor 4 (TLR4) leads to inflammation and oxidative stress and was implicated in diabetes pathophysiology. We hypothesized that bladder hypertrophy and hypercontractility in DBD is mediated by TLR4 activation. Wild-type (WT) and TLR4 knockout (TLR4KO) mice were made diabetic by streptozotocin (STZ) treatment, and bladder contractile function and TLR4 pathway expression were evaluated. Immunohistochemistry confirmed the expression of TLR4 in human and mouse bladder. Recombinant high-mobility group box protein 1 (HMGB1) increased bladder TLR4 and MyD88 expression and enhanced contractile response to electrical field stimulation. Bladder expression of TLR4 and MyD88 and serum expression of HMGB1 were increased in STZ compared with control mice. Carbachol (CCh)-mediated contraction was increased in bladders from STZ mice, and TLR4 inhibitor CLI-095 attenuated this increase. Induction of diabetes by STZ in WT mice increased bladder weight and contractile responses to CCh and to electrical field stimulation. TLR4KO mice were not protected from STZ-induced diabetes; however, despite levels of hyperglycemia similar to those of WT STZ mice, TLR4KO STZ mice were protected from diabetes-induced bladder hypertrophy and hypercontractility. These data suggest that TLR4 activation during diabetes mediates DBD-associated bladder hypertrophy and hypercontractility.

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Section: Discussionsupporting

confidence: 88%

Toll-Like Receptor 4 Activation Contributes to Diabetic Bladder Dysfunction in a Murine Model of Type 1 Diabetes

et al. 2016

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“…In systemic GBS infection, TLR-2 deficiency is associated with impaired host resistance (59); in peritoneal macrophages, GBS induces TLR-2-dependent gene activation (12), and in a neonatal infection model, TLR-2 was necessary for GBS clearance (42). There is little published data on TLR-2 signaling in the bladder; however, a body of recent evidence suggests that TLR-4 is central to the induction of local innate immunity (60,72,73,93). TLR-4 and CXCR1 deficiency predisposes to asymptomatic carriage of E. coli and possibly other uropathogens (60).…”

Section: Figmentioning

confidence: 99%

Genome-Wide Mapping of Cystitis Due to Streptococcus agalactiae and Escherichia coli in Mice Identifies a Unique Bladder Transcriptome That Signifies Pathogen-Specific Antimicrobial Defense against Urinary Tract Infection

et al. 2012

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ABSTRACTThe most common causes of urinary tract infections (UTIs) are Gram-negative pathogens such asEscherichia coli; however, Gram-positive organisms, includingStreptococcus agalactiae, or group B streptococcus (GBS), also cause UTI. In GBS infection, UTI progresses to cystitis once the bacteria colonize the bladder, but the host responses triggered in the bladder immediately following infection are largely unknown. Here, we used genome-wide expression profiling to map the bladder transcriptome of GBS UTI in mice infected transurethrally with uropathogenic GBS that was cultured from a 35-year-old women with cystitis. RNA from bladders was applied to Affymetrix Gene-1.0ST microarrays; quantitative reverse transcriptase PCR (qRT-PCR) was used to analyze selected gene responses identified in array data sets. A surprisingly small significant-gene list of 172 genes was identified at 24 h; this compared to 2,507 genes identified in a side-by-side comparison with uropathogenicE. coli(UPEC). No genes exhibited significantly altered expression at 2 h in GBS-infected mice according to arrays despite high bladder bacterial loads at this early time point. The absence of a marked early host response to GBS juxtaposed with broad-based bladder responses activated by UPEC at 2 h. Bioinformatics analyses, including integrative system-level network mapping, revealed multiple activated biological pathways in the GBS bladder transcriptome that regulate leukocyte activation, inflammation, apoptosis, and cytokine-chemokine biosynthesis. These findings define a novel, minimalistic type of bladder host response triggered by GBS UTI, which comprises collective antimicrobial pathways that differ dramatically from those activated by UPEC. Overall, this study emphasizes the unique nature of bladder immune activation mechanisms triggered by distinct uropathogens.

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“…Zhang et al [14] found that mice pre-administration with APS showed increased DC maturation, T lymphocytes proliferation, and the phagocytic capacity of peritoneal macrophage, indicating enhanced immune status. APS modulates the innate immunity through TLR4 signal pathway in urinary tract under mucosal bacterial infection [15].…”

Section: Introductionmentioning

confidence: 99%

Effect of Astragalus polysaccharide and its sulfated derivative on growth performance and immune condition of lipopolysaccharide-treated broilers

Wang

Shen

et al. 2015

International Journal of Biological Macromolecules

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Enhancement of the innate immune response of bladder epithelial cells by Astragalus polysaccharides through upregulation of TLR4 expression

Cited by 54 publications

References 29 publications

Toll-Like Receptor 4 Activation Contributes to Diabetic Bladder Dysfunction in a Murine Model of Type 1 Diabetes

Toll-Like Receptor 4 Activation Contributes to Diabetic Bladder Dysfunction in a Murine Model of Type 1 Diabetes

Genome-Wide Mapping of Cystitis Due to Streptococcus agalactiae and Escherichia coli in Mice Identifies a Unique Bladder Transcriptome That Signifies Pathogen-Specific Antimicrobial Defense against Urinary Tract Infection

Effect of Astragalus polysaccharide and its sulfated derivative on growth performance and immune condition of lipopolysaccharide-treated broilers

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