Academic Journal
Quartile not availableJournal of Endotoxin Research
About Journal of Endotoxin Research
Journal of Endotoxin Research — Journal Profile
The Journal of Endotoxin Research was a peer-reviewed biomedical journal devoted to endotoxin — the lipopolysaccharide (LPS) component of the outer membrane of Gram-negative bacteria — and to the host responses it triggers. Published in the United Kingdom by Maney Publishing (W. S. Maney & Son, Leeds) as the official journal of the International Endotoxin Society, it ran from volume 1, issue 1 in March 1994 to volume 13, issue 6 in December 2007, appearing six times a year. In 2008 it was continued under the broader title Innate Immunity, published by SAGE Publications on behalf of the International Endotoxin and Innate Immunity Society. The journal therefore no longer accepts submissions under its original title, but its thirteen volumes remain a core archive for sepsis, inflammation and innate-immunity research, and they continue to be cited as J. Endotoxin Res.
Understanding this journal requires understanding its moment. When it launched in 1994, endotoxin research was a distinct, fast-moving field: LPS structure and biosynthesis, the CD14 and Toll-like receptor 4 signalling pathway, endotoxin tolerance, and the search for anti-endotoxin therapies for sepsis all needed a dedicated venue. The journal gave that community a home, publishing structure–function chemistry alongside clinical studies of septic patients. As the field's centre of gravity widened from endotoxin itself to the whole innate immune system, the title followed — hence the continuation as Innate Immunity, which kept the society, the readership and much of the subject matter while widening the remit.
Quick Facts
| Field | Detail |
|---|---|
| Title | Journal of Endotoxin Research |
| Status | Ceased under this title in 2007; continued as Innate Immunity from 2008 |
| Publisher (this title) | Maney Publishing (W. S. Maney & Son Ltd), Leeds, United Kingdom |
| Society | Official journal of the International Endotoxin Society (now the International Endotoxin and Innate Immunity Society) |
| Print ISSN | 0968-0519 |
| Online ISSN | 1743-2839 |
| Run | Vol. 1, no. 1 (March 1994) – vol. 13, no. 6 (December 2007) |
| Frequency | 6 issues per year |
| Language | English |
| Successor title | Innate Immunity (SAGE Publications), ISSN 1753-4259 (print) / 1753-4267 (online) |
| H-index (as listed on Journals World) | 80 |
| Field | Immunology, microbiology, sepsis and inflammation research |
Scope and Subject Coverage
The journal covered endotoxin in the widest sense its community understood the term — bacterial LPS and related microbial products such as lipoteichoic acids from Gram-positive organisms — and the biology they set in motion. Its published content, as reflected in citation records and the Journals World topic profile, clustered around:
- Endotoxin chemistry and structure–function studies — lipid A and LPS structure, lipoteichoic acid characterisation, synthetic analogues and antagonists, and purification methods such as butanol extraction and hydrophobic interaction chromatography.
- Recognition and signalling — CD14, Toll-like receptors (especially TLR4 and its Asp299Gly and Thr399Ile polymorphisms), NF-κB pathway activation, and the cytokine cascades (TNF, IL-1, IL-6, IL-10) that follow LPS exposure.
- Endotoxin tolerance and desensitisation — the reprogrammed, hyporesponsive state of macrophages after prior LPS exposure, and its mechanisms and clinical relevance.
- Sepsis and septic shock — diagnosis, biomarkers, endotoxin measurement in patients, plasma mediator kinetics in neutropenic and critically ill patients, and candidate interventions from anti-endotoxin antibodies to adsorption cartridges and antimicrobial peptides.
- Host defence against Gram-negative infection — Escherichia coli and Pseudomonas aeruginosa studies, biofilm susceptibility, vaccines and immunotherapy, inflammasome activation and inflammation biomarkers.
Article types included original research, invited reviews — the journal's review articles on topics such as tolerance to microbial TLR ligands were widely cited — and shorter communications. A typical article carried a DOI under Maney's prefixes of the era (10.1179 and 10.1177 appear in the run), stated its received, revised and accepted dates, and was typeset to the compact two-column format characteristic of Maney's biomedical list.
The Continuation: Innate Immunity
Library catalogues record the relationship precisely: the Journal of Endotoxin Research ceased with volume 13, issue 6 (December 2007) and was continued by Innate Immunity, published by SAGE from 2008 (volume 14). Some secondary sources date the retitle decision to 2006, when the broadening of scope was announced; the volume record supports 2007 as the last year under the old title and 2008 as the first under the new one. Innate Immunity is published by SAGE Publications on behalf of the International Endotoxin and Innate Immunity Society, appears bimonthly, and covers innate immunity in humans, animals and plants — retaining endotoxin and LPS research within a wider frame that includes pattern-recognition receptors, cytokines, sepsis, inflammation and cell biology. Its editor-in-chief in recent listings is Otto Holst of the Research Center Borstel, Germany. The successor journal is abstracted and indexed in MEDLINE, Scopus and the Science Citation Index Expanded, and it has its own separate Journals World record (post 12612) under its own ISSNs — it is a continuation, not a duplicate of this record.
For authors, the practical consequence is simple: there is no submission route for the Journal of Endotoxin Research today. Manuscripts in its subject area belong with Innate Immunity or another current immunology journal. For readers and citing authors, the backfile remains fully citable: references to J Endotoxin Res resolve through library holdings and publisher archives, and catalogue records (for example the National Library of Medicine-style call number W1 JO643F and LCCN records) link the two titles so that a search under either name surfaces the whole run.
Indexing, Metrics and Standing
During its life the journal was a refereed, peer-reviewed title held by medical and university libraries internationally, with online availability recorded from volume 5 (1999) onward in major aggregations and full holdings of volumes 1–13 in national-licence collections. The H-index of 80 carried in the Journals World record is strikingly high for a thirteen-volume specialist journal, and it reflects reality: endotoxin research of the 1990s and 2000s produced heavily cited methodological and review literature, and papers first published here — on LPS tolerance, TLR signalling and sepsis mediators — accumulated citations for decades. The successor title's SCImago H-index is of the same order (81 in one recent listing, 84 in the Journals World record for Innate Immunity), which is consistent with a single continuing citation community measured under two titles. Citation figures for a ceased title should still be handled with care: the H-index of the old title is frozen as a historical measure, while the living indicator belongs to Innate Immunity.
Why the Journal Still Matters
Three features give the backfile lasting value. First, foundational signalling work: the years in which TLR4 was established as the LPS receptor and its human polymorphisms were mapped across populations fall squarely inside this journal's run, and its pages carry primary studies that later reviews still cite. Second, translational sepsis research: the journal documented the era's therapeutic attempts — mediator kinetics in febrile neutropenia, endotoxin adsorption, peptide antibiotics for Gram-negative sepsis — including negative and equivocal results that remain instructive for trial design. Third, chemical rigour: few clinical journals published LPS and lipoteichoic acid structure work at this depth, and the structure–function literature here is still the reference point for researchers synthesising lipid A analogues. A literature search on endotoxin that omits this title's thirteen volumes is materially incomplete.
How to Cite
The standard abbreviation is J. Endotoxin Res. A complete citation gives authors, title, journal abbreviation, year, volume, issue and pages, plus the DOI where one exists — for example, a 2004 article in volume 10, issue 4, pages 239–248, DOI 10.1179/096805104225005841. Note that journal copyright lines of the period read "© W. S. Maney & Son Ltd". When a reference list crosses the 2008 boundary, cite each article under the title in force when it appeared: Journal of Endotoxin Research up to volume 13 (2007), Innate Immunity from volume 14 (2008).
Frequently Asked Questions
What are the ISSNs of the Journal of Endotoxin Research? Print ISSN 0968-0519 and online ISSN 1743-2839.
Who published it? Maney Publishing (W. S. Maney & Son Ltd) of Leeds, United Kingdom, as the official journal of the International Endotoxin Society.
When did it run? From volume 1, issue 1 (March 1994) to volume 13, issue 6 (December 2007), six issues a year.
Can I still submit to it? No. The title ceased in 2007. Its continuation, Innate Immunity (SAGE Publications), is the current submission venue for this community.
Is Innate Immunity the same journal? It is the successor title of the same journal and society, continued from 2008 with new ISSNs (1753-4259 / 1753-4267) and a broadened scope; catalogues record it as "Continued by: Innate Immunity".
Is the journal peer-reviewed? Yes — library records describe it as a refereed, peer-reviewed periodical.
What was its H-index? The Journals World record lists 80, reflecting the heavy citation of its endotoxin and sepsis literature.
Profile Notes
This profile is based on library catalogue records for the title (publication run, frequency, publisher and ISSNs), the catalogue record of the successor title, the Innate Immunity journal reference entry (former name, society and publisher), and the Journals World record (post 375868). The stored publisher, Maney Publishing (GB), and the stored ISSNs were verified against those catalogue records and are correct for this title's run. One dating nuance is disclosed rather than hidden: some secondary sources give 2006 for the retitling to Innate Immunity, while volume records show the old title completing volume 13 in December 2007 and the new title beginning with volume 14 in 2008; this profile follows the volume record. Impact-factor figures for individual years were not included because no official source for this ceased title's year-by-year values could be verified during this review.
Research Themes in Depth
The journal's contents map the intellectual history of its field with unusual completeness, and four threads deserve particular attention from anyone using the backfile today. The first is the molecular definition of endotoxin itself. Through the 1990s the journal published the painstaking chemistry that turned "endotoxin" from a crude bacterial extract into a defined molecule: the structure of lipid A, the heterogeneity of lipoteichoic acid preparations — including a widely cited 2005 review of lipoteichoic acid structure and function that proposed purification by butanol extraction and hydrophobic interaction chromatography — and the synthesis of lipid A analogues designed as antagonists. That chemical literature is the foundation on which all later receptor biology rests.
The second thread is recognition. The identification of CD14 and then of Toll-like receptor 4 as the signalling receptor for LPS transformed immunology at the turn of the century, and the journal carried both experimental work and population studies of the pathway — including a 2004 investigation of the TLR4 Asp299Gly and Thr399Ile polymorphisms in a twenty-year longitudinal cohort of Chinese textile workers, which found the variants essentially absent in that population and thereby corrected assumptions drawn from European family cohorts. Papers of this kind, testing whether a celebrated finding generalises, are among the most valuable in any backfile.
The third thread is tolerance: the paradoxical state in which prior exposure to endotoxin protects against a later lethal challenge while leaving the host hyporesponsive. The journal's invited reviews and experimental papers on endotoxin desensitisation — the roles of interleukin-10 and transforming growth factor beta, genome-wide analyses of LPS tolerance in macrophages, and the dissociation of interferon-gamma from IL-12 and IL-18 during tolerance — remain standard entry points to a phenomenon now studied under the wider heading of innate immune memory. The fourth thread is the clinic: mediator kinetics in febrile neutropenic patients, methylene blue and cytokine responses in severe sepsis, protegrin peptides against endotoxin-induced mortality, alpha-helical peptides against Pseudomonas biofilm, and the candid reporting of an era's therapeutic hopes. Read together, the four threads explain why a journal of only thirteen volumes could accumulate an H-index of 80: it was the house journal of a field at its moment of maximum fertility.
Production, Access and the Backfile Today
Under Maney, the journal was produced from Leeds in the United Kingdom in both print and online forms; library records show print beginning in March 1994, electronic availability widening from volume 5 (1999), and complete holdings of volumes 1–13 in national-licence and university collections. Articles of the period bear W. S. Maney & Son copyright lines, received/revised/accepted dates and DOIs under the publisher's prefixes, and they are referenced in major bibliographic utilities under OCLC 43072759 and the Library of Congress catalogue records for both titles. The successor title's archive at SAGE is the natural first place to look for the journal's later years, while the 1994–2007 run itself is consulted through library holdings and aggregations; interlibrary-loan requests should cite the ISSN pair 0968-0519 and 1743-2839 and the volume and year, since the title's brevity — the words "endotoxin research" also appear inside many article titles — makes unqualified keyword searching noisy.
For Librarians and Bibliometricians
Cataloguers should treat the two titles as one serial with a title change: Journal of Endotoxin Research (1994–2007, Maney, Leeds) continued by Innate Immunity (2008–, SAGE), with no overlap in volume numbering — the successor continues the sequence, reaching volume 14 in 2008 — and with separate ISSN pairs for each title. Bibliometricians should be equally careful: citation databases that merge the two titles will report a single continuing H-index (values in the low eighties are reported for the combined title), while databases that split them attribute the historical figure of 80 to this title alone, as the Journals World record does. Either treatment is defensible if stated; silently mixing the two is not. Finally, evaluators encountering a 1990s or 2000s publication credit in this journal should read it as a peer-reviewed specialty-society publication of good standing in its field and period — the equivalent, for its community, of the society journals that anchor other biomedical specialties.
Distinguishing Similarly Named Titles
Authors and searchers should take care not to confuse this journal with the Journal of Innate Immunity, a separate Karger title founded later, or with Infection and Immunity, the long-running American Society for Microbiology journal whose subject matter overlaps at the level of bacterial infection but whose history, publisher and ISSNs are entirely different. Nor is the Journal of Endotoxin Research related to review serials with "endotoxin" in an article title, of which there are many. The reliable discriminators are the ones used throughout this profile: the Maney imprint from Leeds, the International Endotoxin Society affiliation, the 1994–2007 volume run ending at volume 13, and above all the ISSN pair 0968-0519 and 1743-2839. A citation that matches those identifiers is this journal; one that does not, however close its title sounds, is something else. The same care protects the successor: Innate Immunity (SAGE, ISSN 1753-4259 / 1753-4267) is this journal's continuation and should be cited under its own name for everything from volume 14 (2008) onward, while the Karger Journal of Innate Immunity is an unrelated title that happens to share two words of it. Keeping these three titles separate in reference lists is a small discipline that materially improves the accuracy of the immunology literature's citation record.
Summary Assessment
For a researcher arriving fresh at the endotoxin literature, this journal is best approached as the field's founding archive. Its thirteen volumes hold the chemical, cellular and clinical work that defined endotoxin science between 1994 and 2007: the structural characterisation of LPS and lipoteichoic acid, the mapping of the CD14–TLR4 pathway and its human variation, the systematic exploration of endotoxin tolerance, and the first translational generation of anti-endotoxin and anti-mediator strategies for sepsis. Its society ownership, refereed status, six-issues-a-year regularity and unusually high citation yield for its size mark it as a serious journal of record, and its seamless continuation as Innate Immunity means the community it built is still publishing today under the broader banner its own success made necessary. Cite it precisely, search it by ISSN, and treat its absence from a bibliography on endotoxin as a gap worth explaining.
Researchers tracing any thread of modern innate-immunity science — a receptor, a polymorphism, a tolerance mechanism, a failed sepsis therapy — will find that the trail repeatedly leads back to these thirteen volumes, which is the surest sign that the journal did the job its founders set for it in 1994.
Journal Metrics
A quartile may vary by subject category. Values without a source or reporting year are unverified historical entries. Verify the current Journal Impact Factor with Clarivate or the publisher before using it.
Aims & Scope
The publisher’s official aims and scope have not yet been verified for this profile. Use the journal website to check subject fit and accepted article types before submitting.
Recent Research Articles
Latest publications matched automatically by ISSN.
Review: Human antimicrobial proteins — effectors of innate immunity
Jürgen Harder, Regine Gläser, Jens-Michael Schröder
2007-12 · DOI: 10.1177/0968051907088275Bikunin suppresses expression of pro-inflammatory cytokines induced by lipopolysaccharide in neutrophils
Seiji Kanayama, Yoshihiko Yamada, Akira Onogi, Hiroshi Shigetomi et al.
2007-12 · DOI: 10.1177/0968051907086464Acknowledgement to Referees 2007
2007-12 · DOI: 10.1177/0968051907087587Low-dose steroid alters in vivo endotoxin-induced systemic inflammation but does not influence autonomic dysfunction
Sonia M. Alvarez, Maria Katsamanis Karavidas, Susette M. Coyle, Shou-En Lu et al.
2007-12 · DOI: 10.1177/0968051907086465Decreased beating rate variability of spontaneously contracting cardiomyocytes after co-incubation with endotoxin
Hendrik Schmidt, Jana Saworski, Karl Werdan, Ursula Müller-Werdan et al.
2007-12 · DOI: 10.1177/0968051907086233Physicochemical characterization and biological activity of lipooligosaccharides and lipid A from Neisseria meningitidis
Susu M. Zughaier, Buko Lindner, Jörg Howe, Patrick Garidel et al.
2007-12 · DOI: 10.1177/0968051907084435Prophylactic effect of liposomal N-acetylcysteine against LPS-induced liver injuries
Misagh Alipour, Abdelwahab Omri, Milton G. Smith, Zacharias E. Suntres et al.
2007-10 · DOI: 10.1177/0968051907085062Review: From therapy to experimental model: a hundred years of endotoxin administration to human subjects
Marjan Bahador, Alan S. Cross
2007-10 · DOI: 10.1177/0968051907085986Differential expression of Toll-like receptor 2 (TLR2) and responses to TLR2 ligands between human and murine vascular endothelial cells
Shuang Chen, Michelle H. Wong, Danica J. Schulte, Moshe Arditi et al.
2007-10 · DOI: 10.1177/0968051907085096IEIIS Meeting minireview: The role of innate immunity in the pathogenesis of asthma: evidence for the involvement of Toll-like receptor signaling
Nicolas W. J. Schröder, Moshe Arditi
2007-10 · DOI: 10.1177/0968051907084652IEIIS Meeting minireview: Bordetella evolution: lipid A and Toll-like receptor 4
Iain MacArthur, Paul B. Mann, Eric T. Harvill, Andrew Preston et al.
2007-08 · DOI: 10.1177/0968051907082609The equine TLR4/MD-2 complex mediates recognition of lipopolysaccharide from Rhodobacter sphaeroides as an agonist
Katharina L. Lohmann, Michel L. Vandenplas, Michelle H. Barton, Clare E. Bryant et al.
2007-08 · DOI: 10.1177/0968051907083193High glucose up-regulates lipopolysaccharide-stimulated inflammatory cytokine production via c-jun N-terminal kinase in the monocytic cell line THP-1
Hirotaka Iwata, Yoshihiko Soga, Michio Meguro, Sayuri Yoshizawa et al.
2007-08 · DOI: 10.1177/0968051907082608Review: Variability of host—pathogen interaction
Corinna Hermann
2007-08 · DOI: 10.1177/0968051907082605Peptostreptococcus micros cell wall elicits a pro-inflammatory response in human macrophages
Shin-ichi Tanabe, Charles Bodet, Daniel Grenier
2007-08 · DOI: 10.1177/0968051907081869Lipopolysaccharide enhances interferon-γ-induced nitric oxide (NO) production in murine vascular endothelial cells via augmentation of interferon regulatory factor-1 activation
Naoki Koide, Mya Mya Mu, Ferdaus Hassan, Shamima Islam et al.
2007-06 · DOI: 10.1177/0968051907080894Recombinant Factor C competes against LBP to bind lipopolysaccharide and neutralizes the endotoxicity
Peng Li, Bow Ho, Jeak Ling Ding
2007-06 · DOI: 10.1177/0968051907079573Invited review: NOD2 and defensins: translating innate to adaptive immunity in Crohn's disease
Laurent Peyrin-Biroulet, Mathias Chamaillard
2007-06 · DOI: 10.1177/0968051907080429IEIIS Meeting minireview: Chemical synthesis of peptidoglycan fragments for elucidation of the immunostimulating mechanism
Yukari Fujimoto, Seiichi Inamura, Akiko Kawasaki, Zenyu Shiokawa et al.
2007-06 · DOI: 10.1177/0968051907080739Potentiation of Toll-like receptor-induced cytokine production by (1→3)-β-D-glucans: implications for the monocyte activation test
Robert Kikkert, Ingrid Bulder, Els R. de Groot, Lucien A. Aarden et al.
2007-06 · DOI: 10.1177/0968051907080024Reviews
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October 16, 2026 at 9:53 am
October 10, 2026