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Data on autophagy markers and anti-candida cytokines expression in mice in response to vaginal infection of Candida albicans.

ABSTRACT: The data presented here are related to the research article entitled "Knockout of autophagy gene, ATG5 in mice vaginal cells abrogates cytokine response and pathogen clearance during vaginal infection of Candida albicans" (Shroff et al., 2018) [1]. The cited research article describes the role of autophagy in host immune response against C. albicans infection of mice vagina. In this data report wild-type C57BL/6 mice were infected intravaginally with C. albicans. Vaginal cells were analyzed for the expression of autophagy marker genes LC3 & ATG5 and lysosome marker LAMP1 at the transcript and protein level. Vaginal lavages were also obtained from these infected mice. The levels of pro-inflammatory and T-helper cell related cytokines were determined in these lavages.

SUBMITTER: Shroff A

PROVIDER: S-EPMC5996161 | biostudies-literature | 2018 Jun

REPOSITORIES: biostudies-literature

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Data on autophagy markers and anti-candida cytokines expression in mice in response to vaginal infection of Candida albicans.

Shroff Ankit A Sequeira Roicy R Patel Vainav V Reddy K V R KVR

Data in brief 20180309

The data presented here are related to the research article entitled "Knockout of autophagy gene, ATG5 in mice vaginal cells abrogates cytokine response and pathogen clearance during vaginal infection of Candida albicans" (Shroff et al., 2018) [1]. The cited research article describes the role of autophagy in host immune response against C. albicans infection of mice vagina. In this data report wild-type C57BL/6 mice were infected intravaginally with C. albicans. Vaginal cel ...[more]

PMID: 29896527

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Project description:Candida albicans is an opportunistic pathogen that causes acute disseminated infections in immunocompromised hosts, representing an important cause of morbidity and mortality in these patients. To study the genetic control of susceptibility to disseminated C. albicans in mice, we phenotyped a group of 23 phylogenetically distant inbred strains for susceptibility to infection as measured by extent of fungal replication in the kidney 48 hours following infection. Susceptibility was strongly associated with the loss-of-function mutant complement component 5 (C5/Hc) allele, which is known to be inherited by approximately 40% of inbred strains. Our survey identified 2 discordant strains, AKR/J (C5-deficient, resistant) and SM/J (C5-sufficient, susceptible), suggesting that additional genetic effects may control response to systemic candidiasis in these strains. Haplotype association mapping in the 23 strains using high density SNP maps revealed several putative loci regulating the extent of C. albicans replication, amongst which the most significant were C5 (P value?=?2.43×10(-11)) and a novel effect on distal chromosome 11 (P value?=?7.63×10(-9)). Compared to other C5-deficient strains, infected AKR/J strain displays a reduced fungal burden in the brain, heart and kidney, and increased survival, concomitant with uniquely high levels of serum IFN?. C5-independent genetic effects were further investigated by linkage analysis in an [A/JxAKR/J]F2 cross (n?=?158) where the mutant Hc allele is fixed. These studies identified a chromosome 11 locus (Carg4, Candida albicans resistance gene 4; LOD?=?4.59), and a chromosome 8 locus (Carg3; LOD?=?3.95), both initially detected by haplotype association mapping. Alleles at both loci were inherited in a co-dominant manner. Our results verify the important effect of C5-deficiency in inbred mouse strains, and further identify two novel loci, Carg3 and Carg4, which regulate resistance to C. albicans infection in a C5-independent manner.

Dataset Information

Data on autophagy markers and anti-candida cytokines expression in mice in response to vaginal infection of Candida albicans.

Publications

Data on autophagy markers and anti-candida cytokines expression in mice in response to vaginal infection of <i>Candida albicans</i>.

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