Evidence map›Paper›PMID 30134802›Full record

ArticleMolecular medicine (Cambridge, Mass.)2018

Microarray analysis of human keratinocytes from different anatomic sites reveals site-specific immune signaling and responses to human papillomavirus type 16 transfection.

Mohd Israr, David Rosenthal, Lidia Frejo-Navarro, James DeVoti, Craig Meyers, Vincent R Bonagura

Open access · goldAbstract readComparative Study
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.1field-weighted citation impact, top 22% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

12 citing papers in PubMed, 19 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 2 countries.

Mohd IsrarThe Feinstein Institute for Medical Research, Manhasset, NY, USA; Division of Allergy and Immunology, Department of Pediatrics, Donald and Barbara Zucker School of Medicine at Hofstra/Northwell, Great Neck, NY, USA.
David RosenthalThe Feinstein Institute for Medical Research, Manhasset, NY, USA; Division of Allergy and Immunology, Department of Pediatrics, Donald and Barbara Zucker School of Medicine at Hofstra/Northwell, Great Neck, NY, USA.
Lidia Frejo-NavarroDepartment of Genomic Medicine, Otology and Neurotology Group CTS495, Centre for Genomics and Oncological Research, Pfizer/Universidad de Granada/Junta de Andalucía (GENYO), Granada, Spain.
James DeVotiThe Feinstein Institute for Medical Research, Manhasset, NY, USA; Division of Allergy and Immunology, Department of Pediatrics, Donald and Barbara Zucker School of Medicine at Hofstra/Northwell, Great Neck, NY, USA.
Craig MeyersDepartment of Microbiology and Immunology, The Pennsylvania State University College of Medicine, Hershey, PA, USA.
Vincent R BonaguraThe Feinstein Institute for Medical Research, Manhasset, NY, USA; Division of Allergy and Immunology, Department of Pediatrics, Donald and Barbara Zucker School of Medicine at Hofstra/Northwell, Great Neck, NY, USA. VBonagura@northwell.edu.ORCID 0000-0002-0681-2099
Feinstein Institute for Medical Research · USPennsylvania State University · USPfizer-University of Granada-Junta de Andalucía Centre for Genomics and Oncological Research · ES

Funding

HPV-Specific, Immune Suppression in Patients with RRPR01DE017227 · NIDCR · FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH · PI BONAGURA, VINCENT ROBERT · 2006 to 2017
$4.5M
ART On Oral Tissue Growth, Function, and HPV InfectionsR01DE018305 · NIDCR · PENNSYLVANIA STATE UNIV HERSHEY MED CTR · PI MEYERS, CRAIG M · 2007 to 2011
$2.1M
Reprogramming Host Immune Responses to Cure or Control Persistent HPV InfectionR21AI105987 · NIAID · FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH · PI BONAGURA, VINCENT ROBERT · 2013 to 2014
$589k
NIAID NIH HHS R21 AI105987NIDCR NIH HHS R01 DE017227NIDCR NIH HHS R01 DE018305
6 · The paper itself

Abstract

backgroundStratified human keratinocytes (SHKs) are an essential part of mucosal innate immune response that modulates adaptive immunity to microbes encountered in the environment. The importance of these SHKs in mucosal integrity and development has been well characterized, however their regulatory immunologic role at different mucosal sites, has not. In this study we compared the immune gene expression of SHKs from five different anatomical sites before and after HPV16 transfection using microarray analyses.

methodsIndividual pools of human keratinocytes from foreskin, cervix, vagina, gingiva, and tonsils (HFKs, HCKs, HVKs, HGKs and HTLKs) were prepared. Organotypic (raft) cultures were established for both normal and HPV16 immortalized HFKs, HCKs, HVKs, HGKs and HTLKs lines which stably maintained episomal HPV16 DNA. Microarray analysis was carried out using the HumanHT-12 V4 gene chip (Illumina). Immune gene expression profiles were obtained by global gene chip (GeneSifter) and Ingenuity pathway analysis (IPA) for each individual site, with or without HPV16 transfection.

resultsWe examined site specific innate immune response gene expression in SHKs from all five different anatomical sites before and after HPV16 transfection. We observed marked differences in SHK immune gene repertoires within and between mucosal tracts before HPV 16 infection. In addition, we observed additional changes in SHKs immune gene repertoire patterns when these SHKs were productively transfected with HPV16. Some immune response genes were similarly expressed by SHKs from different sites. However, there was also variable expression of non-immune response genes, such as keratin genes, by the different SHKs.

conclusionsOur results suggest that keratinocytes from different anatomical sites are likely hard wired in their innate immune responses, and that these immune responses are unique depending on the anatomical site from which the SHKs were derived. These observations may help explain why select HPV types predominate at different mucosal sites, cause persistent infection at these sites, and on occasion, lead to HPV induced malignant and benign tumor development.

Indexed as

Cervix UteriFemaleForeskinGingivaHuman papillomavirus 16HumansImmunity, InnateKeratinocytesMaleMicroarray AnalysisPalatine TonsilPapillomavirus InfectionsSignal TransductionTranscriptomeTransfectionVaginaHPVImmune pathwaysImmune responsesKeratinocytesMicroarrays

Identifiers

PMID30134802
PMCPMC6016891
OpenAlexW2805275614

What OpenQuestion holds

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LicenceCC BY
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.