Regulatory Role of Interleukin-10 in Experimental Group B Streptococcal Arthritis

Puliti, Manuela; Hunolstein, Christina von; Verwaerde, Claudie; Bistoni, Francesco; Orefici, Graziella; Tissi, Luciana

doi:10.1128/iai.70.6.2862-2868.2002

Cited by 32 publications

(34 citation statements)

References 52 publications

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“…In fact, invading macrophages and granulocytes produce cytokines and proteolytic enzymes that contribute to cartilage and bone destruction (38)(39)(40). In addition to proinflammatory cytokine production, in our experimental model the extent of articular inflammatory infiltrate and exudate and the number of microorganisms that reach the joints also dictate the severity of GBS arthritis (41). Selective recruitment of activated leukocytes into a site of inflammation is mediated by many factors, including chemokines (42).…”

Section: Discussionmentioning

confidence: 99%

Role of interleukin‐18 in experimental group B streptococcal arthritis

Tissi¹,

McRae²,

Ghayur³

et al. 2004

Arthritis & Rheumatism

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Objective. To assess the role of interleukin-18 (IL-18) in the evolution of septic arthritis induced by group B streptococci (GBS) in mice.Methods. CD1 mice were inoculated intravenously with 8 ؋ 10 6 colony-forming units (CFU) of type IV GBS (strain 1/82), and administered intraperitoneally 1 hour before infection with anti-IL-18 monoclonal antibodies (0.25 mg/mouse). In a subsequent set of experiments, mice infected with a suboptimal arthritogenic dose of GBS (4 ؋ 10 6 CFU/mouse) were administered different doses of recombinant IL-18 for 4 days, starting 1 hour after infection. Mortality, evolution of arthritis, bacterial clearance, joint histopathology, and cytokine production were examined in infected mice that did or did not receive treatment with anti-IL-18 antibodies or IL-18.Results. IL-18 was produced during GBS infection. Neutralization of IL-18 resulted in a decrease in mortality rates, and in the incidence and severity of arthritis. Amelioration of arthritis was accompanied by a dramatic reduction in local IL-1␤, IL-6, macrophage inflammatory protein 1␣ (MIP-1␣) and MIP-2 production, and reduced bacterial burden. Administration of exogenous IL-18 resulted in increased mortality rates and increased incidence and severity of GBS arthritis, concomitant with a higher number of GBS and increased levels of IL-6, IL-1␤, MIP-1␤, and MIP-2 production in the joints.Conclusion. The present study indicated some involvement of IL-18 in the pathogenesis of GBSinduced arthritis. The role of IL-18 in joint pathology is shown by a regulatory effect on inflammatory mediator levels and local cell influx. Thus, IL-18 should be regarded as a potential therapeutic target in GBS infection and arthritis.

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Section: Discussionmentioning

confidence: 99%

Role of interleukin‐18 in experimental group B streptococcal arthritis

Tissi¹,

McRae²,

Ghayur³

et al. 2004

Arthritis & Rheumatism

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“…Increased production of proinflammatory cytokines by A549 and HEp-2 cells in response to GAS infection was significantly increased compared to the control, indicating that bacterial infection stimulates human cells for immune response (Table 4). IL-6 and IL-8 up-regulate activity by macrophages/monocytes and polymorphonuclear cells and leukocyte chemotaxis [45][46][47][48]. Greater production of IL-6 and IL-8 and lower production of IL-10 by A549 and HEp-2 cells in all conditions was observed in this study (Table 4), which suggests that in the first phase of infection, human cells respond immunologically to up-regulate activity of macrophages/monocytes, inflammatory cells, and polymorphonuclear cells to phagocytize and clear bacteria from the cellular environment.…”

Section: Discussionmentioning

confidence: 99%

Molecular epidemiology and virulence characteristics of prevalent group A streptococci recovered from patients in northern India

Arya

Sharma

Mehta

et al. 2014

J Infect Dev Ctries

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Introduction: In this study, the prevalence of M types of Group A Streptococcus (GAS) in North India, invasive behavior of prevalent M types, and inflammatory immune response by host cells were studied. Methodology: A total of 1,047 clinical samples were collected between 2004 and 2010. Confirmation of GAS was determined by serotyping and M types were identified by emm gene sequencing. The most prevalent serotypes were selected to study their invasive behavior and inflammatory immune response under different temperatures and salt concentrations in A549 and HEp-2 cells. Results: Ninety-two isolates were identified as GAS of which 17 were M types with 18.5% heterogeneity. The most prevalent M types were M1 (21.73%) and M49 (8.7%), respectively. M1 and M49 were used to study virulence potential and inflammatory immune responses. The efficiency of cell infection decreased with increased temperature for both M types, increasing with lowering temperatures compared to the uninfected control (37°C). As salt concentration was increased, cell infection efficiency was lowered with some exceptions; the infection efficiency of M1 strain in A549 cells with 0.6 M NaCl was 50 fold higher (p ≤ 0.03). Significantly increased production of IL-6 and IL-8 was observed in both cell lines infected with GAS and when grown under different environmental conditions compared to uninfected cell lines. Conclusions: This study determined the prevalence of different M types in North India and showed that environmental conditions can regulate cell infection by GAS . This information may influence the selection of GAS serotypes used in vaccine development.

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“…IL-10 has been shown to inhibit the production of many proinflammatory cytokines, including IL-1, IL-6, TNF-␣, IL-8, granulocyte-monocyte colony-stimulating factor, and granulocyte colony-stimulating factor; to down-regulate activity by macrophages/monocytes and polymorphonuclear cells (1,3,38); and to inhibit leukocyte chemotaxis (17). The presence of IL-10 may represent a cellular response to the increasing levels of TNF-␣, since this has been described as an autoregulatory mechanism to decrease the production of TNF-␣.…”

Section: Discussionmentioning

confidence: 99%

Adherence to, Invasion by, and Cytokine Production in Response to Serotype VIII Group B Streptococci

Mikamo¹,

Johri²,

Paoletti³

et al. 2004

Infect Immun

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The adherence to and invasion of the human epithelial cell line A549 by group B streptococcus (GBS) serotype VIII strains were compared with those of serotype III strains by a conventional method and the dynamic in vitro attachment and invasion system. Twenty GBS strains, including nine vaginal isolates and one invasive isolate each of serotypes III and VIII, were used in the conventional attachment and invasion assay. Adherence to and invasion of A549 cells by serotype VIII GBS strains were significantly greater (P < 0.0001) than those by serotype III strains for both the invasive strain and vaginal isolates. Cytokine production by A549 cells following stimulation with GBS serotypes III and VIII or their purified capsular polysaccharides (CPS) was measured. Serotype III strains stimulated significantly greater tumor necrosis factor alpha (TNF-α) (P < 0.0001) and interleukin-10 (IL-10) (P < 0.05) production than did serotype VIII strains. IL-8 production in response to serotype VIII was significantly higher (P < 0.001) than that in response to serotype III. TNF-α, IL-8, and IL-10 production was greater in A549 cells infected with GBS than in the untreated control cells. TNF-α production was significantly greater (P < 0.005) after stimulation with purified GBS serotype III CPS than after stimulation with serotype VIII CPS, a result similar to that after stimulation with whole GBS. IL-12 production by A549 cells was observed only in response to infection with GBS serotype III, resulting in the possibility of a greater TH1 response in serotype III GBS. These results suggest differences in immune responses to infection with GBS serotypes III and VIII

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Regulatory Role of Interleukin-10 in Experimental Group B Streptococcal Arthritis

Cited by 32 publications

References 52 publications

Role of interleukin‐18 in experimental group B streptococcal arthritis

Role of interleukin‐18 in experimental group B streptococcal arthritis

Molecular epidemiology and virulence characteristics of prevalent group A streptococci recovered from patients in northern India

Adherence to, Invasion by, and Cytokine Production in Response to Serotype VIII Group B Streptococci

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