scholarly journals Renal CD169++ resident macrophages are crucial for protection against acute systemic candidiasis

2021 ◽  
Vol 4 (5) ◽  
pp. e202000890
Author(s):  
Yi Juan Teo ◽  
See Liang Ng ◽  
Keng Wai Mak ◽  
Yolanda Aphrilia Setiagani ◽  
Qi Chen ◽  
...  
Keyword(s):  
Immune Response ◽  
Mortality Rate ◽  
Fungal Infection ◽  
Innate Immune Response ◽  
Host Resistance ◽  
Protective Role ◽  
Innate Immune ◽  
Systemic Candidiasis ◽  
Ifn Γ ◽  
Hospital Acquired

Disseminated candidiasis remains as the most common hospital-acquired bloodstream fungal infection with up to 40% mortality rate despite the advancement of medical and hygienic practices. While it is well established that this infection heavily relies on the innate immune response for host survival, much less is known for the protective role elicited by the tissue-resident macrophage (TRM) subsets in the kidney, the prime organ for Candida persistence. Here, we describe a unique CD169++ TRM subset that controls Candida growth and inflammation during acute systemic candidiasis. Their absence causes severe fungal-mediated renal pathology. CD169++ TRMs, without being actively involved in direct fungal clearance, increase host resistance by promoting IFN-γ release and neutrophil ROS activity.

scholarly journals CpG Oligodeoxynucleotides Increase the Susceptibility of Normal Mice to Infection by Candida albicans

2005 ◽  
Vol 73 (9) ◽  
pp. 6154-6156 ◽  
Author(s):  
Shuichi Ito ◽  
Joao Pedras-Vasconcelos ◽  
Dennis M. Klinman
Keyword(s):  
Immune Response ◽  
Candida Albicans ◽  
Innate Immune Response ◽  
Host Resistance ◽  
Cytokine Production ◽  
Innate Immune ◽  
Interleukin 12 ◽  
Cpg Oligodeoxynucleotides ◽  
Cpg Motifs ◽  
Resistance To Infection

ABSTRACT Synthetic oligodeoxynucleotides containing CpG motifs trigger an innate immune response that typically increases host resistance to infection. Yet CpG treatment reduces the resistance of normal mice to Candida albicans infection. This effect is mediated by CpG-induced interleukin-12, indicating that CpG-dependent cytokine production may have adverse consequences for the host.

scholarly journals The Exopolysaccharide of Lactobacillus fermentum UCO-979C Is Partially Involved in Its Immunomodulatory Effect and Its Ability to Improve the Resistance against Helicobacter pylori Infection

2020 ◽  
Vol 8 (4) ◽  
pp. 479
Author(s):  
Valeria Garcia-Castillo ◽  
Guillermo Marcial ◽  
Leonardo Albarracín ◽  
Mikado Tomokiyo ◽  
Patricia Clua ◽  
...  
Keyword(s):  
Immune Response ◽  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Innate Immune Response ◽  
Innate Immune ◽  
Helicobacter Pylori Infection ◽  
Beneficial Effects ◽  
Ifn Γ ◽  
H Pylori

Lactobacillus fermentum UCO-979C (Lf979C) beneficially modulates the cytokine response of gastric epithelial cells and macrophages after Helicobacter pylori infection in vitro. Nevertheless, no in vivo studies were performed with this strain to confirm its beneficial immunomodulatory effects. This work evaluated whether Lf979C improves protection against H. pylori infection in mice by modulating the innate immune response. In addition, we evaluated whether its exopolysaccharide (EPS) was involved in its beneficial effects. Lf979C significantly reduced TNF-α, IL-8, and MCP-1 and augmented IFN-γ and IL-10 in the gastric mucosa of H. pylori-infected mice. The differential cytokine profile induced by Lf979C in H. pylori-infected mice correlated with an improved reduction in the pathogen gastric colonization and protection against inflammatory damage. The purified EPS of Lf979C reduced IL-8 and enhanced IL-10 levels in the gastric mucosa of infected mice, while no effect was observed for IFN-γ. This work demonstrates for the first time the in vivo ability of Lf979C to increase resistance against H. pylori infection by modulating the gastric innate immune response. In addition, we advanced knowledge of the mechanisms involved in the beneficial effects of Lf979C by demonstrating that its EPS is partially responsible for its immunomodulatory effect.

scholarly journals Innate Immune Responses of Bat and Human Cells to Filoviruses: Commonalities and Distinctions

2017 ◽  
Vol 91 (8) ◽  
Author(s):  
Ivan V. Kuzmin ◽  
Toni M. Schwarz ◽  
Philipp A. Ilinykh ◽  
Ingo Jordan ◽  
Thomas G. Ksiazek ◽  
...  
Keyword(s):  
Immune Response ◽  
Immune Responses ◽  
Innate Immune Response ◽  
Antiviral Effect ◽  
Human Cells ◽  
Innate Immune ◽  
Innate Immune Responses ◽  
Symptomatic Disease ◽  
Ifn Γ

ABSTRACT Marburg (MARV) and Ebola (EBOV) viruses are zoonotic pathogens that cause severe hemorrhagic fever in humans. The natural reservoir of MARV is the Egyptian rousette bat (Rousettus aegyptiacus); that of EBOV is unknown but believed to be another bat species. The Egyptian rousette develops subclinical productive infection with MARV but is refractory to EBOV. Interaction of filoviruses with hosts is greatly affected by the viral interferon (IFN)-inhibiting domains (IID). Our study was aimed at characterization of innate immune responses to filoviruses and the role of filovirus IID in bat and human cells. The study demonstrated that EBOV and MARV replicate to similar levels in all tested cell lines, indicating that permissiveness for EBOV at cell and organism levels do not necessarily correlate. Filoviruses, particularly MARV, induced a potent innate immune response in rousette cells, which was generally stronger than that in human cells. Both EBOV VP35 and VP24 IID were found to suppress the innate immune response in rousette cells, but only VP35 IID appeared to promote virus replication. Along with IFN-α and IFN-β, IFN-γ was demonstrated to control filovirus infection in bat cells but not in human cells, suggesting host species specificity of the antiviral effect. The antiviral effects of bat IFNs appeared not to correlate with induction of IFN-stimulated genes 54 and 56, which were detected in human cells ectopically expressing bat IFN-α and IFN-β. As bat IFN-γ induced the type I IFN pathway, its antiviral effect is likely to be partially induced via cross talk. IMPORTANCE Bats serve as reservoirs for multiple emerging viruses, including filoviruses, henipaviruses, lyssaviruses, and zoonotic coronaviruses. Although there is no evidence for symptomatic disease caused by either Marburg or Ebola viruses in bats, spillover of these viruses into human populations causes deadly outbreaks. The reason for the lack of symptomatic disease in bats infected with filoviruses remains unknown. The outcome of a virus-host interaction depends on the ability of the host immune system to suppress viral replication and the ability of a virus to counteract the host defenses. Our study is a comparative analysis of the host innate immune response to either MARV or EBOV infection in bat and human cells and the role of viral interferon-inhibiting domains in the host innate immune responses. The data are useful for understanding the interactions of filoviruses with natural and accidental hosts and for identification of factors that influence filovirus evolution.

scholarly journals Multi-walled carbon nanotubes enhanced fungal colonization and suppressed innate immune response to fungal infection in nematodes

2016 ◽  
Vol 5 (2) ◽  
pp. 492-499 ◽  
Author(s):  
Shumaila Shakoor ◽  
Lingmei Sun ◽  
Dayong Wang
Keyword(s):  
Carbon Nanotubes ◽  
Immune Response ◽  
Fungal Infection ◽  
Signaling Pathway ◽  
Innate Immune Response ◽  
Mapk Signaling ◽  
Innate Immune ◽  
Fungal Colonization ◽  
Multi Walled Carbon Nanotubes ◽  
Walled Carbon Nanotubes

MWCNTs require the involvement of p38 MAPK signaling pathway to enhance toxicity of fungal infection.

scholarly journals Induction of an Embryonic Mouse Innate Immune Response following Inoculation In Utero with Minute Virus of Mice

2014 ◽  
Vol 89 (4) ◽  
pp. 2182-2191 ◽  
Author(s):  
Irina Rostovsky ◽  
Claytus Davis
Keyword(s):  
Immune Response ◽  
Innate Immune Response ◽  
In Utero ◽  
Innate Immune ◽  
Productive Infection ◽  
Interferon Response ◽  
Minute Virus Of Mice ◽  
Embryonic Mouse ◽  
Minute Virus ◽  
Ifn Γ

ABSTRACTWe used an embryonic-infection model system to show that MVMp, the prototypic minute virus of mice (MVM) serotype and a member of the genusProtoparvovirus, triggers a comprehensive innate immune response in the developing mouse embryo. Direct inoculation of the midtrimester embryoin uterowith MVMp results in a widespread, productive infection. During a 96-h infection course, embryonic beta interferon (IFN-β) and IFN-γ transcription were induced 90- and 60-fold, respectively. IFN-β levels correlated with the embryo viral burden, while IFN-γ levels first increased and then decreased. Production of proinflammatory cytokines, interleukin 1β (IL-1β) and tumor necrosis factor alpha (TNF-α), also increased, but by smaller amounts, approximately 7-fold each. We observed increased levels of downstream antiviral effector molecules, PKR and phosphorylated STAT2. Finally, we showed that there is an immune cell response to the virus infection. Infected tissues in the embryo exhibited an increased density of mature leukocytes compared to the same tissues in uninfected embryos. The responses we observed were almost completely restricted to the infected embryos. Uninfected littermates routinely exhibited small increases in innate immune components that rarely reached statistical significance compared to negative controls. Similarly, the placentae of infected embryos did not show any significant increase in transcription of innate immune cytokines. Since the placenta has both embryonic and maternal components, we suggest there is minimal involvement of the dam in the response to infection.IMPORTANCEInteraction between the small single-stranded vertebrate DNA viruses, the protoparvoviruses, and the host innate immune system has been unclear. The issue is important practically given the potential use of these viruses as oncotherapeutic agents. The data reported here stand in contrast to studies of innate immune response during protoparvovirus infection of adult hosts, which invariably reported no or minimal and sporadic induction of an interferon response during infection. We conclude that under conditions of robust and productive MVM infection, a normal murine host is able to mount a significant and broad innate immune response.

scholarly journals Memory CD8+ T Cells Provide Innate Immune Protection against Listeria monocytogenes in the Absence of Cognate Antigen

2003 ◽  
Vol 198 (10) ◽  
pp. 1583-1593 ◽  
Author(s):  
Rance E. Berg ◽  
Emily Crossley ◽  
Sean Murray ◽  
James Forman
Keyword(s):  
Immune Response ◽  
T Cells ◽  
Listeria Monocytogenes ◽  
Innate Immune Response ◽  
Cd8 T Cells ◽  
Primary Source ◽  
Innate Immune ◽  
Memory Cd8 T Cells ◽  
Cognate Antigen ◽  
Ifn Γ

Interferon (IFN)-γ plays an important role in the innate immune response against intracellular bacterial pathogens. It is commonly thought that natural killer cells are the primary source of this cytokine that is involved in activating antibacterial effects in infected cells and polarizing CD4+ T cells toward the Th1 subset. However, here we show that both effector and memory CD8+ T cells have the potential to secrete IFN-γ in response to interleukin (IL)-12 and IL-18 in the absence of cognate antigen. We demonstrate that memory CD8+ T cells specific for the ovalbumin protein secrete IFN-γ rapidly after infection with wild-type Listeria monocytogenes (LM). Furthermore, small numbers of ovalbumin-specific, memory CD8+ T cells can reduce spleen and liver bacterial counts in IFN-γ–deficient mice 3 d after LM infection. Up-regulation of the receptors for IL-12 and IL-18 provides a mechanism for the ability of memory CD8+ T cells to respond in this antigen nonspecific manner. Thus, CD8+ T cells play an important role in the innate immune response against intracellular pathogens by rapidly secreting IFN-γ in response to IL-12 and IL-18.

scholarly journals Mycobacterium tuberculosis Strains Lacking Surface Lipid Phthiocerol Dimycocerosate Are Susceptible to Killing by an Early Innate Host Response

2014 ◽  
Vol 82 (12) ◽  
pp. 5214-5222 ◽  
Author(s):  
Tracey A. Day ◽  
John E. Mittler ◽  
Molly R. Nixon ◽  
Cullen Thompson ◽  
Maurine D. Miner ◽  
...  
Keyword(s):  
Immune Response ◽  
Mycobacterium Tuberculosis ◽  
Innate Immune Response ◽  
Host Response ◽  
Innate Immune ◽  
Dependent Manner ◽  
Surface Lipid ◽  
Content Type ◽  
Ifn Γ ◽  
Phthiocerol Dimycocerosate

ABSTRACTThe innate immune response plays an important but unknown role in host defense againstMycobacterium tuberculosis. To define the function of innate immunity during tuberculosis, we evaluatedM. tuberculosisreplication dynamics during murine infection. Our data show that the early pulmonary innate immune response limitsM. tuberculosisreplication in a MyD88-dependent manner. Strikingly, we found that littleM. tuberculosiscell death occurs during the first 2 weeks of infection. In contrast,M. tuberculosiscells deficient in the surface lipid phthiocerol dimycocerosate (PDIM) exhibited significant death rates, and consequently, total bacterial numbers were reduced. Host restriction of PDIM-deficientM. tuberculosiswas not alleviated by the absence of interferon gamma (IFN-γ), inducible nitric oxide synthase (iNOS), or the phagocyte oxidase subunit p47. Taken together, these data indicate that PDIM protectsM. tuberculosisfrom an early innate host response that is independent of IFN-γ, reactive nitrogen intermediates, and reactive oxygen species. By employing a pathogen replication tracking tool to evaluateM. tuberculosisreplication and death during infection, we identify both host and pathogen factors affecting the outcome of infection.

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