CD14 Genotype

This test reports your genotype at CD14 -159 C/T (rs2569190), also called CD14 -260 C/T. It is a fixed germline result: CC, CT, or TT. A saliva swab, cheek swab, or blood draw should give the same genotype if the lab gets enough of your DNA.

The marker is research-grade. It has functional studies and many association studies, but it is not a standard diagnostic test for gum disease, sepsis, tuberculosis, heart disease, asthma, or allergy. Use it as context, not as a verdict.

What CD14 Actually Does

CD14 is a bacterial-sensing protein used by the first-line immune system. Monocytes circulate in blood. Macrophages live in tissues. Both use CD14 to notice bacterial material early.

The best-known trigger is lipopolysaccharide, often called LPS or endotoxin. It is a piece of the outer coat of gram-negative bacteria. CD14 helps hand LPS to TLR4. TLR4 then starts an inflammatory response, including signals such as TNF-alpha.

Some CD14 is attached to immune cells. Some is soluble CD14, a floating protein found in blood and saliva. Soluble CD14 is a different test from this genotype. It changes with infection, age, and inflammation.

The -159 change is in the CD14 promoter. The promoter is the stretch of DNA that helps control how much CD14 gets made. The T version changes how Sp-family control proteins bind there. In several studies, TT carriers had higher soluble CD14, and this effect appears to attenuate across childhood alongside increasing CD14 methylation. Cell-surface CD14 and TNF-alpha responses have been less consistent. One in vivo study of monocytes found stronger RNA polymerase II recruitment on the T-allele haplotype but no difference in actual transcript numbers, and a Chinese Han functional study found the opposite direction, with the C allele reducing promoter activity and inducible sCD14 and TNF-alpha. The functional literature genuinely conflicts.

Gum Disease and Oral Health

The most practical human data are in oral disease, but even here the signal is not clean enough for a diagnosis. In one Chinese study of chronic periodontitis, 43 percent of patients carried TT, compared with 26 percent of controls. TT carriers had about twice the odds of moderate to severe disease. A larger meta-analysis found no overall CD14-periodontitis link, though it did find signals tied to disease severity. One nuance worth flagging: a separate meta-analysis found TT associated with lower odds of mild-to-moderate periodontitis compared with CC (odds ratio about 0.42). Taken together, the pattern suggests TT may shift disease toward the more severe end when it develops, rather than raising overall risk.

Bacteria start gum disease, but tissue damage also depends on the immune response to those bacteria. If CD14 changes the response to the same bacterial load, it could change how much gum tissue gets damaged.

In one Suriname cohort of children with severe cavities, TT was linked to lower odds of abscess or fistula formation. In Czech children, CT and TT were linked to plaque-induced gingivitis only when Porphyromonas gingivalis was present. Same genotype, different setting. The bacteria in the mouth matter.

Once active periodontitis is present, soluble CD14 can rise no matter what genotype you carry. During a flare, a salivary or serum CD14 protein result mostly reflects current inflammation. The genotype tells you what you inherited.

Infection Susceptibility and Sepsis

CD14 is close to the start of antibacterial defense, so researchers have tested this variant in severe infections. In a prospective study of 417 sepsis patients of western European descent, TT carriers had lower 30-day mortality than people carrying a C allele (multivariate hazard ratio 2.11 for the C allele). Earlier work pointed the other way: a multicenter septic-shock study found TT overrepresented among septic-shock patients and independently linked to higher mortality (odds ratio around 5.3), and a retrospective surgical septic-shock cohort found the CC genotype associated with death. A broader meta-analysis did not find a consistent mortality effect, and its susceptibility signal was mainly in Asian burn ICU studies. The direction of the TT effect in sepsis is not settled; treat this as unresolved rather than a clean survival advantage.

In critical care patients, TT has been linked to more positive bacterial cultures, especially gram-negative bacteria, but not to septic shock or 28-day survival. For tuberculosis, several meta-analyses found higher susceptibility in T carriers, especially TT carriers in Asian populations, with no clear effect in Caucasian populations. A 2025 Kurdish Iranian study found the same direction for rs2569190, with TT carriers having about 1.7-fold higher odds of tuberculosis. These findings do not change infection prevention: vaccination, prompt care for serious symptoms, and source control still matter more than genotype.

Heart Disease Risk

CD14 attracted heart-disease research because bacterial sensing and inflammation can affect plaque biology. An early German study found no overall link, but TT was tied to prior myocardial infarction in a small low-risk subgroup older than 62, with nearly fourfold higher odds. In the original Czech myocardial infarction study, the T allele frequency was 0.49 in cases versus 0.35 in controls, and TT carriers had higher CD14 receptor density on monocytes. A Chinese Han study also linked the T allele to myocardial infarction, especially in men, smokers, and people with hypertension. A cardiovascular meta-analysis found the clearest pooled signal in East Asian datasets, with a T-allele odds ratio around 1.24.

The stronger test of prediction was less convincing. In the Physicians' Health Study, nearly 15,000 apparently healthy men were followed for 12 years, and CD14 genotype did not predict future myocardial infarction. A separate study of 789 people found no independent link to stable coronary artery disease after adjustment. One Indian coronary artery disease study even found the CC genotype was the risk factor and TT was protective. Treat CD14 as background biology. ApoB, Lp(a), blood pressure, smoking, and metabolic health carry far more weight.

Allergies, Asthma, and Endotoxin

The most useful allergy finding is a gene-environment interaction. In children with CC, higher household endotoxin exposure was linked to less allergic sensitization and eczema, but more nonallergic wheeze. In CT and TT children, that endotoxin pattern was not seen. Same exposure, different response. Other cohorts, including a Barbados study, have shown the direction of the CD14-endotoxin interaction can even reverse depending on exposure level, so the effect is real but age- and exposure-dependent.

Asthma results do not give a clean answer. One adult Caucasian study found the T allele and TT genotype were linked to lower risk of allergic asthma and higher soluble CD14. A large German cohort found higher soluble CD14 in TT carriers but no link to IgE or atopic disease. A family-based test and meta-analysis also failed to find a clear asthma association. Do not order this test expecting it to explain asthma or allergies by itself.

How to Read the Result

CD14 genotype is a context marker. The T allele has been linked in some studies to higher soluble CD14 and stronger downstream signaling, but the functional evidence is mixed, and whether that helps or hurts depends on the exposure. It may be helpful in one infection setting and unhelpful in chronic gum inflammation. Context decides the effect.

CC means you do not carry the T version at this site. It does not prove low gum, allergy, infection, or heart risk. CT means you carry one T allele. TT means you carry two. For TT, the best-supported practical use is to take recurrent gingivitis or periodontitis seriously and look harder for the bacterial driver.

Why This Test Is One-Time

Your CD14 genotype is set at conception. There is no reason to repeat it unless the first variant call may be wrong. The useful follow-up is not another CD14 genotype. It is watching the things this result might modify: periodontal exams, bleeding gums, oral pathogen testing when gum disease recurs, and standard cardiovascular markers when family history points that way.

Soluble CD14 protein levels are a different measurement. Those can move with H. pylori, periodontitis, aging, and other inflammatory states. If you want to track current immune activation, that is a protein test. This test tells you one inherited setting.

When Results Can Be Misleading

Genetic results have a different set of pitfalls from ordinary blood markers:

• Single-variant coverage: this test looks at rs2569190. It does not sequence the whole CD14 gene or rule out rare variants elsewhere.
• Study-population mismatch: many associations are strongest in specific ancestry groups or clinical settings. The tuberculosis signal, for example, sits mainly in Asian populations, and a result from an East Asian sepsis study should not be read as the same risk estimate for everyone.
• Clinical-grade versus direct-to-consumer data: if a major decision depends on the result, confirm it with a clinical-grade assay. A different lab method is better than repeating the same consumer file.
• Broader sequencing reports: a single rs2569190 result is usually CC, CT, or TT. If CD14 appears on a larger sequencing report, uncertain rare variants should not be interpreted like this common variant.
• Sample quality: saliva and cheek swabs work for germline DNA, but a poor swab can fail. It should not turn CC into TT if the lab has good quality controls.
• Tumor-only versus inherited DNA: this result should come from normal DNA, not tumor tissue. A tumor-only sequencing result is not a family-risk result unless it is confirmed in normal DNA.
• Confusion with soluble CD14: soluble CD14 in blood or saliva measures current protein level. It is not the same as CD14 genotype.

What to Do With Your Result

If the result came from a clinical-grade lab and the call is clear, treat it as permanent. If it came from a raw consumer genotype file, or if it conflicts with another report, confirm it before using it in family or medical decisions.

For gum health, use the result as a reason to be less casual about bleeding, pockets, and recurrent inflammation. The action is still ordinary periodontal care: plaque control, interdental cleaning, professional assessment, and shorter maintenance intervals if a dentist finds active or recurrent periodontitis. CD14 can explain part of the host response. It does not replace an oral exam.

For heart disease, do not let CD14 drive the plan. If family history is strong, check the markers that change decisions: ApoB, Lp(a), blood pressure, glucose control, and smoking status. If a broader genetics panel finds a high-impact lipid or cardiomyopathy variant, that is when a genetic counselor or specialist becomes useful.

For family members, the practical value is narrow. Children, siblings, and parents may share the allele, but testing them usually matters only if severe periodontitis, unusual infection patterns, or early heart disease runs through the family. Carrying T changes odds in some studies. It does not decide what will happen.