Insufficient generation of Th17 cells in <scp>IL</scp>‐23p19‐deficient <scp>BALB</scp>/c mice protects against progressive cutaneous leishmaniasis

Dietze-Schwonberg, Kirsten; Lorenz, Beate; Kostka, Susanna Lopez; Schumak, Beatrix; Gessner, André; Stebut, Esther von

doi:10.1111/exd.13455

Cited by 9 publications

(6 citation statements)

References 9 publications

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“…Our findings are thus in line with prior observations in C57BL/6 mice showing that MCprimed dendritic cells induced higher frequencies of IL-17Aeproducing Th17 cells (Dudeck et al, 2011). This has a strong effect on pathology in cutaneous leishmaniasis in BALB/c mice because IL-17 induction is highly relevant in leishmaniasis of susceptible BALB/c mice (Dietze-Schwonberg et al, 2018;Lopez Kostka et al, 2009), whereas in C57BL/6 mice, the absence of IL-17A does not affect disease outcome (Dietze-Schwonberg et al, 2019). Only artificial overexpression of IL-17A in CD4 þ T cells of C57BL/6 mice led to disease aggravation (Dietze-Schwonberg et al, 2019); thus, it appears that in Kit W-sh /Kit W-sh mice, MCassociated decreased levels of IFN-g are responsible for the worsening of the disease, whereas in the same mice on BALB/c background, IL-17Aedependent neutrophil recruitment dominates disease outcome.…”

Section: Abbreviations: MC Mast Cell; Th T Helpersupporting

confidence: 92%

Mast Cell Deficiency Protects Susceptible BALB/c Mice from Progressive Murine Cutaneous Leishmaniasis

Dietze-Schwonberg

Lorenz

Hartmann

et al. 2021

Journal of Investigative Dermatology

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Section: Abbreviations: MC Mast Cell; Th T Helpersupporting

confidence: 92%

Mast Cell Deficiency Protects Susceptible BALB/c Mice from Progressive Murine Cutaneous Leishmaniasis

Dietze-Schwonberg

Lorenz

Hartmann

et al. 2021

Journal of Investigative Dermatology

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“…Th17 cells and IL-17A are also implicated in the immunopathology of murine models of CL [66–70]. Susceptible BALB/c mice have higher IL-17A levels in L .…”

Section: Discussionmentioning

confidence: 99%

Coinfection with Leishmania major and Staphylococcus aureus enhances the pathologic responses to both microbes through a pathway involving IL-17A

et al. 2019

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Cutaneous leishmaniasis (CL) is a parasitic disease causing chronic, ulcerating skin lesions. Most humans infected with the causative Leishmania protozoa are asymptomatic. Leishmania spp. are usually introduced by sand flies into the dermis of mammalian hosts in the presence of bacteria from either the host skin, sand fly gut or both. We hypothesized that bacteria at the dermal inoculation site of Leishmania major will influence the severity of infection that ensues. A C57BL/6 mouse ear model of single or coinfection with Leishmania major , Staphylococcus aureus , or both showed that single pathogen infections caused localized lesions that peaked after 2–3 days for S . aureus and 3 weeks for L . major infection, but that coinfection produced lesions that were two-fold larger than single infection throughout 4 weeks after coinfection. Coinfection increased S . aureus burdens over 7 days, whereas L . major burdens (3, 7, 28 days) were the same in singly and coinfected ears. Inflammatory lesions throughout the first 4 weeks of coinfection had more neutrophils than did singly infected lesions, and the recruited neutrophils from early (day 1) lesions had similar phagocytic and NADPH oxidase capacities. However, most neutrophils were apoptotic, and transcription of immunomodulatory genes that promote efferocytosis was not upregulated, suggesting that the increased numbers of neutrophils may, in part, reflect defective clearance and resolution of the inflammatory response. In addition, the presence of more IL-17A-producing γδ and non-γδ T cells in early lesions (1–7 days), and L . major antigen-responsive Th17 cells after 28 days of coinfection, with a corresponding increase in IL-1β, may recruit more naïve neutrophils into the inflammatory site. Neutralization studies suggest that IL-17A contributed to an enhanced inflammatory response, whereas IL-1β has an important role in controlling bacterial replication. Taken together, these data suggest that coinfection of L . major infection with S . aureus exacerbates disease, both by promoting more inflammation and neutrophil recruitment and by increasing neutrophil apoptosis and delaying resolution of the inflammatory response. These data illustrate the profound impact that coinfecting microorganisms can exert on inflammatory lesion pathology and host adaptive immune responses.

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“…For instance, autoimmune diseases such as rheumatoid arthritis5 and inflammatory skin diseases6 caused by immunological imbalances have been frequently linked with chronic lesion inflammation. Likewise, pro-inflammatory cytokines can promote the progression of immune diseases by generating pathogenic B- and T-cells 7. Therefore, immune responses are important parts of inflammation.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA expression profile in chronic nonbacterial prostatitis revealed by next-generation small RNA sequencing

et al. 2019

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MicroRNAs (miRNAs) are considered to be involved in the pathogenic initiation and progression of chronic nonbacterial prostatitis (CNP); however, the comprehensive expression profile of dysregulated miRNAs, relevant signaling pathways, and core machineries in CNP have not been fully elucidated. In the current research, CNP rat models were established through the intraprostatic injection of carrageenan into the prostate. Then, next-generation sequencing was performed to explore the miRNA expression profile in CNP. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) bioinformatical analyses were conducted to reveal the enriched biological processes, molecular functions, and cellular components and signaling pathways. As a result, 1224, 1039, and 1029 known miRNAs were annotated in prostate tissues from the blank control (BC), normal saline injection (NS), and carrageenan injection (CAR) groups ( n = 3 for each group), respectively. Among them, 84 miRNAs (CAR vs BC) and 70 miRNAs (CAR vs NS) with significantly different expression levels were identified. Compared with previously reported miRNAs with altered expression in various inflammatory diseases, the majority of deregulated miRNAs in CNP, such as miR-146b-5p, miR-155-5p, miR-150-5p, and miR-139-5p, showed similar expression patterns. Moreover, bioinformatics analyses have enriched mitogen-activated protein kinase (MAPK), cyclic adenosine monophosphate (cAMP), endocytosis, mammalian target of rapamycin (mTOR), and forkhead box O (FoxO) signaling pathways. These pathways were all involved in immune response, which indicates the critical regulatory role of the immune system in CNP initiation and progression. Our investigation has presented a global view of the differentially expressed miRNAs and potential regulatory networks containing their target genes, which may be helpful for identifying the novel mechanisms of miRNAs in immune regulation and effective target-specific theragnosis for CNP.

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Insufficient generation of Th17 cells in IL‐23p19‐deficient BALB/c mice protects against progressive cutaneous leishmaniasis

Cited by 9 publications

References 9 publications

Mast Cell Deficiency Protects Susceptible BALB/c Mice from Progressive Murine Cutaneous Leishmaniasis

Mast Cell Deficiency Protects Susceptible BALB/c Mice from Progressive Murine Cutaneous Leishmaniasis

Coinfection with Leishmania major and Staphylococcus aureus enhances the pathologic responses to both microbes through a pathway involving IL-17A

MicroRNA expression profile in chronic nonbacterial prostatitis revealed by next-generation small RNA sequencing

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