Immersion infection of germ-free zebrafish with Listeria monocytogenes induces transient expression of innate immune response genes

Mice deficient in lymphocytes are more resistant than normal mice to Listeria monocytogenes infection during the early innate immune response. This paradox remains unresolved: lymphocytes are required for sterilizing immunity, but their presence during the early stage of the infection is not an asset and may even be detrimental. We found that lymphocyte-deficient mice, which showed limited apoptosis in infected organs, were resistant during the first four days of infection but became susceptible when engrafted with lymphocytes. Engraftment with lymphocytes from type I interferon receptor–deficient (IFN-αβR−/−) mice, which had reduced apoptosis, did not confer increased susceptibility to infection, even when the phagocytes were IFN-αβR+/+. The attenuation of innate immunity was due, in part, to the production of the antiinflammatory cytokine interleukin 10 by phagocytic cells after the apoptotic phase of the infection. Thus, immunodeficient mice were more resistant relative to normal mice because the latter went through a stage of lymphocyte apoptosis that was detrimental to the innate immune response. This is an example of a bacterial pathogen creating a cascade of events that leads to a permissive infective niche early during infection.

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Expression of Innate Immune Response Genes in Liver and Three Types of Adipose Tissue in Cloned Pigs

Cellular Reprogramming ◽

10.1089/cell.2012.0026 ◽

2012 ◽

Vol 14 (5) ◽

pp. 407-417 ◽

Cited By ~ 4

Author(s):

Tina Rødgaard ◽

Kerstin Skovgaard ◽

Jan Stagsted ◽

Peter M.H. Heegaard

Keyword(s):

Immune Response ◽

Adipose Tissue ◽

Innate Immune Response ◽

Innate Immune ◽

Immune Response Genes

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Rapid evolution of innate immune response genes

Rapidly Evolving Genes and Genetic Systems ◽

10.1093/acprof:oso/9780199642274.003.0020 ◽

2012 ◽

pp. 203-210 ◽

Cited By ~ 7

Author(s):

Brian P. Lazzaro ◽

Andrew G. Clark

Keyword(s):

Immune Response ◽

Innate Immune Response ◽

Rapid Evolution ◽

Innate Immune ◽

Immune Response Genes

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Abstract A31: The two most potent PARP inhibitors increase expression levels of innate immune response genes in BRCA wild-type HGSC tumors

10.1158/1557-3265.ovca19-a31 ◽

2020 ◽

Author(s):

Monica Wielgos-Bonvallet ◽

Danhui Weng ◽

Petar Jelinic ◽

Douglas A. Levine

Keyword(s):

Immune Response ◽

Innate Immune Response ◽

Parp Inhibitors ◽

Innate Immune ◽

Wild Type ◽

Expression Levels ◽

Immune Response Genes

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Effects of Regulatory T Cell Depletion on NK Cell Responses against Listeria monocytogenes in Feline Immunodeficiency Virus Infected Cats

Viruses ◽

10.3390/v11110984 ◽

2019 ◽

Vol 11 (11) ◽

pp. 984

Author(s):

Simões ◽

LaVoy ◽

Dean

Keyword(s):

Immune Response ◽

Listeria Monocytogenes ◽

Dendritic Cell ◽

Innate Immune Response ◽

Feline Immunodeficiency Virus ◽

Innate Immune ◽

Treg Depletion ◽

Cell Responses ◽

Immunodeficiency Virus

Regulatory T cells (Treg) are key players in the maintenance of peripheral tolerance, preventing autoimmune diseases and restraining chronic inflammatory diseases. Evidence suggests Treg cells and NK cells have important roles in feline immunodeficiency virus (FIV) pathogenesis; however, in vivo studies investigating the interplay between these two cell populations are lacking. We previously described innate immune defects in FIV-infected cats characterized by cytokine deficits and impaired natural killer cell (NK) and NK T cell (NKT) functions. In this study, we investigated whether in vivo Treg depletion by treatment with an anti-feline CD25 monoclonal antibody would improve the innate immune response against subcutaneous challenge with Listeria monocytogenes (Lm). Treg depletion resulted in an increased overall number of cells in Lm-draining lymph nodes and increased proliferation of NK and NKT cells in FIV-infected cats. Treg depletion did not normalize expression of perforin or granzyme A by NK and NKT cells, nor did Treg depletion result in improved clearance of Lm. Thus, despite the quantitative improvements in the NK and NKT cell responses to Lm, there was no functional improvement in the early control of Lm. CD1a+ dendritic cell percentages in the lymph nodes of FIV-infected cats were lower than in specific-pathogen-free control cats and failed to upregulate CD80 even when Treg were depleted. Taken together, Treg depletion failed to improve the innate immune response of FIV-infected cats against Lm and this may be due to dendritic cell dysfunction.

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Survival Following Traumatic Brain Injury in Drosophila Is Increased by Heterozygosity for a Mutation of the NF-κB Innate Immune Response Transcription Factor Relish

Genetics ◽

10.1534/genetics.120.303776 ◽

2020 ◽

Vol 216 (4) ◽

pp. 1117-1136 ◽

Cited By ~ 1

Author(s):

Laura C. Swanson ◽

Edna A. Trujillo ◽

Gene H. Thiede ◽

Rebeccah J. Katzenberger ◽

Evgenia Shishkova ◽

...

Keyword(s):

Traumatic Brain Injury ◽

Immune Response ◽

Brain Injury ◽

Innate Immune Response ◽

Genetic Background ◽

Cellular Response ◽

Expression Profiles ◽

Innate Immune ◽

Immune Response Genes ◽

Secondary Injuries

Traumatic brain injury (TBI) pathologies are caused by primary and secondary injuries. Primary injuries result from physical damage to the brain, and secondary injuries arise from cellular responses to primary injuries. A characteristic cellular response is sustained activation of inflammatory pathways commonly mediated by nuclear factor-κB (NF-κB) transcription factors. Using a Drosophila melanogaster TBI model, we previously found that the main proximal transcriptional response to primary injuries is triggered by activation of Toll and Imd innate immune response pathways that engage NF-κB factors Dif and Relish (Rel), respectively. Here, we found by mass spectrometry that Rel protein level increased in fly heads at 4–8 hr after TBI. To investigate the necessity of Rel for secondary injuries, we generated a null allele, Reldel, by CRISPR/Cas9 editing. When heterozygous but not homozygous, the Reldel mutation reduced mortality at 24 hr after TBI and increased the lifespan of injured flies. Additionally, the effect of heterozygosity for Reldel on mortality was modulated by genetic background and diet. To identify genes that facilitate effects of Reldel on TBI outcomes, we compared genome-wide mRNA expression profiles of uninjured and injured +/+, +/Reldel, and Reldel/Reldel flies at 4 hr following TBI. Only a few genes changed expression more than twofold in +/Reldel flies relative to +/+ and Reldel/Reldel flies, and they were not canonical innate immune response genes. Therefore, Rel is necessary for TBI-induced secondary injuries but in complex ways involving Rel gene dose, genetic background, diet, and possibly small changes in expression of innate immune response genes.

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