A novel IL‐17‐dependent mechanism of cross protection: Respiratory infection with mycoplasma protects against a secondary listeria infection

Sieve, Amy N.; Meeks, Karen D.; Bodhankar, Sheetal; Lee, Suheung; Kolls, Jay K.; Simecka, Jerry W.; Berg, Rance E.

doi:10.1002/eji.200838726

Cited by 33 publications

(34 citation statements)

References 52 publications

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“…in 30). More recently, the involvement of Th17/IL-17 in protective immunity against intracellular bacterial infections was also reported (31)(32)(33)(34). In particular, we and others reported that IL-17 is important in host defense against chlamydial lung infection (31,34).…”

Section: Enhanced Inducible Costimulator Ligand (Icos-l) Expression Osupporting

confidence: 61%

Enhanced Inducible Costimulator Ligand (ICOS-L) Expression on Dendritic Cells in Interleukin-10 Deficiency and Its Impact on T-Cell Subsets in Respiratory Tract Infection

Gao

Zhao

Wang

et al. 2013

Mol Med

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An association between inducible costimulator ligand (ICOS-L) expression and interleukin (IL)-10 production by dendritic cells (DCs) has been commonly found in infectious disease. DCs with higher ICOS-L expression and IL-10 production are reportedly more efficient in inducing regulatory T cells (Tregs). Here we use the Chlamydia muridarum (Cm) lung infection model in IL-10 knockout (KO) mice to test the relationship between IL-10 production and ICOS-L expression by DCs. We examined ICOS-L expression, the development of T-cell subsets, including Treg, Th17 and Th1 cell, in the background of IL-10 deficiency and its relationship with ICOS-L/ICOS signaling after infection. Surprisingly, we found that the IL-10 KO mice exhibited significantly higher ICOS-L expression by DCs. Moreover, IL-10 KO mice showed lower Tregs but higher Th17 and Th1 responses, but only the Th17 response depended on ICOS signaling. Consistently, most of the Th17 cells were ICOS + , whereas most of the Th1 cells were ICOS -in the infected mice. Furthermore, neutralization of IL-17 in IL-10 KO mice significantly exacerbated lung infection.

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Section: Enhanced Inducible Costimulator Ligand (Icos-l) Expression Osupporting

confidence: 61%

Enhanced Inducible Costimulator Ligand (ICOS-L) Expression on Dendritic Cells in Interleukin-10 Deficiency and Its Impact on T-Cell Subsets in Respiratory Tract Infection

Gao

Zhao

Wang

et al. 2013

Mol Med

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“…This includes, but is not limited to, models of Mycobacterium tuberculosis (45), Salmonella (46), and Listeria monocytogenes infection in which IL-17 deficiency is associated with an enhanced inflammatory response (47) and substantial neutrophil-mediated tissue pathology (48). Contrary to the data we have presented in this study, IL-17 was proinflammatory in nature in these infections, and a deficiency in IL-17 resulted in higher pathogen burdens, stemming from uncontrolled pathogen growth.…”

Section: Discussionmentioning

confidence: 99%

IL-17A–Producing γδ T Cells Suppress Early Control of Parasite Growth by Monocytes in the Liver

Sheel

Beattie

Frame

et al. 2015

The Journal of Immunology

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Intracellular infections, such as those caused by the protozoan parasite Leishmania donovani, a causative agent of visceral leishmaniasis (VL), require a potent host proinflammatory response for control. IL-17 has emerged as an important proinflammatory cytokine required for limiting growth of both extracellular and intracellular pathogens. However, there are conflicting reports on the exact roles for IL-17 during parasitic infections and limited knowledge about cellular sources and the immune pathways it modulates. We examined the role of IL-17 in an experimental model of VL caused by infection of C57BL/6 mice with L. donovani and identified an early suppressive role for IL-17 in the liver that limited control of parasite growth. IL-17–producing γδ T cells recruited to the liver in the first week of infection were the critical source of IL-17 in this model, and CCR2+ inflammatory monocytes were an important target for the suppressive effects of IL-17. Improved parasite control was independent of NO generation, but associated with maintenance of superoxide dismutase mRNA expression in the absence of IL-17 in the liver. Thus, we have identified a novel inhibitory function for IL-17 in parasitic infection, and our results demonstrate important interactions among γδ T cells, monocytes, and infected macrophages in the liver that can determine the outcome of parasitic infection.

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“…In contrast, it is generally thought that IL-17/Th17 responses have limited role in intracellular bacterial infections mainly based on the theoretical insufficiency of neutrophils in killing intracellular bacteria. Indeed, IL-17 gene knockout (KO) 3 and IL-17R KO mice are not more susceptible to primary Mycobacterium tuberculosis and Listeria monocytogenes infections than wild-type mice (17)(18)(19). However, the involvement of IL-17 in host defense against M. tuberculosis was also reported, especially in inducing recall response following vaccination (20,21).…”

mentioning

confidence: 99%

IL-17/Th17 Promotes Type 1 T Cell Immunity against Pulmonary Intracellular Bacterial Infection through Modulating Dendritic Cell Function

Bai

Cheng

Gao

et al. 2009

The Journal of Immunology

146

164

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Although their contribution to host defense against extracellular infections has been well defined, IL-17 and Th17 are generally thought to have limited impact on intracellular infections. In this study, we investigated the role and mechanisms of IL-17/Th17 in host defense against Chlamydia muridarum, an obligate intracellular bacterium, lung infection. Our data showed rapid increase in IL-17 production and expansion of Th17 cells following C. muridarum infection and significant detrimental impact of in vivo IL-17 neutralization by anti-IL-17 mAb on disease course, immune response, and dendritic cell (DC) function. Specifically, IL-17-neutralized mice exhibited significantly greater body weight loss, higher organism growth, and much more severe pathological changes in the lung compared with sham-treated control mice. Immunological analysis showed that IL-17 neutralization significantly reduced Chlamydia-specific Th1 responses, but increased Th2 responses. Interestingly, the DC isolated from IL-17-neutralized mice showed lower CD40 and MHC II expression and IL-12 production, but higher IL-10 production compared with those from sham-treated mice. In two DC-T cell coculture systems, DC isolated from IL-17-neutralized mice induced higher IL-4, but lower IFN-γ production by Ag-specific T cells than those from sham-treated mice in cell priming and reaction settings. Adoptive transfer of DC isolated from IL-17-neutralized mice, unlike those from sham-treated mice, failed to protect the recipients against challenge infection. These findings provide in vivo evidence that IL-17/Th17 plays an important role in host defense against intracellular bacterial infection, and suggest that IL-17/Th17 can promote type 1 T cell immunity through modulating DC function.

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A novel IL‐17‐dependent mechanism of cross protection: Respiratory infection with mycoplasma protects against a secondary listeria infection

Cited by 33 publications

References 52 publications

Enhanced Inducible Costimulator Ligand (ICOS-L) Expression on Dendritic Cells in Interleukin-10 Deficiency and Its Impact on T-Cell Subsets in Respiratory Tract Infection

Enhanced Inducible Costimulator Ligand (ICOS-L) Expression on Dendritic Cells in Interleukin-10 Deficiency and Its Impact on T-Cell Subsets in Respiratory Tract Infection

IL-17A–Producing γδ T Cells Suppress Early Control of Parasite Growth by Monocytes in the Liver

IL-17/Th17 Promotes Type 1 T Cell Immunity against Pulmonary Intracellular Bacterial Infection through Modulating Dendritic Cell Function

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