Surfactant Protein D Inhibits Adherence of Uropathogenic Escherichia coli to the Bladder Epithelial Cells and the Bacterium-induced Cytotoxicity

Kurimura, Yuichiro; Nishitani, Chiaki; Ariki, Shigeru; Saito, Atsushi; Hasegawa, Yoshihiro; Takahashi, Motoko; Hashimoto, Jiro; Takahashi, Satoshi; Tsukamoto, Taiji; Kuroki, Yoshio

doi:10.1074/jbc.m112.380287

Cited by 23 publications

(28 citation statements)

References 42 publications

(47 reference statements)

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“…We previously showed that SP-D functions as an innate immune factor and modulates inflammation in renal tubular epithelial cells in vitro 26 . Recently, it has been shown that SP-D protein could inhibit adherence of UPEC to bladder epithelial cells and the bacterium-induced cytotoxicity 29 . The current study examines the role of SP-A and SP-D in murine UTI and provides evidence that SP-A and SP-D function as mediators of innate immunity by inhibiting bacterial growth and modulating renal inflammation in part by regulating p38 MAPK-related pathways in murine UTI.…”

Section: Introductionmentioning

confidence: 99%

Innate immunity of surfactant proteins A and D in urinary tract infection with uropathogenic Escherichia coli

Ding

Zhang

et al. 2015

Innate Immun

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To investigate the effects of surfactant proteins A and D (SP-A, SP-D) in urinary tract infection (UTI), SP-A and SP-D double knockout (SP-A/D KO) and wild type (WT) C57BL/6 female mice were infected with uropathogenic Escherichia coli by intravesical inoculation. Compared with WT mice SP-A/D KO mice showed increased susceptibility to UTI as evidenced by higher bacterial CFU, more infiltrating neutrophils and severe pathological changes. Keratinocyte-derived chemokine increased in the kidney of WT mice but not in SP-A/D KO mice 24 h post-infection. Compared to control, level of IL-17 was elevated in the kidney of infected WT and SP-A/D KO mice and the level of IL-17 was higher in the infected SP-A/D KO mice than infected WT mice 24 and 48 h post-infection. Basal level of p38 MAPK phosphorylation in SP-A/D KO mice was higher compared to WT mice. Phosphorylated-p38 level was elevated in the kidney of WT mice post-infection but not in SP-A/D KO mice. Furthermore, in vitro growth of uropathogenic E. coli was inhibited by SP-A and SP-D. We conclude that SP-A and SP-D function as mediators of innate immunity by inhibiting bacterial growth and modulating renal inflammation in part by regulating p38 MAPK-related pathway in murine UTI.

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Section: Introductionmentioning

confidence: 99%

Innate immunity of surfactant proteins A and D in urinary tract infection with uropathogenic Escherichia coli

Ding

Zhang

et al. 2015

Innate Immun

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“…Among these is the flow of urine that can wash away non-adherent microbes, the secretion of anti-adherence factors like Tamm-Horsfall protein (THP) and Surfactant Protein D, and the production of antibacterial proteins such as secretory IgA, Ribonuclease 7, and defensins (132–137). When overwhelmed with bacteria, bladder epithelial cells can also initiate programmed cell death pathways that lead to their exfoliation and eventual clearance from the urinary tract with the flow of urine.…”

Section: Anti-bacterial Defenses and Liabilitiesmentioning

confidence: 99%

Invasion of Host Cells and Tissues by Uropathogenic Bacteria

2016

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Within the mammalian urinary tract uropathogenic bacteria face many challenges, including the shearing flow of urine, numerous antibacterial molecules, the bactericidal effects of phagocytes, and a scarcity of nutrients. These problems may be circumvented in part by the ability of uropathogenic Escherichia coli (UPEC) and several other uropathogens to invade the epithelial cells that line the urinary tract. By entering host cells, uropathogens can gain access to additional nutrients and protection from both host defenses and antibiotic treatments. Translocation through host cells can facilitate bacterial dissemination within the urinary tract, while the establishment of stable intracellular bacterial populations may create reservoirs for relapsing and chronic urinary tract infections (UTIs). Here we review the mechanisms and consequences of host cell invasion by uropathogenic bacteria, with consideration of the defenses that are brought to bear against facultative intracellular pathogens within the urinary tract. The relevance of host cell invasion to the pathogenesis of UTIs in human patients is also assessed, along with some of the emerging treatment options that build upon our growing understanding of the infectious life cycle of UPEC and other uropathogenic bacteria.

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“…The kidneys of wildtype mice were histologically normal after infection, whereas in the knockout mice, neutrophil and monocyte infiltrates were noted in the medulla, indicating a higher inflammatory response in these mice [37] . Additionally, mice infected with uropathogenic E. coli exhibited higher levels of SP-D mRNA in the bladder as compared to uninfected mice [39] . SP-D may also play a protective role against tubulointerstitial fibrosis (the common pathway to end-stage renal disease), as overexpressing SP-D in human kidney proximal tubular cells inhibits the expression of monocyte chemoattractant protein-1, a protein that when upregulated leads to disease progression [40] .…”

Section: The Urinary Tractmentioning

confidence: 99%

“…SP-A and SP-D have been detected by RT-PCR and immunohistochemistry in the kidney and epithelium of the ureter and bladder [37,38] , and they are likely to have a protective role in these regions. In vitro , SP-A and SP-D inhibit the growth of uropathogenic Escherichia coli [37] , and SP-D reduces bacterial adherence to human bladder cells [39] . In vivo experiments on SP-A and SP-D double-knockout mice showed that these mice have an increased susceptibility to urinary tract infections by uropathogenic E. coli , as measured by higher bacterial loads in the kidney and urine [37] .…”

Section: The Urinary Tractmentioning

confidence: 99%

Non-Pulmonary Immune Functions of Surfactant Proteins A and D

Ujma

Horsnell²,

Katz³

et al. 2016

J Innate Immun

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Surfactant proteins A (SP-A) and D (SP-D) are established as essential components of our innate immune system for protecting the lung from pathogens and allergens. They essentially exert their protective functions by regulating pulmonary homeostasis. Both proteins are however widely expressed throughout the body, including the female reproductive tract, urinary tract, gastrointestinal tract, the eye, ear, nasal compartment, central nervous system, the coronary artery and the skin. The functions of SP-A and SP-D at these sites are a relatively underinvestigated area, but it is emerging that both SP-A and SP-D contribute significantly to the regulation of inflammation and protection from infection at these sites. This review presents our current understanding of the roles of SP-A and SP-D in non-pulmonary sites.

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Surfactant Protein D Inhibits Adherence of Uropathogenic Escherichia coli to the Bladder Epithelial Cells and the Bacterium-induced Cytotoxicity

Cited by 23 publications

References 42 publications

Innate immunity of surfactant proteins A and D in urinary tract infection with uropathogenic Escherichia coli

Innate immunity of surfactant proteins A and D in urinary tract infection with uropathogenic Escherichia coli

Invasion of Host Cells and Tissues by Uropathogenic Bacteria

Non-Pulmonary Immune Functions of Surfactant Proteins A and D

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