Interleukin‐10 plays a key role in the modulation of neutrophils recruitment and lung inflammation during infection by <i>Streptococcus pneumoniae</i>

Peñaloza, Hernán F.; Nieto, Pamela A.; Muñoz‐Durango, Natalia; Salazar-Echegarai, Francisco J.; Torres, Javiera; Parga, María José; Álvarez-Lobos, Manuel; Riedel, Claudia A.; Kalergis, Alexis M.; Bueno, Susan M.

doi:10.1111/imm.12486

Cited by 90 publications

(87 citation statements)

References 50 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…[20][21][22] IL-10 could prevent pulmonary inflammation from aggravation induced by S pneumoniae, the lack of which may cause the rising mortality. 23 IL-8 is also called chemokine 8, which is secreted by monocytes/macrophages and dendritic cells.…”

Section: Discussionmentioning

confidence: 99%

Impact of different Streptococcus pneumoniae on the secretion of interleukin and adhesin from THP‐1 monocytes

Ren

Zhang

et al. 2019

Clinical Laboratory Analysis

View full text Add to dashboard Cite

BackgroundTo investigate the secretion of interleukin‐1β (IL‐1β), IL‐6, IL‐10, IL‐8, and soluble intercellular adhesin molecule 1 (sICAM‐1) from THP‐1 monocytes stimulated by different Streptococcus pneumoniae (S pneumoniae) strains.MethodsFifty‐eight strains of S pneumoniae were collected: ATCC49619, 23 from sputum (sd‐SP), 23 from blood (bd‐SP), and 11 from cerebrospinal fluid (CSF; cd‐SP). Such strains were cultured and suspended at 0.5 McFarland. THP‐1 monocytes were cultured and resuspended at 5.0 × 108/L, which were stimulated by S pneumoniae for 4, 8, and 12 hours, respectively. The suspensions were analyzed for IL‐1β, IL‐6, IL‐10, IL‐8, and sICAM‐1 using an ELISA method. The data were assayed with SPSS 19.0.ResultsContrary to IL‐10, the concentrations of IL‐1β, IL‐6, IL‐8, and sICAM‐1 all increased first and then decreased. IL‐1β and sICAM‐1 levels in the ATCC49619 group were both higher than all the clinical S pneumoniae groups (sd‐SP, bd‐SP, and cd‐SP), IL‐6 and IL‐8 versa, and IL‐10 equal. The difference among clinical S pneumoniae groups lay only in sICAM‐1. cd‐SP group showed lower sICAM‐1 concentrations than sd‐SP and bd‐SP groups at both 4 and 8 hours. However, they became equal at 12 hours.ConclusionsThe secretion summit is 8 hours for IL‐1β, IL‐6, IL‐8, and sICAM‐1, bottom for IL‐10. Different clinical S pneumoniae strains show similar ability to induce THP‐1 cells secreting interleukins. However, cd‐SP induces THP‐1 cells secreting lower sICAM‐1 than sd‐SP and bd‐SP, which may in turn facilitate its invasion into CSF.

show abstract

Section: Discussionmentioning

confidence: 99%

Impact of different Streptococcus pneumoniae on the secretion of interleukin and adhesin from THP‐1 monocytes

Ren

Zhang

et al. 2019

Clinical Laboratory Analysis

View full text Add to dashboard Cite

show abstract

“…The increased secretion of IL-4, IL-5 and IL-10 suggests that rFBA immunization elicits a Th2-type immune response, which may be important for protection. Recently, IL-10 has been shown to be important to avoid excessive tissue inflammation and to improve host survival, despite the fact that bacterial dissemination is less efficient in the presence of this cytokine (55).…”

Section: Discussionmentioning

confidence: 99%

Streptococcus pneumoniae fructose-1, 6-bisphosphate aldolase, a protein vaccine candidate, elicits Th1/Th2/Th17-type cytokine responses in mice

Goldman

Dotan²,

Talias

et al. 2016

International Journal of Molecular Medicine

View full text Add to dashboard Cite

Streptococcus pneumoniae (S. pneumoniae) is a major pathogen worldwide. The currently available polysaccharide-based vaccines significantly reduce morbidity and mortality. However, the inherent disadvantages of the currently available polysaccharide-based vaccines have motivated the search for other bacterial immunogens capable of eliciting a protective immune response against S. pneumoniae. Fructose-1,6-bisphosphate aldolase (FBA) is a glycolytic enzyme, which was found to localize to the bacterial surface, where it functions as an adhesin. Previously, immunizing mice with recombinant FBA (rFBA) in the presence of alum elicited a protective immune response against a lethal challenge with S. pneumoniae. Thus, the aim of the present study was to determine the cytokine responses that are indicative of protective immunity following immunization with rFBA. The protective effects against pneumococcal challenge in mice immunized with rFBA with complete Freund's adjuvant (CFA) in the initial immunization and with incomplete Freund's adjuvant (IFA) in booster immunizations surpassed the protective effects observed following immunization with either rFBA + alum or pVACfba. CD4+ T-cells obtained from the rFBA/CFA/IFA/IFA-immunized mice co-cultured with rFBA-pulsed antigen-presenting cells (APCs), exhibited a significantly greater proliferative ability than CD4+ T-cells obtained from the adjuvant-immunized mice co-cultured with rFBA‑pulsed APCs. The levels of the Th1-type cytokines, interferon (IFN)-γ, interleukin (IL)-2, tumor necrosis factor (TNF)-α and IL-12, the Th2-type cytokines, IL-4, IL-5 and IL-10, and the Th17-type cytokine, IL-17A, significantly increased within 72 h of the initiation of co-culture with CD4+ T-cells obtained from the rFBA‑immunized mice, in comparison with the co-cultures with CD4+ T-cells obtained from the adjuvant-immunized mice. Immunizing mice with rFBA resulted in an IgG1/IgG2 ratio of 41, indicating a Th2 response with substantial Th1 involvement. In addition, rabbit and mouse anti-rFBA antisera significantly protected the mice against a lethal S. pneumoniae challenge in comparison with preimmune sera. Our results emphasize the mixed involvement of the Th1, Th2 and Th17 arms of the immune system in response to immunization with pneumococcal rFBA, a potential vaccine candidate.

show abstract

“…and macrophage recruitment into the lungs (27)(28)(29). In particular, increased Il10 expression suggests greater suppression of the inflammatory response to the 4496⌬PPI1 mutant, which may be a reflection of the fact the mutant is more readily cleared from the lungs than the wild type.…”

Section: Discussionmentioning

confidence: 99%

The Variable Region of Pneumococcal Pathogenicity Island 1 Is Responsible for Unusually High Virulence of a Serotype 1 Isolate

et al. 2016

View full text Add to dashboard Cite

Streptococcus pneumoniae is the leading infectious cause of death in children in the world. However, the mechanisms that drive the progression from asymptomatic colonization to disease are poorly understood. Two virulence-associated genomic accessory regions (ARs) were deleted in a highly virulent serotype 1 clinical isolate (strain 4496) and examined for their contribution to pathogenesis. Deletion of a prophage encoding a platelet-binding protein (PblB) resulted in reduced adherence, biofilm formation, reduced initial infection within the lungs, and a reduction in the number of circulating platelets in infected mice. However, the region's overall contribution to the survival of mice was not significant. In contrast, deletion of the variable region of pneumococcal pathogenicity island 1 (vPPI1) was also responsible for a reduction in adherence and biofilm formation but also reduced survival and invasion of the pleural cavity, blood, and lungs. While the 4496⌬PPI1 strain induced higher expression of the genes encoding interleukin-10 (IL-10) and CD11b in the lungs of challenged mice than the wild-type strain, very few other genes exhibited altered expression. Moreover, while the level of IL-10 protein was increased in the lungs of 4496⌬PPI1 mutant-infected mice compared to strain 4496-infected mice, the levels of gamma interferon (IFN-␥), CXCL10, CCL2, and CCL4 were not different in the two groups. However, the 4496⌬PPI1 mutant was found to be more susceptible than the wild type to phagocytic killing by a macrophage-like cell line. Therefore, our data suggest that vPPI1 may be a major contributing factor to the heightened virulence of certain serotype 1 strains, possibly by influencing resistance to phagocytic killing. Streptococcus pneumoniae (the pneumococcus) is a significant cause of human morbidity and mortality and is a leading cause of pneumonia, bacteremia, meningitis, and otitis media (1). However, the mechanism by which the pathogen progresses from asymptomatic colonization to disease is poorly understood. Moreover, significant variations in virulence exist even between strains of the same serotype (2-5). For example, outbreaks of unusually severe invasive pneumococcal disease (IPD) caused by serotype 1 strains belonging to clonal lineage group B have been reported in parts of Africa (6, 7), while clustered cases of carriage without disease caused by serotype 1 strains belonging to clonal lineage A, which include the common clonal complex (CC) CC227, have been reported within Australia (8). Furthermore, disease caused by invasive lineage A strains has been reported to be of relatively low severity (9). These naturally occurring differences in virulence provide opportunities to investigate the molecular processes that drive progression to disease by comparing closely related invasive and noninvasive strains. In previous work, the pathogenesis of noninvasive and invasive serotype 1 clinical isolates was characterized in mice (10,11 CC615]), belonging to serotype 1 lineages B and C, respectively, were foun...

show abstract

Interleukin‐10 plays a key role in the modulation of neutrophils recruitment and lung inflammation during infection by Streptococcus pneumoniae

Cited by 90 publications

References 50 publications

Impact of different Streptococcus pneumoniae on the secretion of interleukin and adhesin from THP‐1 monocytes

Impact of different Streptococcus pneumoniae on the secretion of interleukin and adhesin from THP‐1 monocytes

Streptococcus pneumoniae fructose-1, 6-bisphosphate aldolase, a protein vaccine candidate, elicits Th1/Th2/Th17-type cytokine responses in mice

The Variable Region of Pneumococcal Pathogenicity Island 1 Is Responsible for Unusually High Virulence of a Serotype 1 Isolate

Contact Info

Product

Resources

About