IL-17 Is Necessary for Host Protection against Acute-Phase <i>Trypanosoma cruzi</i> Infection

Miyazaki, Y.; Hamano, Shinjiro; Wang, Seng; Shimanoe, Yohei; Iwakura, Yoichiro; Yoshida, Hiroki

doi:10.4049/jimmunol.0900047

Cited by 136 publications

(144 citation statements)

References 50 publications

Supporting

Mentioning

131

Contrasting

Unclassified

Order By: Relevance

“…Infants diagnosed for T. cruzi infection later after birth (i.e., 6-12 mo of age) had not only lower IFN-g levels but also higher IL-17A and IL-6 levels throughout the follow-up period than children diagnosed at 1 mo of age. We speculate that, as reported in experimental models of T. cruzi infection, IL-17 might have a protective role recruiting and activating neutrophils and monocytes required for early control of the pathogen (28,29). Other studies have shown that IL-17 is also crucial in the control of cardiac inflammation and host survival, playing a negative feedback role in the production of IFN-g and chemokines during T. cruzi infection in humans and mice (30).…”

Section: Discussionmentioning

confidence: 99%

Serum Cytokines as Biomarkers of Early Trypanosoma cruzi infection by Congenital Exposure

Volta

Bustos

Cardoni

et al. 2016

The Journal of Immunology

View full text Add to dashboard Cite

Trypanosoma cruzi, the causing agent of Chagas disease, leads to an activation of the immune system in congenitally infected infants. In this study, we measured a set of cytokines/chemokines and the levels of parasitemia by quantitative PCR in the circulation of neonates born to T. cruzi–infected mothers to evaluate the predictive value of these mediators as biomarkers of congenital transmission. We conducted a retrospective cohort study of 35 infants with congenital T. cruzi infection, of which 15 and 10 infants had been diagnosed by detection of parasites by microscopy in the first and sixth month after delivery, respectively, and the remaining 10 had been diagnosed by the presence of T. cruzi–specific Abs at 10–12 mo old. Uninfected infants born to either T. cruzi–infected or uninfected mothers were also evaluated as controls. The plasma levels of IL-17A, MCP-1, and monokine induced by IFN-γ were increased in infants congenitally infected with T. cruzi, even before they developed detectable parasitemia or seroconversion. Infants diagnosed between 6 and 12 mo old also showed increased levels of IL-6 and IL-17F at 1 mo of age. Conversely, infants who did not develop congenital T. cruzi infection had higher levels of IFN-γ than infected infants born to uninfected mothers. Monokine induced by IFN-γ, MCP-1, and IFN-γ production induced in T. cruzi–infected infants correlated with parasitemia, whereas the plasma levels of IL-17A, IL-17F, and IL-6 were less parasite load dependent. These findings support the existence of a distinct profile of cytokines and chemokines in the circulation of infants born to T. cruzi–infected mothers, which might predict congenital infection.

show abstract

Section: Discussionmentioning

confidence: 99%

Serum Cytokines as Biomarkers of Early Trypanosoma cruzi infection by Congenital Exposure

Volta

Bustos

Cardoni

et al. 2016

The Journal of Immunology

View full text Add to dashboard Cite

show abstract

“…Similarly, IL-22 is essential for maintaining mucosal barrier function and for the enhanced epithelial cell proliferation and cytokine production required to control K. pneumoniae infection (9). High levels of IL-17A and IL-22 also strongly correlate with protective immunity in human populations infected with Leishmania donovani (39), and IL-17A 2/2 mice fail to control Trypanosoma cruzi infection, which leads to multiple organ failure and mortality (40). However, to date no protective role for IL-22 has been shown in parasite infections.…”

Section: Discussionmentioning

confidence: 99%

IL-22 Mediates Host Defense against an Intestinal Intracellular Parasite in the Absence of IFN-γ at the Cost of Th17-Driven Immunopathology

Stange

Hepworth

Rausch

et al. 2012

The Journal of Immunology

View full text Add to dashboard Cite

The roles of Th1 and Th17 responses as mediators of host protection and pathology in the intestine are the subjects of intense research. In this study, we investigated a model of intestinal inflammation driven by the intracellular apicomplexan parasite Eimeria falciformis. Although IFN-γ was the predominant cytokine during E. falciformis infection in wild-type mice, it was found to be dispensable for host defense and the development of intestinal inflammation. E. falciformis-infected IFN-γR−/− and IFN-γ−/− mice developed dramatically exacerbated body weight loss and intestinal pathology, but they surprisingly harbored fewer parasites. This was associated with a striking increase in parasite-specific IL-17A and IL-22 production in the mesenteric lymph nodes and intestine. CD4+ T cells were found to be the source of IL-17A and IL-22, which drove the recruitment of neutrophils and increased tissue expression of anti-microbial peptides (RegIIIβ, RegIIIγ) and matrix metalloproteinase 9. Concurrent neutralization of IL-17A and IL-22 in E. falciformis-infected IFN-γR−/− mice resulted in a reduction in infection-induced body weight loss and inflammation and significantly increased parasite shedding. In contrast, neutralization of IL-22 alone was sufficient to increase parasite burden, but it had no effect on body weight loss. Treatment of an E. falciformis-infected intestinal epithelial cell line with IFN-γ, IL-17A, or IL-22 significantly reduced parasite development in vitro. Taken together, to our knowledge these data demonstrate for the first time an antiparasite effect of IL-22 during an intestinal infection, and they suggest that IL-17A and IL-22 have redundant roles in driving intestinal pathology in the absence of IFN-γ signaling.

show abstract

“…We focused our efforts on IL-17A and IL-17F (IL-17A/F), two main factors in the IL-17 protein family that are known to play an important role in antimicrobial host defenses and immunological responses to a variety of infections, including fungi, bacteria, viruses, and parasites (6,15,16,26,29). IL-17A and IL-17F appear to bind the same receptor complexes, comprising IL-17 receptor A and IL-17 receptor C (42,54), and therefore appear to have similar biological functions (16).…”

mentioning

confidence: 99%

Roles of Interleukin-17 in an Experimental Legionella pneumophila Pneumonia Model

et al. 2012

Self Cite

View full text Add to dashboard Cite

Interleukin-17 (IL-17) is a key factor in T helper type 17 (Th17) lineage host responses and plays critical roles in immunological control of a variety of infectious diseases. Although Legionella pneumophila, an intracellular bacterium found widely in the environment, often causes a serious and life-threatening pneumonia in humans, the contribution of IL-17 to immune function during Legionella pneumonia is unknown. In the present study, we used an experimental Legionella pneumonia infection to clarify the role of IL-17 in the resulting immune response. We observed robust production of pulmonary IL-17A and IL-17F (IL-17A/ F), peaking on day 1 and declining thereafter. Upregulated production of tumor necrosis factor alpha (TNF-␣), IL-6, and IL-1␤, but not monocyte chemotactic protein 1 (MCP-1), was observed in Legionella-infected bone marrow-derived macrophages from BALB/c mice that had been stimulated with IL-17A or IL-17F. A significant decrease in the production of proinflammatory cytokines IL-6 and TNF-␣ was observed in IL-17A/F-deficient mice (BALB/c background) infected with L. pneumophila. Moreover, we found impaired neutrophil migration and lower numbers of chemokines (KC, LIX, and MIP-2) in IL-17A/F-deficient mice. IL-17A/F-deficient mice also eliminated L. pneumophila more slowly and were less likely to survive a lethal challenge. These results demonstrate that IL-17A/F plays a critical role in L. pneumophila pneumonia, probably through induction of proinflammatory cytokines and accumulation of neutrophils at the infection site.

show abstract

IL-17 Is Necessary for Host Protection against Acute-Phase Trypanosoma cruzi Infection

Abstract: Material Supplementary 7.DC1http://www.jimmunol.org/content/suppl/2010/06/18/jimmunol.090004

Cited by 136 publications

References 50 publications

Serum Cytokines as Biomarkers of Early Trypanosoma cruzi infection by Congenital Exposure

Serum Cytokines as Biomarkers of Early Trypanosoma cruzi infection by Congenital Exposure

IL-22 Mediates Host Defense against an Intestinal Intracellular Parasite in the Absence of IFN-γ at the Cost of Th17-Driven Immunopathology

Roles of Interleukin-17 in an Experimental Legionella pneumophila Pneumonia Model

Contact Info

Product

Resources

About