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Anatomy and Physiology of the Urinary Tract: Relation to Host Defense and Microbial Infection

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  • Authors: Duane R. Hickling1, Tung-Tien Sun2, Xue-Ru Wu3
  • Editors: Matthew A. Mulvey5, Ann E. Stapleton6, David J. Klumpp7
  • VIEW AFFILIATIONS HIDE AFFILIATIONS
    Affiliations: 1: Division of Urology, Ottawa Hospital Research Institute, The Ottawa Hospital, University of Ottawa, Ottawa, ON K1Y 4E9, Canada; 2: Departments of Cell Biology, Biochemistry and Molecular Pharmacology, Departments of Dermatology and Urology, New York University School of Medicine, New York, NY, 10016; 3: Departments of Urology and Pathology, New York University School of Medicine, New York, NY, 10016; 4: Veterans Affairs, New York Harbor Healthcare Systems, Manhattan Campus, New York, NY 10016; 5: University of Utah, Salt Lake City, UT; 6: University of Washington, Seattle, WA; 7: Northwestern University, Chicago, IL
  • Source: microbiolspec July 2015 vol. 3 no. 4 doi:10.1128/microbiolspec.UTI-0016-2012
  • Received 11 November 2012 Accepted 03 April 2015 Published 31 July 2015
  • Xue-Ru Wu. xue-ru.wu@med.nyu.edu
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  • Abstract:

    The urinary tract exits to a body surface area that is densely populated by a wide range of microbes. Yet, under most normal circumstances, it is typically considered sterile, i.e., devoid of microbes, a stark contrast to the gastrointestinal and upper respiratory tracts where many commensal and pathogenic microbes call home. Not surprisingly, infection of the urinary tract over a healthy person’s lifetime is relatively infrequent, occurring once or twice or not at all for most people. For those who do experience an initial infection, the great majority (70% to 80%) thankfully do not go on to suffer from multiple episodes. This is a far cry from the upper respiratory tract infections, which can afflict an otherwise healthy individual countless times. The fact that urinary tract infections are hard to elicit in experimental animals except with inoculum 3–5 orders of magnitude greater than the colony counts that define an acute urinary infection in humans (10 cfu/ml), also speaks to the robustness of the urinary tract defense. How can the urinary tract be so effective in fending off harmful microbes despite its orifice in a close vicinity to that of the microbe-laden gastrointestinal tract? While a complete picture is still evolving, the general consensus is that the anatomical and physiological integrity of the urinary tract is of paramount importance in maintaining a healthy urinary tract. When this integrity is breached, however, the urinary tract can be at a heightened risk or even recurrent episodes of microbial infections. In fact, recurrent urinary tract infections are a significant cause of morbidity and time lost from work and a major challenge to manage clinically. Additionally, infections of the upper urinary tract often require hospitalization and prolonged antibiotic therapy. In this chapter, we provide an overview of the basic anatomy and physiology of the urinary tract with an emphasis on their specific roles in host defense. We also highlight the important structural and functional abnormalities that predispose the urinary tract to microbial infections.

  • Citation: Hickling D, Sun T, Wu X. 2015. Anatomy and Physiology of the Urinary Tract: Relation to Host Defense and Microbial Infection. Microbiol Spectrum 3(4):UTI-0016-2012. doi:10.1128/microbiolspec.UTI-0016-2012.

Key Concept Ranking

Urinary Tract Infections
0.48799685
Upper Respiratory Tract Infections
0.4433595
0.48799685

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/content/journal/microbiolspec/10.1128/microbiolspec.UTI-0016-2012
2015-07-31
2017-11-19

Abstract:

The urinary tract exits to a body surface area that is densely populated by a wide range of microbes. Yet, under most normal circumstances, it is typically considered sterile, i.e., devoid of microbes, a stark contrast to the gastrointestinal and upper respiratory tracts where many commensal and pathogenic microbes call home. Not surprisingly, infection of the urinary tract over a healthy person’s lifetime is relatively infrequent, occurring once or twice or not at all for most people. For those who do experience an initial infection, the great majority (70% to 80%) thankfully do not go on to suffer from multiple episodes. This is a far cry from the upper respiratory tract infections, which can afflict an otherwise healthy individual countless times. The fact that urinary tract infections are hard to elicit in experimental animals except with inoculum 3–5 orders of magnitude greater than the colony counts that define an acute urinary infection in humans (10 cfu/ml), also speaks to the robustness of the urinary tract defense. How can the urinary tract be so effective in fending off harmful microbes despite its orifice in a close vicinity to that of the microbe-laden gastrointestinal tract? While a complete picture is still evolving, the general consensus is that the anatomical and physiological integrity of the urinary tract is of paramount importance in maintaining a healthy urinary tract. When this integrity is breached, however, the urinary tract can be at a heightened risk or even recurrent episodes of microbial infections. In fact, recurrent urinary tract infections are a significant cause of morbidity and time lost from work and a major challenge to manage clinically. Additionally, infections of the upper urinary tract often require hospitalization and prolonged antibiotic therapy. In this chapter, we provide an overview of the basic anatomy and physiology of the urinary tract with an emphasis on their specific roles in host defense. We also highlight the important structural and functional abnormalities that predispose the urinary tract to microbial infections.

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Figures

Image of FIGURE 1
FIGURE 1

Normal anatomy of the kidney and upper urinary tract. (Reprinted from reference 163, Fig. 74.8, with permission of the publisher.) doi:10.1128/microbiolspec.UTI-0016-2012.f1

Source: microbiolspec July 2015 vol. 3 no. 4 doi:10.1128/microbiolspec.UTI-0016-2012
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Image of FIGURE 2
FIGURE 2

The ureterovesical junction. In this figure, A represents an orthotopic ureteral orifice. There is adequate length of ureteral tunnel in the bladder and therefore no reflux. Lateral and/or superior insertion of the ureteral orifice (B & C) can lead to inadequate submucosal ureter length and, potentially, reflux. (Reprinted from reference 162 with permission of the publisher.) doi:10.1128/microbiolspec.UTI-0016-2012.f2

Source: microbiolspec July 2015 vol. 3 no. 4 doi:10.1128/microbiolspec.UTI-0016-2012
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Image of FIGURE 3
FIGURE 3

Assembly, intracelluar trafficking and structure of uroplakins. (a) Luminal portion of a superficial umbrella cell of mouse urothelium visualized by transmission electron microscopy (inset: an urothelial plaque exhibiting asymmetric unit membrane or AUM). (b) Quick-freeze deep-etch showing 16-nm uroplakin particles arranged in hexagonal arrays comprising the urothelial plaques (P) interconnected by particle-free hinges (H). (c) Vesicular trafficking in umbrella cells. Uroplakin heterodimer formation takes place in the endoplasmic reticulum (ER) and undergoes modification in the Golgi apparatus. Assembled uroplakins then amass in small vesicles and bud off the trans-Golgi network (TGN), forming discoidal vesicles (DVs). The next- stage, fusiform vesicles (FVs) pass through an intermediate-filament (IF) network and ultimately fuse with the apical membrane, a process mediated by Rab27b. Apical plaque-associated UPs are internalized via endocytic pathways and/or modified FVs that form sorting endosomes (SE) and multivesicular bodies (MVB), which merge with lysosomes (LYS) for degradation. (d) A hypothetical model of uroplakin assembly into 2-D crystals. Stages A and B: The four major uroplakins (UPIa, Ib, II, and IIIa) are modified with high-mannose glycans in the ER and hetero- dimerize forming UPIa/II and UPIb/IIIa and undergo major conformational changes. Symbols: the small, horizontal arrows on UPII denote the furin cleavage site at the end of the prosequence; the open and closed circles denote high-mannose and complex glycans, respectively. With urothelium (pathway on the right), the glycans on two of the three N-glycosylation sites on the prosequence of UPII become complex glycans in the TGN (stage C2), and the cleavage of the prosequence by furin in the TGN (stage D2) then triggers oligomerization to form a 16-nm particle. In cultured urothelial cells (pathway on the left), the differentiation-dependent glycosylation of pro-UPII is defective, preventing the formation of the uroplakin heterotetramer and the 16-nm particle, thus the lack of asymmetric-unit membrane. (Reprinted and adapted from reference 16 with permission of the publisher.) doi:10.1128/microbiolspec.UTI-0016-2012.f3

Source: microbiolspec July 2015 vol. 3 no. 4 doi:10.1128/microbiolspec.UTI-0016-2012
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Image of FIGURE 4
FIGURE 4

Mechanism of storage and voiding. A. Storage of urine. Low-level bladder afferent firing, secondary to bladder distension, increases sympathetic outflow to the bladder outlet and external urethral sphincter (‘guarding reflex’). Sympathetic signaling also acts to inhibit detrusor-muscle contractions. B. Voiding. At bladder capacity, high-level bladder afferent activity activates the pontine-micturition center. This, in turn, inhibits the guarding reflex. The activated pontine-micturition center, under appropriate conditions, will lead to parasympathetic outflow to the bladder and internal-sphincter smooth muscle. Urinary sphincter relaxation is soon followed by a large, coordinated detrusor contraction leading to expulsion of urine from the bladder. (Reprinted and adapted from reference 58 with permission of the publisher.) doi:10.1128/microbiolspec.UTI-0016-2012.f4

Source: microbiolspec July 2015 vol. 3 no. 4 doi:10.1128/microbiolspec.UTI-0016-2012
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Tables

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TABLE 1

Anatomic causes of ureteral obstruction

Source: microbiolspec July 2015 vol. 3 no. 4 doi:10.1128/microbiolspec.UTI-0016-2012

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