Estrogens and Infection

Styrt, Barbara; Sugarman, Barrett

doi:10.1093/clinids/13.6.1139

Cited by 113 publications

(72 citation statements)

References 135 publications

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“…The mechanisms underlying gender-or, strictly, sex-based differences in susceptibility to infection and diseases remain ill defined (3,35,36); however, several recent studies suggest that differences in immune responses may involve gender. Gamma interferon (IFN-␥), an important immunoregulatory cytokine, plays a key role in the development of balanced Th1/Th2 responses that are essential for efficient control of infectious intracellular pathogens.…”

mentioning

confidence: 99%

Gender Influences Herpes Simplex Virus Type 1 Infection in Normal and Gamma Interferon-Mutant Mice

Han¹,

Lundberg²,

Tanamachi³

et al. 2001

J Virol

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Gender influences the incidence and severity of some bacterial and viral infections and autoimmune diseases in animal models and humans. To determine a gender-based difference, comparisons were made between male and female mice inoculated with herpes simplex virus type 1 (HSV-1) by the corneal route. Mortality was higher in the male mice of the three strains tested: 129/Sv//Ev wild type, gamma interferon (IFN-␥) knockout (GKO), and IFN-␥ receptor knockout (RGKO). Similarly, in vivo HSV-1 reactivation occurred more commonly in male mice, but the male-female difference in reactivation was restricted to the two knockout strains and was not seen in the 129/Sv//Ev control. Comparison among male mice of the three strains showed a higher mortality of the RGKO mice and a higher reactivation rate of the GKO and RGKO mice than of the 129/Sv//Ev males. In contrast, female RGKO and GKO mice did not differ from female 129/Sv//Ev controls in either mortality or reactivation. HSV-1 periocular and eyelid disease was also more severe in male and dihydrotestosterone (DHT)-treated female mice than in control female mice. These results show a consistent gender difference in HSV-1 infection, with a worse outcome in male mice. In addition, the results comparing GKO and RGKO mice to controls show differences only in male mice, suggesting that some effects of IFN-␥, a key immunoregulatory molecule, are gender specific.

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mentioning

confidence: 99%

Gender Influences Herpes Simplex Virus Type 1 Infection in Normal and Gamma Interferon-Mutant Mice

Han¹,

Lundberg²,

Tanamachi³

et al. 2001

J Virol

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“…[44][45][46][47][48] It has been suggested that this influence on immunity may, in part, be due to inherent physiological differences between males and females or the different levels and actions of sex hormones. 49 A sex difference in susceptibility to an infectious agent unique to the F2 population derived from phenotypically divergent inbred strains has been Figure 4 Sex-stratified marker regression scan of complete CBAB6F2 population. Logarithm of odds (LOD) score plots for separate genomewide marker regression scans on 203 female (a) and 210 male (b) CBAB6F2 progeny using R and R/qtl.…”

Section: Discussionmentioning

confidence: 99%

Sex differences in the genetic architecture of susceptibility to Cryptococcus neoformans pulmonary infection

et al. 2008

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Cryptococcus neoformans is a major cause of fungal pneumonia, meningitis and disseminated disease in the immune compromised host. Here we have used a clinically relevant model to investigate the genetic determinants of susceptibility to progressive cryptococcal pneumonia in C57BL/6J and CBA/J inbred mice. At 5 weeks after infection, the lung fungal burden was over 1000-fold higher in C57BL/6J compared to CBA/J mice. A genome-wide scan performed on 210 male and 203 female (CBA/J Â C57BL/6J) F2 progeny using lung colony-forming units as a quantitative trait revealed a sex difference in genetic architecture with three loci (designated Cnes1-Cnes3) associated with susceptibility to cryptococcal pneumonia. Single locus analysis identified significant loci on chromosomes 3 (Cnes1) and 17 (Cnes2) with logarithm of the odds (LOD) scores of 4.09 (P ¼ 0.0110) and 7.30 (Po0.0001) that explained 8.9 and 15.9% of the phenotypic variance, respectively, in female CBAB6F2 and one significant locus on chromosome 17 (Cnes3) with a LOD score of 4.04 (P ¼ 0.010) that explained 8.6% of the phenotypic variance in male CBAB6F2 mice. Genome-wide pair-wise analysis revealed significant quantitative trait locus interactions in both the female and male CBAB6F2 progeny that collectively explained 43.8 and 19.5% of phenotypic variance in each sex, respectively.

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“…It is remarkable that the sexual dimorphism was only statistically significant in two strains, indicating a combined effect of background and sex in the susceptibility of the RCS mice to influenza. Sexual dimorphism with enhanced male susceptibility has been seen in model infections with many pathogens and are hypothesized to reflect endocrine-immune interactions (58,59). For example, in the case of Listeria monocytogenes infection, increased female resistance was linked to estrogen-mediated inhibition of proinflammatory caspase-12 expression (60).…”

Section: Complex Genetic Control Of Influenza Virus Infection In Micementioning

confidence: 99%

Mapping of Clinical and Expression Quantitative Trait Loci in a Sex-Dependent Effect of Host Susceptibility to Mouse-Adapted Influenza H3N2/HK/1/68

Boivin

Pothlichet

Skamene

et al. 2012

The Journal of Immunology

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Seasonal influenza outbreaks and recurrent influenza pandemics present major challenges to public health. By studying immunological responses to influenza in different host species, it may be possible to discover common mechanisms of susceptibility in response to various influenza strains. This could lead to novel therapeutic targets with wide clinical application. Using a mouse-adapted strain of influenza (A/HK/1/68-MA20 [H3N2]), we produced a mouse model of severe influenza that reproduces the hallmark high viral load and overexpression of cytokines associated with susceptibility to severe influenza in humans. We mapped genetic determinants of the host response using a panel of 29 closely related mouse strains (AcB/BcA panel of recombinant congenic strains) created from influenza-susceptible A/J and influenza-resistant C57BL/6J (B6) mice. Combined clinical quantitative trait loci (QTL) and lung expression QTL mapping identified candidate genes for two sex-specific QTL on chromosomes 2 and 17. The former includes the previously described Hc gene, a deficit of which is associated with the susceptibility phenotype in females. The latter includes the phospholipase gene Pla2g7 and Tnfrsf21, a member of the TNFR superfamily. Confirmation of the gene underlying the chromosome 17 QTL may reveal new strategies for influenza treatment.

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Estrogens and Infection

Cited by 113 publications

References 135 publications

Gender Influences Herpes Simplex Virus Type 1 Infection in Normal and Gamma Interferon-Mutant Mice

Gender Influences Herpes Simplex Virus Type 1 Infection in Normal and Gamma Interferon-Mutant Mice

Sex differences in the genetic architecture of susceptibility to Cryptococcus neoformans pulmonary infection

Mapping of Clinical and Expression Quantitative Trait Loci in a Sex-Dependent Effect of Host Susceptibility to Mouse-Adapted Influenza H3N2/HK/1/68

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