Transcriptome analysis unveils survival strategies of Streptococcus parauberis against fish serum

Streptococcus parauberis is an important bacterial fish pathogen that causes streptococcosis in a variety of fish species including the olive flounder. Despite its importance in the aquaculture industry, little is known about the survival strategy of S. parauberis in the host. Therefore, the objective of this study was to produce genome-wide transcriptome data and identify key factors for the survival of S. parauberis SPOF3K in its host. To this end, S. parauberis SPOF3K was incubated in olive flounder serum and nutrient-enriched media as a control. Although S. parauberis SPOF3K proliferated in both culture conditions, the transcriptomic patterns of the two groups were very different. Interestingly, the expression levels of genes responsible for the replication of an S. parauberis plasmid in the presence of olive flounder serum were higher than those in the absence of olive flounder serum, indicating that this plasmid may play an important role in the survival and proliferation of S. parauberis in the host. Several ATP-binding cassette transporters known to transport organic substrates (e.g., biotin and osmoprotectants) that are vital for bacterial survival in the host were significantly up-regulated in S. parauberis cultured in serum. In addition, groEL, dnaK operon, and members of the clp protease family, which are known to play important roles in response to various stressors, were up-regulated in S. parauberis incubated in serum, thus limiting damage and facilitating cellular recovery. Moreover, important virulence factors including the hyaluronic acid capsule (has operon), sortase A (srtA), C5a peptidase (scp), and peptidoglycan O-acetyltransferase (oatA) were significantly upregulated in S. paraubers in serum. These results indicate that S. paraubers can resist and evade the humoral immune responses of fish. The transcriptomic data obtained in this study provide a better understanding of the mode of action of S. parauberis in fish.

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Faculty Opinions recommendation of Identifying the MAGUK protein Carma-1 as a central regulator of humoral immune responses and atopy by genome-wide mouse mutagenesis.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.1014045.194307 ◽

2003 ◽

Author(s):

Andy Chan

Keyword(s):

Immune Responses ◽

Humoral Immune ◽

Humoral Immune Responses ◽

Genome Wide ◽

Maguk Protein ◽

Mouse Mutagenesis

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Faculty Opinions recommendation of Identifying the MAGUK protein Carma-1 as a central regulator of humoral immune responses and atopy by genome-wide mouse mutagenesis.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.1014045.192325 ◽

2003 ◽

Author(s):

Paul Lyons

Keyword(s):

Immune Responses ◽

Humoral Immune ◽

Humoral Immune Responses ◽

Genome Wide ◽

Maguk Protein ◽

Mouse Mutagenesis

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Jun et al. Identifying the MAGUK protein Carma-1 as a central regulator of humoral immune responses and atopy by genome-wide mouse mutagenesis. Immunity 2003;18:751–62

Journal of Allergy and Clinical Immunology ◽

10.1016/j.jaci.2003.10.030 ◽

2004 ◽

Vol 113 (2) ◽

pp. 370-370

Keyword(s):

Immune Responses ◽

Humoral Immune ◽

Humoral Immune Responses ◽

Genome Wide ◽

Maguk Protein ◽

Mouse Mutagenesis

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Genetic factors and age are the strongest predictors of humoral immune responses to common pathogens and vaccines

10.1101/254706 ◽

2018 ◽

Author(s):

Petar Scepanovic ◽

Cécile Alanio ◽

Christian Hammer ◽

Flavia Hodel ◽

Jacob Bergstedt ◽

...

Keyword(s):

Immune Responses ◽

Genetic Variants ◽

Genetic Factors ◽

Humoral Response ◽

Genome Wide Association ◽

Healthy Individuals ◽

Humoral Immune ◽

Humoral Immune Responses ◽

Genome Wide ◽

Age And Sex

AbstractIntroductionHumoral immune responses to infectious agents or vaccination vary substantially among individuals, and many of the factors responsible for this variability remain to be defined. Current evidence suggests that human genetic variation influences (i) serum immunoglobulin levels, (ii) seroconversion rates, and (iii) intensity of antigen-specific immune responses. Here, we evaluate the impact of intrinsic (age and sex), environmental and genetic factors on the variability of humoral response to common pathogens and vaccines.MethodsWe characterized the serological response to 15 antigens from common human pathogens or vaccines, in an age‐ and sex-stratified cohort of 1,000 healthy individuals (Milieu Intérieur cohort). Using clinical-grade serological assays, we measured total IgA, IgE, IgG and IgM levels, as well as qualitative (serostatus) and quantitative IgG responses to cytomegalovirus, Epstein-Barr virus, herpes simplex virus 1 & 2, varicella zoster virus, Helicobacter pylori, Toxoplasma gondii, influenza A virus, measles, mumps, rubella, and hepatitis B virus. Following genome-wide genotyping of single nucleotide polymorphisms and imputation, we examined associations between ~5 million genetic variants and antibody responses using single marker and gene burden tests.Results and discussionWe identified age and sex as important determinants of humoral response, with older individuals and women having higher rates of seropositivity for most antigens. Genome-wide association studies revealed significant associations between variants in the human leucocyte antigen (HLA) class II region on chromosome 6 and anti-EBV and anti-rubella IgG levels. We used HLA imputation to fine map these associations to amino acid variants in the peptide-binding groove of HLA-DRβ1 and HLA-DPβ1, respectively. We also observed significant associations for total IgA levels with two loci on chromosome 2 and with specific KIR-HLA combinations.ConclusionsUsing extensive serological testing and genome-wide association analyses in a well-characterized cohort of healthy individuals, we demonstrate that age, sex and specific human genetic variants contribute to inter-individual variability in humoral response. By highlighting genes and pathways implicated in the normal antibody response to frequently encountered antigens, these findings provide a basis to better understand disease pathogenesis.

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