Microbiome Interpretation Structured microbiome reference
← Foundations

Gut inflammation markers

Intestinal inflammation on a clinical pathway is measured with fecal calprotectin or lactoferrin, not with vendor sequencing scores. Low Faecalibacterium and elevated blood LPS are different constructs, each has association literature but none replaces inflammatory workup when alarm features are present.

Gut inflammation markers

Gut inflammation in clinic usually means neutrophil-driven mucosal activity measurable in stool (calprotectin, lactoferrin) or systemic acute-phase response (CRP). Consumer microbiome reports sometimes add proprietary inflammation scores or highlight low butyrate producers such as Faecalibacterium prausnitzii. Those layers answer different questions and are not interchangeable, a surprising but common pattern is a high vendor inflammation flag with normal calprotectin, which often reflects algorithm design or taxon proxies rather than active IBD-like inflammation.

For how immunity, barrier, and composition threads fit together: Gut–immune axis.

Three different questions

QuestionBetter toolsStool microbiome sequencing alone?
Is there neutrophilic intestinal inflammation?Fecal calprotectin, lactoferrinNo, see Calprotectin test page
Is there systemic inflammation?CRP, ESR (clinical context)No
Does community composition correlate with inflammatory states in research?Metagenomics in cohortsAssociation only, not individual diagnosis

When red flags are present, the first branch is clinical inflammatory workup, not probiotic-first interpretation of taxa lists.

Marker comparison

MarkerSourceHigh may suggestLimits
Fecal calprotectinStool proteinIBD activity, some infectionsNot sensitive for pure IBS; interpret with symptoms
Fecal lactoferrinStoolInflammatory diarrhoeaSimilar niche to calprotectin
CRPBloodSystemic inflammationNon-specific; normal CRP does not exclude focal gut inflammation
Plasma LPS / LBP / sCD14BloodMetabolic endotoxemia hypotheses in obesity/metabolic researchConfounders; not direct mucosal inflammation test
Sequencing “inflammation index”Vendor algorithmUnknown per lab, ask validation dataNot interchangeable with calprotectin
Low F. prausnitziiTaxon abundanceIBD association in cohorts (Sokol et al., 2008)Also varies with diet, antibiotics, method

What not to conclude

FindingWeak conclusionStronger next step
Low Faecalibacterium on report“I have gut inflammation”Symptom review; calprotectin if diarrhoea, blood, or weight loss
High vendor inflammation score“Same as raised calprotectin”Compare to fecal calprotectin if available; do not skip scope when alarms exist
Normal calprotectin“Microbiome proves no IBD ever”Functional pathway possible; follow-up if symptoms change
Elevated CRP“Must be gut source”Non-gut causes common, clinical context

Species page: Faecalibacterium prausnitzii. Synthesis: Multi-marker report synthesis.

Clinical routing

  • Elevated calprotectin → gastroenterology workup (endoscopy, treatment pathway), not a probiotic-first algorithm.
  • Normal calprotectin + IBS-type symptoms → functional hypotheses: FODMAPs, motility, barrier, each evidence-tiered, not diagnostic from sequencing alone.
  • IBD vs functional overlap → IBD vs functional gut.
Context if you're reading a report

Consumers often treat a microbiome inflammation index like calprotectin, or infer mucosal inflammation from a single low butyrate producer. That misclassification can delay IBD evaluation or drive unnecessary supplement protocols when functional pathways fit better.

Tier markers: validated fecal proteins (calprotectin, lactoferrin) > clinical CRP > research blood endotoxin proxies > vendor sequencing indexes > single-taxon abundance flags.

That a sequencing inflammation score equals calprotectin; that normal calprotectin rules out all immune activation in the gut; that plasma LPS in research cohorts diagnoses leaky gut in an individual; or that low Faecalibacterium alone proves active colitis.

Related on this site: Sokol et al., 2008, PNAS