Evidence map›Paper›PMID 38572923›Full record

ArticleJournal of medical virology2024

The use of human iPSC-derived alveolar organoids to explore SARS-CoV-2 variant infections and host responses.

Chaitanya Gandikota, Kishore Vaddadi, Pulavendran Sivasami, Chaoqun Huang, Yurong Liang, Samuel Pushparaj, Xufang Deng, Rudragouda Channappanava, Jordan P Metcalf, Lin Liu

Open access · greenAbstract read
In one paragraph

Article in Journal of medical virology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
4.7field-weighted citation impact, top 4% 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

9 citing papers in PubMed, 1 synthesis or guideline pooled it, 12 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
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

10 authors at 1 institution in 1 country.

Chaitanya GandikotaDepartment of Physiological Sciences, The Lundberg-Kienlen Lung Biology and Toxicology Laboratory, Oklahoma State University, Stillwater, Oklahoma, USA.ORCID 0000-0001-8876-4168
Kishore VaddadiDepartment of Physiological Sciences, The Lundberg-Kienlen Lung Biology and Toxicology Laboratory, Oklahoma State University, Stillwater, Oklahoma, USA.ORCID 0000-0003-0320-9064
Pulavendran SivasamiDepartment of Physiological Sciences, The Lundberg-Kienlen Lung Biology and Toxicology Laboratory, Oklahoma State University, Stillwater, Oklahoma, USA.
Chaoqun HuangDepartment of Physiological Sciences, The Lundberg-Kienlen Lung Biology and Toxicology Laboratory, Oklahoma State University, Stillwater, Oklahoma, USA.
Yurong LiangDepartment of Physiological Sciences, The Lundberg-Kienlen Lung Biology and Toxicology Laboratory, Oklahoma State University, Stillwater, Oklahoma, USA.
Samuel PushparajDepartment of Physiological Sciences, The Lundberg-Kienlen Lung Biology and Toxicology Laboratory, Oklahoma State University, Stillwater, Oklahoma, USA.
Xufang DengOklahoma Center for Respiratory and Infectious Diseases, Oklahoma State University, Stillwater, Oklahoma, USA.
Rudragouda ChannappanavaOklahoma Center for Respiratory and Infectious Diseases, Oklahoma State University, Stillwater, Oklahoma, USA.
Jordan P MetcalfOklahoma Center for Respiratory and Infectious Diseases, Oklahoma State University, Stillwater, Oklahoma, USA.
Lin LiuDepartment of Physiological Sciences, The Lundberg-Kienlen Lung Biology and Toxicology Laboratory, Oklahoma State University, Stillwater, Oklahoma, USA.ORCID 0000-0002-4811-4897
Oklahoma State University · US

Funding

ZFC3H1 Regulation of Host Defense and Influenza A Virus PathogenesisP20GM103648 · NIGMS · OKLAHOMA STATE UNIVERSITY STILLWATER · PI CHANNAPPANAVAR, RUDRAGOUDA · 2013 to 2022
$22.3M
Pilot Project Grant ProgramP30GM149368 · NIGMS · OKLAHOMA STATE UNIVERSITY STILLWATER · PI LIN LIU · 2023 to 2026
$5.5M
The Role of Iron In Pulmonary FibrosisR01HL157450 · NHLBI · OKLAHOMA STATE UNIVERSITY STILLWATER · PI LIN LIU · 2023 to 2026
$2.0M
Lnc-PINK regulation of innate immunity in lung epithelial cellsR21AI152004 · NIAID · OKLAHOMA STATE UNIVERSITY STILLWATER · PI LIU, LIN · 2021 to 2022
$411k
Reversing Cigarette Smoke-Induced Antiviral ImmunosuppressionI01BX005023 · VA · OKLAHOMA CITY VA MEDICAL CENTER · PI METCALF, JORDAN PATRICK · 2021 to 2024
–
BLRD VA I01 BX005023NHLBI NIH HHS R01 HL157450NIAID NIH HHS R21 AI152004NIGMS NIH HHS P20 GM103648NIGMS NIH HHS P30 GM149368NIH HHS AI152004NIH HHS GM103648NIH HHS GM149368NIH HHS HL157450
6 · The paper itself

Abstract

Severe acute respiratory syndrome-related coronavirus 2 (SARS-CoV-2) primarily targets the respiratory system. Physiologically relevant human lung models are indispensable to investigate virus-induced host response and disease pathogenesis. In this study, we generated human induced pluripotent stem cell (iPSC)-derived alveolar organoids (AOs) using an established protocol that recapitulates the sequential steps of in vivo lung development. AOs express alveolar epithelial type II cell protein markers including pro-surfactant protein C and ATP binding cassette subfamily A member 3. Compared to primary human alveolar type II cells, AOs expressed higher mRNA levels of SARS-CoV-2 entry factors, angiotensin-converting enzyme 2 (ACE2), asialoglycoprotein receptor 1 (ASGR1) and basigin (CD147). Considering the localization of ACE2 on the apical side in AOs, we used three AO models, apical-in, sheared and apical-out for SARS-CoV-2 infection. All three models of AOs were robustly infected with the SARS-CoV-2 irrespective of ACE2 accessibility. Antibody blocking experiment revealed that ASGR1 was the main receptor for SARS-CoV2 entry from the basolateral in apical-in AOs. AOs supported the replication of SARS-CoV-2 variants WA1, Alpha, Beta, Delta, and Zeta and Omicron to a variable degree with WA1 being the highest and Omicron being the least. Transcriptomic profiling of infected AOs revealed the induction of inflammatory and interferon-related pathways with NF-κB signaling being the predominant host response. In summary, iPSC-derived AOs can serve as excellent human lung models to investigate infection of SARS-CoV-2 variants and host responses from both apical and basolateral sides.

Indexed as

COVID-19Induced Pluripotent Stem CellsAngiotensin-Converting Enzyme 2Asialoglycoprotein ReceptorHumansLungOrganoidsRNA, ViralSARS-CoV-2Angiotensin-Converting Enzyme 2ASGR1 protein, humanAsialoglycoprotein ReceptorRNA, Viralimmune responsesinnate immunitypathogenesisSARS coronavirusvirus classification

Identifiers

PMID38572923
PMCPMC11603130
OpenAlexW4393934717

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

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.