Hexa-LPS producing microbes
What this marker measures
The collective capacity of the microbial community to produce hexa-acylated lipopolysaccharides (hexa-LPS), an immunostimulatory outer membrane component of some Gram-negative bacteria, particularly Gammaproteobacteria1,2. Elevated hexa-LPS-producing potential may increase microbial inflammatory potential and may be relevant in intestinal inflammation, systemic inflammation, or impaired gut barrier integrity1,3–7.
Clinical associations
Consider this marker when your patient presents with:
Interpreting the result
All results are compared to Microba's healthy cohort to determine whether they fall within or outside the expected range.
Action: see patient management insights
Patient management insights
Limit Gammaproteobacteria overgrowth and reduce inflammatory triggers.
GRADE D
GRADE D
Tips for patients discussion
Your report shows elevated levels of gut microbes that can produce hexa-LPS, a bacterial compound that can strongly stimulates immune signalling, particularly when the gut barrier is under stress. Increasing fibre-rich plant foods and omega-3s while reducing excess saturated fat can help.
The community
Hexa-LPS is not produced by a single species, it's a community-level function. Below are some of the most common, though this list is not exhaustive.
- Citrobacter freundii
- Escherichia sp000208585
- Haemophilus_D sp001815355
- Haemophilus_D pittmaniae
- Enterobacter himalayensis
- Haemophilus_D MIC7468
- Klebsiella pneumoniae
- Enterobacter kobei
- Haemophilus_D parainfluenzae
- Klebsiella_A michiganensis
- Klebsiella_A oxytoca
- Enterobacter ludwigii
- Haemophilus_D parainfluenzae_K
- Haemophilus_D parainfluenzae_L
- Haemophilus_D parainfluenzae_L
- Enterobacter nimipressuralis
- Pseudomonas aeruginosa
- Haemophilus_D parainfluenzae_M
- Escherichia dysenteriae
- Escherichia coli
- Haemophilus_D parainfluenzae_N
- Raoultella ornithinolytica
- Escherichia flexneri
- Haemophilus_D sp001679485
How results are calculated
All microbiome marker results are compared against the Microba Healthy Cohort — a purpose-built reference group of more than 450 healthy individuals, collected and analysed using the same workflow as patient samples.
Each marker is scored by comparing the patient's relative abundance against the cohort average. The distance from this average is expressed as standard deviations, and determines whether a result is classified as Low, Borderline, or High.
Source references for all clinical associations, interpretation definitions, and patient management insights on this card.
1. Zamyatina, A. & Heine, H. Lipopolysaccharide Recognition in the Crossroads of TLR4 and Caspase-4/11 Mediated Inflammatory Pathways. Frontiers in Immunology 11, (2020).
2. Matsuura, M. Structural Modifications of Bacterial Lipopolysaccharide that Facilitate Gram-Negative Bacteria Evasion of Host Innate Immunity. Frontiers in Immunology 4, 109 (2013).
3. Thompson, K. N. et al. Alterations in the gut microbiome implicate key taxa and metabolic pathways across inflammatory arthritis phenotypes. Science Translational Medicine 15, eabn4722 (2023).
4. Anhê, F. F., Barra, N. G., Cavallari, J. F., Henriksbo, B. D. & Schertzer, J. D. Metabolic endotoxemia is dictated by the type of lipopolysaccharide. Cell Reports 36, (2021).
5. Tulkens, J. et al. Increased levels of systemic LPS-positive bacterial extracellular vesicles in patients with intestinal barrier dysfunction. Gut 69, 191–193 (2020).
6. d’Hennezel, E., Abubucker, S., Murphy, L. O. & Cullen, T. W. Total Lipopolysaccharide from the Human Gut Microbiome Silences Toll-Like Receptor Signaling. mSystems 2, e00046-17 (2017).
7. Nighot, M. et al. Lipopolysaccharide-Induced Increase in Intestinal Epithelial Tight Permeability Is Mediated by Toll-Like Receptor 4/Myeloid Differentiation Primary Response 88 (MyD88) Activation of Myosin Light Chain Kinase Expression. The American Journal of Pathology 187, 2698–2710 (2017).
8. Khorsand, B. et al. Overrepresentation of Enterobacteriaceae and Escherichia coli is the major gut microbiome signature in Crohn’s disease and ulcerative colitis; a comprehensive metagenomic analysis of IBDMDB datasets. Front. Cell. Infect. Microbiol. 12, (2022).
9. Vich Vila, A. et al. Gut microbiota composition and functional changes in inflammatory bowel disease and irritable bowel syndrome. Science Translational Medicine 10, eaap8914 (2018).
10. López-Moreno, J. et al. Effect of Dietary Lipids on Endotoxemia Influences Postprandial Inflammatory Response. J. Agric. Food Chem. 65, 7756–7763 (2017).
11. Lyte, J. M., Gabler, N. K. & Hollis, J. H. Postprandial serum endotoxin in healthy humans is modulated by dietary fat in a randomized, controlled, cross-over study. Lipids Health Dis 15, 186 (2016).
12. Harte, A. L. et al. High fat intake leads to acute postprandial exposure to circulating endotoxin in type 2 diabetic subjects. Diabetes care 35, 375–382 (2012).
13. Vulevic, J., Drakoularakou, A., Yaqoob, P., Tzortzis, G. & Gibson, G. R. Modulation of the fecal microflora profile and immune function by a novel trans-galactooligosaccharide mixture (B-GOS) in healthy elderly volunteers2. The American Journal of Clinical Nutrition 88, 1438–1446 (2008)
.14. Spaiser, S. J. et al. Lactobacillus gasseri KS-13, Bifidobacterium bifidum G9-1, and Bifidobacterium longum MM-2 Ingestion Induces a Less Inflammatory Cytokine Profile and a Potentially Beneficial Shift in Gut Microbiota in Older Adults: A Randomized, Double-Blind, Placebo-Controlled, Crossover Study. J Am Coll Nutr 34, 459–469 (2015).