Induction of Cytokine Production by Different Staphylococcal Strains

Megyeri, Klára; Mándi, Yvette; Degré, Miklos; Rosztóczy, I

doi:10.1006/cyto.2002.0876

Cited by 31 publications

(26 citation statements)

References 19 publications

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“…In addition to the previously reported high-level induction of IL-1␤ and IL-6 (27), this study revealed that the levels TNF-␣, IL-17, G-CSF, and RANTES secreted in the kidneys were ϳ100-fold greater than the levels secreted in the bladder at the height of induction. Low-level induction of MCP-1, MIP-1␤, IL-12, and KC was also observed.…”

Section: Discussionsupporting

confidence: 71%

“…IL-8 can be detected in the urine of patients infected with many uropathogens, including E. faecalis and other Gram-positive cocci (32). In vitro, human mononuclear cells secrete IL-1␤ and IL-6 in response to S. saprophyticus (27). To gain greater insight into the host response to S. saprophyticus UTI, we examined soluble factors induced in vivo during infection.…”

Section: Vol 78 2010 New Model Of S Saprophyticus Murine Uti 1945mentioning

confidence: 99%

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Characterization of a Novel Murine Model of Staphylococcus saprophyticus Urinary Tract Infection Reveals Roles for Ssp and SdrI in Virulence

et al. 2010

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Staphylococcus saprophyticus, an obligate human pathogen, is the most common Gram-positive causative agent of urinary tract infection (UTI) in young, healthy women. Despite the clinical importance of S. saprophyticus, little is known about how it causes disease in the urinary tract or how the host responds to the infection. Here we established an in vivo model to study both host and bacterial factors contributing to S. saprophyticus UTI. Using this model, we show that S. saprophyticus preferentially infects C3H/HeN murine kidneys instead of the bladder, a trait observed for multiple clinical isolates. Bacterial persistence in the kidneys was observed in C3H/HeN mice but not in C57BL/6 mice, indicating that host factors strongly contribute to the ability of S. saprophyticus to cause UTI. Using C3H/HeN mice as a model, histologic and immunofluorescence analyses of infected tissues revealed that S. saprophyticus induced epithelial cell shedding in the bladder and an inflammatory response characterized by macrophage and neutrophil infiltration in the bladder and kidneys. The inflammatory response correlated with increased production of proinflammatory cytokines and chemokines in both the bladder and the kidneys. Finally, we observed that the putative S. saprophyticus virulence factors Ssp and SdrI were important for persistence, but not for initial colonization, in the murine urinary tract. Thus, we characterized both host and bacterial factors involved in progression of S. saprophyticus UTI, and we describe a useful model system for studying factors involved in the pathogenesis of this Gram-positive uropathogen.Urinary tract infections (UTI) affect over 11 million women annually in the United States (11). The primary cause of UTI is the Gram-negative bacterium Escherichia coli. However, the Gram-positive bacterium Staphylococcus saprophyticus can cause up to 10 to 15% of uncomplicated UTI (33). Thus, it is estimated that S. saprophyticus causes up to 1 million UTI each year and is the second most common cause of UTI in sexually active women (41). Moreover, Gram-positive bacteria, such as S. saprophyticus, often coexist with dominant uropathogens in the urine of infected patients, although the concentrations are lower, and therefore tend to be overlooked by routine laboratory diagnostics (35). Thus, the reported estimates of the incidence of this organism may be artificially low. Interestingly, there is a seasonal pattern for S. saprophyticus UTI; such infections peak during late summer and fall, a pattern similar to that observed for sexually transmitted diseases (23). Other Gram-positive bacteria that cause UTI include Enterococcus faecalis and Enterococcus faecium (3). In contrast to S. saprophyticus, Enterococcus spp. cause UTI in healthy young women infrequently, but they contribute to ϳ19% of complicated UTI and are often nosocomially acquired (31). Despite the fact that S. saprophyticus is the predominant cause of Gram-positive UTI, relatively little is known about how this organism causes disease in the urin...

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Section: Discussionsupporting

confidence: 71%

Section: Vol 78 2010 New Model Of S Saprophyticus Murine Uti 1945mentioning

confidence: 99%

Characterization of a Novel Murine Model of Staphylococcus saprophyticus Urinary Tract Infection Reveals Roles for Ssp and SdrI in Virulence

et al. 2010

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“…aureus elicits a strong inflammatory response, resulting in the migration of large numbers of neutrophils and macrophages to the site of infection. A majority of S. aureus strains have been shown to elicit the production of interleukin-1␤ (IL-1␤), IL-6, and IL-12 p70 in monocytes in vitro, and this may result in biasing the immune response toward a Th1-type response in vivo (33). Staphylococcal enterotoxin B (SEB) has been shown to induce in vitro expression of IL-2 and gamma interferon (IFN-␥) with rapid and intermediate kinetics, respectively, but slow expression of IL-10, a Th2 cytokine (2).…”

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confidence: 99%

Murine Immune Response to a Chronic Staphylococcus aureus Biofilm Infection

et al. 2011

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Staphylococcus aureus has reemerged as an important human pathogen in recent decades. Although many infections caused by this microbial species persist through a biofilm mode of growth, little is known about how the host's adaptive immune system responds to these biofilm infections. In this study, S. aureus cells adhered to pins in culture and were subsequently inserted into the tibiae of C57BL/6 mice, with an infecting dose of 2 ؋

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“…TLRs are surface molecules on phagocytes and other immune cells involved in identifying microbial structures (like endotoxin) and generating signals that lead to the activation of innate immune responses. The primary response to S. aureus infection is thought to be a T helper 1 (Th1) type in vivo (Megyeri et al, 2002). Recent studies evaluated the adaptive immune response to MRSA biofilms (using MRSA-M2, an ST30, spa type T019 and agr type III strain) in a mouse model and found that Th2 cell and T regulatory cell (Th2/ Treg) responses protected against biofilm formation, while Th1/Th17 responses promote the development of chronic implant infection (Prabhakara et al, 2011a(Prabhakara et al, , 2011b.…”

Section: Biofilms In Mrsa Infectionsmentioning

confidence: 99%