The DOI matches its Crossref record; 31 of the 31 references it cites were found in a registry or an index.
Maternal TLR signaling is required for prenatal asthma protection by the nonpathogenic microbe Acinetobacter lwoffii F78
Open accessAbstract
The pre- and postnatal environment may represent a window of opportunity for allergy and asthma prevention, and the hygiene hypothesis implies that microbial agents may play an important role in this regard. Using the cowshed-derived bacterium Acinetobacter lwoffii F78 together with a mouse model of experimental allergic airway inflammation, this study investigated the hygiene hypothesis, maternal (prenatal) microbial exposure, and the involvement of Toll-like receptor (TLR) signaling in prenatal protection from asthma. Maternal intranasal exposure to A. lwoffii F78 protected against the development of experimental asthma in the progeny. Maternally, A. lwoffii F78 exposure resulted in a transient increase in lung and serum proinflammatory cytokine production and up-regulation of lung TLR messenger RNA. Conversely, suppression of TLRs was observed in placental tissue. To investigate further, the functional relevance of maternal TLR signaling was tested in TLR2/3/4/7/9−/− knockout mice. The asthma-preventive effect was completely abolished in heterozygous offspring from A. lwoffii F78–treated TLR2/3/4/7/9−/− homozygous mother mice. Furthermore, the mild local and systemic inflammatory response was also absent in these A. lwoffii F78–exposed mothers. These data establish a direct relationship between maternal bacterial exposures, functional maternal TLR signaling, and asthma protection in the progeny.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Analysis of Relative Gene Expression Data Using Real-Time Quantitative PCR and the 2−ΔΔCT Method
Livak, K. J., & Schmittgen, T. D. (2001) · Methods · doi:10.1006/meth.2001.1262 · Cited by 180,860
A Toll-like receptor recognizes bacterial DNA
Hemmi, H., Takeuchi, O., Kawai, T., Kaisho, T., Sato, S., Sanjo, H., Matsumoto, M., Hoshino, K., Wagner, H., Takeda, K., et al. (2000) · Nature · doi:10.1038/35047123 · Cited by 6,491 · cited 4×
“, 2002), and TLR9/ (Hemmi et al., 2000) mice were backcrossed toward”
InfluentialSelf-citationHoshino, K., Takeuchi, O., Kawai, T., Sanjo, H., Ogawa, T., Takeda, Y., Takeda, K., & Akira, S. (1999) · The Journal of Immunology · doi:10.4049/jimmunol.162.7.3749 · Cited by 3,374
Self-citationRecognition of microorganisms and activation of the immune response
Medzhitov, R. (2007) · Nature · doi:10.1038/nature06246 · Cited by 2,862
Small anti-viral compounds activate immune cells via the TLR7 MyD88–dependent signaling pathway
Hemmi, H., Kaisho, T., Takeuchi, O., Sato, S., Sanjo, H., Hoshino, K., Horiuchi, T., Tomizawa, H., Takeda, K., & Akira, S. (2002) · Nature Immunology · doi:10.1038/ni758 · Cited by 2,522
Self-citationThe roles of TLRs, RLRs and NLRs in pathogen recognition
Kawai, T., & Akira, S. (2009) · International Immunology · doi:10.1093/intimm/dxp017 · Cited by 1,670
Self-citationGenetic variants regulating ORMDL3 expression contribute to the risk of childhood asthma
Moffatt, M. F., Kabesch, M., Liang, L., Dixon, A. L., Strachan, D., Heath, S., Depner, M., von Berg, A., Bufe, A., Rietschel, E., et al. (2007) · Nature · doi:10.1038/nature06014 · Cited by 1,604
Self-citationExposure to farming in early life and development of asthma and allergy: a cross-sectional survey
Riedler, J., Braun-Fahrländer, C., Eder, W., Schreuer, M., Waser, M., Maisch, S., Carr, D., Schierl, R., Nowak, D., & von Mutius, E. (2001) · The Lancet · doi:10.1016/s0140-6736(01)06252-3 · Cited by 1,520
Family size, infection and atopy: the first decade of the 'hygiene hypothesis'
Strachan, D. (2000) · Thorax · doi:10.1136/thorax.55.suppl_1.s2 · Cited by 1,183
Treatment strategies for allergy and asthma
Holgate, S. T., & Polosa, R. (2008) · Nature Reviews Immunology · doi:10.1038/nri2262 · Cited by 691
Cited by
Host microbiota constantly control maturation and function of microglia in the CNS
Erny, D., Hrabě de Angelis, A. L., Jaitin, D., Wieghofer, P., Staszewski, O., David, E., Keren-Shaul, H., Mahlakoiv, T., Jakobshagen, K., Buch, T., et al. (2015) · Nature Neuroscience · doi:10.1038/nn.4030 · Cited by 3,569
Environmental biodiversity, human microbiota, and allergy are interrelated
Hanski, I., von Hertzen, L., Fyhrquist, N., Koskinen, K., Torppa, K., Laatikainen, T., Karisola, P., Auvinen, P., Paulin, L., Mäkelä, M. J., et al. (2012) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1205624109 · Cited by 1,063
Intestinal barrier and gut microbiota: Shaping our immune responses throughout life
Takiishi, T., Fenero, C. I. M., & Câmara, N. O. S. (2017) · Tissue Barriers · doi:10.1080/21688370.2017.1373208 · Cited by 1,009
The influence of the microbiome on respiratory health
Wypych, T. P., Wickramasinghe, L. C., & Marsland, B. J. (2019) · Nature Immunology · doi:10.1038/s41590-019-0451-9 · Cited by 611
Ganal, S. C., Sanos, S. L., Kallfass, C., Oberle, K., Johner, C., Kirschning, C., Lienenklaus, S., Weiss, S., Staeheli, P., Aichele, P., et al. (2012) · Immunity · doi:10.1016/j.immuni.2012.05.020 · Cited by 484
Self-citation
Metadata
- Authors
- Conrad, M. L., Ferstl, R., Teich, R., Brand, S., Blümer, N., Yildirim, A. Ö., Patrascan, C. C., Hanuszkiewicz, A., Akira, S., Wagner, H., Holst, O., von Mutius, E., Pfefferle, P. I., Kirschning, C. J., Garn, H., & Renz, H.
- Venue
- Journal of Experimental Medicine
- Publisher
- Rockefeller University Press
- Published
- 2009-12-07
- Volume
- 206
- Issue
- 13
- Pages
- 2869-2877
- ISSN
- 0022-1007 (ISSN-L)
- 1540-9538
- OpenAlex
- W2032096424
- Cited by
- 320
- References
- 31
- FWCI
- 16.73
- Type
- journal article
- Language
- en
- Open access
- bronze
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
How to cite
Cite CoChat for the checks on this page, and the paper for its own findings.
- This page
- CoChat. (2026). Citation check: Maternal TLR signaling is required for prenatal asthma protection by the nonpathogenic microbe Acinetobacter lwoffii F78. https://app.cochat.ai/papers/10.1084/jem.20090845
- The paper
- Conrad, M. L., Ferstl, R., Teich, R., Brand, S., Blümer, N., Yildirim, A. Ö., Patrascan, C. C., Hanuszkiewicz, A., Akira, S., Wagner, H., Holst, O., von Mutius, E., Pfefferle, P. I., Kirschning, C. J., Garn, H., & Renz, H. (2009). Maternal TLR signaling is required for prenatal asthma protection by the nonpathogenic microbe Acinetobacter lwoffii F78. Journal of Experimental Medicine. https://doi.org/10.1084/jem.20090845
Data sources
Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.