Interleukin‐10: Potential Benefits and Possible Risks in Clinical Infectious Diseases

Opal, Steven M.; Wherry, Janice C.; Grint, P.

doi:10.1086/515032

Cited by 102 publications

(75 citation statements)

References 87 publications

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“…23 Prematurely downregulated Th1 activity by IL-10 and other anti-inflammatory factors can lead to persistent C trachomatis infection where the presence of infectious organisms maintain continuous inflammation leading to tissue damage. 24 Especially genital strains of C trachomatis have adapted to host IFN-g-mediated defence mechanisms by developing genetically regulated means to replace IFN-g-induced tryptophane depletion. 25 Moreover, concomitant infection with another Th2 activating microorganism, 26 preexistence of microenvironmental cytokines, 27 or hormonal status of the host 28 may compromise Th1 activation following C trachomatis infection.…”

Section: Discussionmentioning

confidence: 99%

IL-10 polymorphism and cell-mediated immune response to Chlamydia trachomatis

Öhman¹,

Tiitinen

Halttunen

et al. 2006

Genes Immun

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Chlamydia trachomatis infection induces an inflammatory response that is crucial in resolving acute infection but may also play a key role in the pathogenesis of C trachomatis associated infertility. The immune response is linked to cytokine secretion pattern which is influenced by the host genetic background. To study a relationship between interleukin-10 (IL-10) promoter À1082 polymorphism and cell-mediated immune response during C trachomatis infection in vitro, lymphocyte proliferation and cytokine (IL-10, IFN-g, TNF-a, IL-2, IL-4 and IL-5) secretion were analysed in subjects with different IL-10 genotypes. Enhanced IL-10 secretion and reduced antigen-specific lymphocyte proliferative and IFN-g responses were found in subjects with IL-10 À1082 GG genotype when compared to those with À1082 AA genotype. CD14 þ monocytes were main source of IL-10 indicating that these cells are important regulators of the antigen-specific cell-mediated responses during active C trachomatis infection. We conclude that impaired cell-mediated response to C trachomatis is associated with IL-10 genotype in subjects with high IL-10 producing capacity. A comparison of immune markers between subjects with a history of noncomplicated and complicated infection is needed to further understand the confounding factors associated with the development of C trachomatis associated sequelae.

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Section: Discussionmentioning

confidence: 99%

IL-10 polymorphism and cell-mediated immune response to Chlamydia trachomatis

Öhman¹,

Tiitinen

Halttunen

et al. 2006

Genes Immun

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“…The mechanisms involved in the improved clearance of bacteria from the peritoneal cavity of IL-10 Ϫ/Ϫ mice remain to be established. IL-10 may exert direct anti-inflammatory effects on cells involved in host defense against bacteria, i.e., IL-10 can decrease neutrophil degranulation and chemotaxis, and can suppress oxygen radical and NO synthesis (21). The net effect of the increased influx of neutrophils in peritoneal fluid of IL-10 Ϫ/Ϫ mice, likely at least in part mediated by locally elevated concentrations of the CXC chemokines MIP-2 and KC (45,46), is uncertain.…”

Section: Discussionmentioning

confidence: 99%

“…IL-10 is an 18-kDa cytokine produced under different conditions of immune activation by a variety of cell types, including T cells, B cells, monocytes, and macrophages (20,21). IL-10 is considered a prototypic anti-inflammatory cytokine and potently inhibits the production of proinflammatory cytokines in vitro and in vivo (22)(23)(24)(25)(26).…”

Section: Il-10-deficient Mice Demonstrate Multiple Organ Failure and mentioning

confidence: 99%

IL-10-Deficient Mice Demonstrate Multiple Organ Failure and Increased Mortality DuringEscherichia coliPeritonitis Despite an Accelerated Bacterial Clearance

Sewnath¹,

Olszyna

Birjmohun³

et al. 2001

The Journal of Immunology

151

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To determine the role of endogenous IL-10 in local antibacterial host defense and in the development of a systemic inflammatory response syndrome during abdominal sepsis, IL-10 gene-deficient (IL-10−/−) and wild-type (IL-10+/+) mice received an i.p. injection with Escherichia coli. Peritonitis was associated with a bacterial dose-dependent increase in IL-10 concentrations in peritoneal fluid and plasma. The recovery of E. coli from the peritoneal fluid, blood, and lungs was diminished in IL-10−/− mice, indicating that endogenous IL-10 impaired bacterial clearance. Despite a lower bacterial load, IL-10−/− mice had higher concentrations of TNF, macrophage inflammatory protein-2 and keratinocyte in peritoneal fluid and plasma, and demonstrated more severe multiple organ damage as indicated by clinical chemistry and histopathology. Furthermore, IL-10−/− mice showed an increased neutrophil recruitment to the peritoneal cavity. To examine the role of elevated TNF levels in the altered host response in IL-10−/− mice, the effect of a neutralizing anti-TNF mAb was determined. Anti-TNF did not influence the clearance of E. coli in either IL-10+/+ or IL-10−/− mice. Furthermore, anti-TNF did not affect leukocyte influx in the peritoneal fluid, multiple organ damage, or survival in IL-10+/+ mice. In IL-10−/− mice, anti-TNF partially attenuated neutrophil recruitment and multiple organ damage, and prevented the increased lethality. These data suggest that although endogenous IL-10 facilitates the outgrowth and dissemination of bacteria during E. coli peritonitis, it protects mice from lethality by attenuating the development of a systemic inflammatory response syndrome by a mechanism that involves inhibition of TNF release.

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“…[16][17][18][19][20][21][22] However, the role of IL-10 in renal tubulointerstitial fibrosis has not been studied. Here, we used IL-10 À / À mice [23][24][25][26] with unilateral ureteral obstruction (UUO), a well-established model for kidney fibrosis, to investigate the roles of IL-10 in the progression of renal fibrosis.…”

mentioning

confidence: 99%