Direct evidence that capsaicin-induced plasma protein extravasation is mediated through tachykinin NK1 receptors

Eglezos, Anthony; Giuliani, Sandro; Viti, Giovanni; Maggi, Carlo Alberto

doi:10.1016/0014-2999(91)90183-q

Cited by 87 publications

(32 citation statements)

References 8 publications

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“…This is an inflammatory response triggered by the release of proinflammatory neuropeptides and activation of surface receptors, including NK1R, on the surface of sensory neurons (40). However, our data indicate that the NK1R-mediated neurogenic inflammatory response is not a major contributor of implant-induced cystitis in mice since treatment with specific NK1R antagonists and iNOS inhibitors did not prevent plasma protein leakage and edema as was previously shown in cystitis or other experimental models involving activation of the neurogenic pathway (32,41,42). Although the contributions of other factors involved in the neurogenic inflammatory response, including mast cells, bradykinins, and NK2 receptors, need to be assessed, identifying the effects of urinary implantation on factors involved in vascular permeability, such as calcium channels, calveolin, RhoGTPases, sphingosine kinases (SPHK1), and protein tyrosine phosphatases (SHP2) (43), may shed light on the mechanisms underlying the onset of bladder wall edema following catheterization.…”

Section: Discussionmentioning

confidence: 41%

Enterococcus faecalis Overcomes Foreign Body-Mediated Inflammation To Establish Urinary Tract Infections

et al. 2013

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Urinary catheterization elicits major histological and immunological changes that render the bladder susceptible to microbial invasion, colonization, and dissemination. However, it is not understood how catheters induce these changes, how these changes act to promote infection, or whether they may have any protective benefit. In the present study, we examined how catheter-associated inflammation impacts infection by Enterococcus faecalis, a leading cause of catheter-associated urinary tract infection (CAUTI), a source of significant societal and clinical challenges. Using a recently optimized murine model of foreign body-associated UTI, we found that the implanted catheter itself was the primary inducer of inflammation. In the absence of the silicone tubing implant, E. faecalis induced only minimal inflammation and was rapidly cleared from the bladder. The catheter-induced inflammation was only minimally altered by subsequent enterococcal infection and was not suppressed by inhibitors of the neurogenic pathway and only partially by dexamethasone. Despite the robust inflammatory response induced by urinary implantation, E. faecalis produced biofilm and high bladder titers in these animals. Induction of inflammation in the absence of an implanted catheter failed to promote infection, suggesting that the presence of the catheter itself is essential for E. faecalis persistence in the bladder. Immunosuppression prior to urinary catheterization enhanced E. faecalis colonization, suggesting that implant-mediated inflammation contributes to the control of enterococcal infection. Thus, this study underscores the need for novel strategies against CAUTIs that seek to reduce the deleterious effects of implant-mediated inflammation on bladder homeostasis while maintaining an active immune response that effectively limits bacterial invaders. U rinary catheterization is directly associated with 80% of hospital-acquired urinary tract infections (UTIs) (1). The insertion and presence of indwelling urinary catheters disrupt the normal mechanical and host defenses of the urinary tract, allow extracellular microbes access to the sterile environment of the bladder by ascending through the catheter lumen or from the urethral meatus along the catheter, and provide an additional surface for biofilm formation and the establishment of antibioticrecalcitrant chronic or recurrent infections (2-9). Even in the absence of microbial colonization, urinary catheterization was shown to be associated with histological and immunological alterations in the bladder, including urothelial damage and exfoliation, bladder wall edema, inflammatory cytokine production, immune cell infiltration, and mucosal lesions of the bladders and kidneys (7, 10-13) which can lead to bladder cancers (14, 15). However, there remains a need to uncover molecular details and the functional role of the catheter-induced host responses during bacterial colonization and catheter-associated UTIs (CAUTIs).We recently optimized a murine model of foreign body-associated UTI to inv...

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Section: Discussionmentioning

confidence: 41%

Enterococcus faecalis Overcomes Foreign Body-Mediated Inflammation To Establish Urinary Tract Infections

et al. 2013

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“…Airway oedema is an important component of airway obstruction, both in asthma and in chronic airflow limitation, but is not susceptible to acute reversal by conventional bronchodilator agents. Inhibition of airway oedema by NK, receptor antagonists, including FK888, has been demonstrated in animal models (Eglezos et al, 1991;Lei et al, 1992;Delay-Goyet et al, 1992;Hirayama et al, 1993;Murai et al, 1993 (Maggi et al, 1990). Endothelium-dependent vasodilation, as in the systemic circulation, is NK, receptor mediated, while endothelium-independent vasoconstriction is predominantly NK2 receptor mediated.…”

Section: Discussionmentioning

confidence: 99%

Differences in the distribution and characteristics of tachykinin NK₁ binding sites between human and guinea pig lung

Walsh

Salmon

Featherstone

et al. 1994

British J Pharmacology

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“…With the use of the selective, non-peptide NKI receptor antagonist, RP 67,580 (Garret et al, 1991), it would seem that at least part of the response to CYP at the 2 h timepoint is mediated through activation of these receptors by endogenous tachykinins, the most probable candidate for this being substance P. In fact, studies investigating the inflammatory effects of direct application of capsaicin to the urinary bladder have demonstrated that the ensuing PPE is due to activation of tachykinin NKI receptors (Eglezos et al, 1991). Pretreatment with Hoe 140, the selective, potent bradykinin B2 receptor antagonist (Lembeck et al, 1991;Wirth et al, 1991), also resulted in a significant inhibition of the oedema response.…”

Section: Plasma Protein Extravasationmentioning

confidence: 99%

Characterization of the capsaicin‐sensitive component of cyclophosphamide‐induced inflammation in the rat urinary bladder

Ahluwalia

Maggi

Santicioli

et al. 1994

British J Pharmacology

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Direct evidence that capsaicin-induced plasma protein extravasation is mediated through tachykinin NK1 receptors

Cited by 87 publications

References 8 publications

Enterococcus faecalis Overcomes Foreign Body-Mediated Inflammation To Establish Urinary Tract Infections

Enterococcus faecalis Overcomes Foreign Body-Mediated Inflammation To Establish Urinary Tract Infections

Differences in the distribution and characteristics of tachykinin NK₁ binding sites between human and guinea pig lung

Characterization of the capsaicin‐sensitive component of cyclophosphamide‐induced inflammation in the rat urinary bladder

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Direct evidence that capsaicin-induced plasma protein extravasation is mediated through tachykinin NK1 receptors

Cited by 87 publications

References 8 publications

Enterococcus faecalis Overcomes Foreign Body-Mediated Inflammation To Establish Urinary Tract Infections

Enterococcus faecalis Overcomes Foreign Body-Mediated Inflammation To Establish Urinary Tract Infections

Differences in the distribution and characteristics of tachykinin NK1 binding sites between human and guinea pig lung

Characterization of the capsaicin‐sensitive component of cyclophosphamide‐induced inflammation in the rat urinary bladder

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Differences in the distribution and characteristics of tachykinin NK₁ binding sites between human and guinea pig lung