DIAGNOSIS OF DYSBIOSIS:

Evaluation sometimes employs stool, breath, urine, or blood testing to find microbial imbalance, inflammation, or aberrant fermentation by-products, often in the setting of conditions like IBD or IBS. ^6.

1. Urine Tests: Using methods like nuclear magnetic resonance (NMR) spectroscopy, which detects metabolic signatures associated with dysbiosis, such as phenols, indoles, and short-chain fatty acids, urine analysis evaluates microbial-derived metabolites. Mass spectrometry (MS) is another, more sensitive method used in urine metabolomics, which usually entails sample preparation (centrifugation, filtration), normalization (e.g., creatinine adjustment), and multivariate statistical analysis. ^14.

2. The hydrogen-methane breath test: It gauges how much bacterial fermentation takes place following the consumption of an indigestible substrate (such as lactulose). To find increases in hydrogen or methane, breath samples are taken at baseline and every 20 minutes. Dysbiosis, or small intestine overgrowth, is indicated by early or persistent gas rises, with diagnostic criteria of >20 ppm hydrogen or >10 ppm methane rise. For diseases like SIBO or leaky gut, serial testing is helpful for tracking therapy response. ^15-16.

3. Stool tests: The composition of gut microbes, including yeasts, opportunistic and pathogenic bacteria (including E. coli, Proteus, Pseudomonas, Salmonella, Shigella, and Vibrio), and beneficial bacteria (like Lactobacillus and Bifidobacterium), is evaluated by a Comprehensive Digestive Stool Analysis (CDSA). Several panels also assess the overall makeup of the microbiome and dysbiosis scores ^17-18.DNA sequencing, metagenomics/metatranscriptomics, and the detection of microbial compounds such as short-chain fatty acids (SCFAs) are examples of contemporary CDSA. Because it is easy to gather and provides an excellent picture of gut microbes, stool is frequently employed. Whole-genome shotgun sequencing (functional potential) and 16S rRNA gene sequencing (taxonomic identification) are significant sequencing techniques. ^19.

4. Indices of dysbiosis: These indices measure microbiome imbalance using phylum distributions, alpha-diversity (such as Shannon, Simpson, and Chao-1), and beta-diversity (such as Bray-Curtis). Reduced alpha-diversity is linked to several illnesses, and indices are evaluated in conjunction with clinical data. ^20-21.

5. Neighborhood classification: This technique quantifies deviation by comparing an individual's microbiome profile to healthy reference groups using similarity and distance metrics. ^22.

6. Identification of gut microbial metabolites: In order to evaluate functional activity, metabolomics uses both targeted and untargeted methods to quantify microbial chemicals. Metabolites such as SCFAs, lipopolysaccharides, secondary bile acids, and tryptophan derivatives that play roles in inflammation or therapeutic response can be detected by NMR or MS in feces, blood, urine, or CSF. ^23-24.

7. Oral carnitine challenge test: By giving carnitine and examining microbial-derived metabolites in blood or urine, this functional test assesses microbiome metabolic activity and aids in the development of personalized dietary recommendations. ^25.

8. Intestinal permeability test: The mannitol-lactulose test quantifies the amount of these sugars excreted in the urine following a meal in order to evaluate "leaky gut"; elevated levels suggest decreased barrier function as a result of dysbiosis. ^26.

Identification of biomarkers: A biomarker is a measurable indicator of disease states, normal biological processes, or therapeutic responses at the molecular, cellular, or systemic levels ^27-28. Examples include blood pressure, C-reactive protein (CRP), which indicates inflammation, and gut microbial metabolites that show dysbiosis or eubiosis. ^29.

The importance of biomarkers:

Early disease detection, risk prediction, disease development tracking, and therapy efficacy evaluation are all made possible by biomarkers. They aid in detecting microbial imbalance in gut dysbiosis, evaluating its severity, tracking probiotic therapies, and forecasting diseases like IBD. ^29-30.

Types of Biomarkers:

Risk, safety, pharmacodynamics, prognosis, monitoring, and prediction using biomarkers ^28.

By type: microorganisms (e.g., reduced Faecalibacterium prausnitzii), metabolites (SCFAs), genetic or protein markers, and host-response markers (calprotectin, CRP) ^29-30.

Identification Techniques:

Dysbiosis-related biomarkers can be found by sequencing (16S rRNA, metagenomics), metabolomics (SCFAs, bile acids via LC-MS/GC-MS), proteomics/transcriptomics, and multi-omics in conjunction with AI or machine learning. ^29–32

Gut Dysbiosis-Related Inflammation Biomarkers:

Acute-phase proteins, microbial compounds, barrier proteins, metabolites, cytokines, antibodies, and microRNAs are among the markers associated with dysbiosis-related inflammation. Frequently used markers are highlighted in this section. ³³

C-Reactive Protein (CRP): The acute-phase protein CRP is produced by the liver and can rise up to 1000 times during inflammation, primarily due to IL-6. Low Firmicutes-to-Bacteroidota ratios and LPS-induced TNF-α signaling are two characteristics of gut dysbiosis that are linked to elevated CRP. CRP is a commonly used, non-specific indicator of systemic inflammation. By blocking HDAC, mTOR-S6K signaling, and G-protein-coupled receptors, SCFAs lower inflammation. They maintain the integrity of the intestinal barrier, encourage the production of Tregs, regulate the polarization of macrophages, and reduce inflammation caused by autoimmune disorders and obesity. Inflammation.^34.

Short-Chain Fatty Acids (SCFAs): By blocking HDAC, mTOR-S6K signaling, and G-protein-coupled receptors, SCFAs lower inflammation. They maintain the integrity of the intestinal barrier, encourage the production of Tregs, regulate the polarization of macrophages, and reduce inflammation caused by autoimmune disorders and obesity.^35-36

MicroRNAs (miRNAs): miRNAs regulate inflammatory processes as well as host-microbe interactions. MiR-21 enhances inflammation via TNF-α signaling, whereas miR-320 targets NOD2 to reduce inflammation. MiR-155, which is elevated in inflammation and boosts IL-8 production, exacerbates gut inflammation. By reacting to and regulating inflammatory signals, miRNAs produce feedback loops.³⁷

Inflammatory metabolites (e.g., ImP, TMAO): The dysbiotic microbiota produces imidazole propionate (ImP), which interferes with insulin signaling and lessens the effectiveness of metformin in type 2 diabetes. The microbial breakdown of choline and carnitine produces trimethylamine N-oxide (TMAO), which triggers inflammatory pathways, damages the heart, and activates the NLRP3 inflammasome.^38-41.

BIOMARKERS:

1. Zonulin acts as a precursor to pre-haptoglobin 2 and uses PAR2 receptors to control intestinal epithelial cell tight junctions. The intestinal barrier is weakened by increased zonulin release caused by gut dysbiosis. Autoimmune illnesses, including type 1 diabetes and celiac disease, are associated with elevated zonulin levels, which permit toxins and antigens to pass through the epithelium, trigger immunological responses, and release cytokines (like TNF-α and IFN-γ). This starts a vicious cycle of inflammation and barrier deterioration.^42–43.

Herbal Phytotherapies: Plants, Phytochemicals, and Therapeutic Approaches:

Many diseases are caused by gut dysbiosis, which emphasizes the need for treatments other than antibiotics. The antibacterial, anti-inflammatory, prebiotic, and immunomodulatory properties of herbal phytotherapies result in multi-target effects. There is mounting evidence that herbal remedies profoundly alter the gut microbiome. Dietary composition and function enhance microbial diversity and improve immunity, digestion, metabolism, and mental health ^[59-60].Reduced inflammation, enhanced immunity, better food absorption, and favorable results in metabolic illnesses, including type 2 diabetes and obesity, are all linked to herbal remedies ^[60]. Their effects are mediated by host immunological modulation, selective antibacterial activity against pathogens, and prebiotic support of beneficial microbes. Additionally, intestinal bacteria produce more active metabolites from herbal substances.^61-62.

Investigated Therapeutic Plants That Have Been Shown to Change Microbial Communities:

1. Aloe vera (Aloe vera (L.) Burm. F): Succulents from the Asphodelaceae family have long been used to enhance digestive health and digestion. The inner leaf gel is safe, but because of its laxative and cytotoxic qualities, whole-leaf formulations containing anthraquinones (such as aloin) should be taken with caution⁶³ Polysaccharides such as acemannan, phenolics, vitamins, and minerals are responsible for its medicinal properties. Acemannan influences immunity, lowers inflammation, and functions as a prebiotic ^64-65. Aloe vera also preserves the integrity of the intestinal barrier and encourages the microbial fermentation of short-chain fatty acids. It also possesses antioxidant, anti-inflammatory, and antibacterial qualities ^66–68.Aloe vera's function in gut health and microbiome modulation is highlighted by a clinical trial, which suggests that it may lessen IBS symptoms, particularly constipation-predominant forms, by increasing motility and mucus secretion.

2. Dandelion (Taraxacum officinale) F.H. Wigg: Fructans (inulin, FOS) prebiotically improve Bifidobacterium, Olsenella, and Dialister; sesquiterpene lactones (taraxacin, taraxinic acid) increase bile flow, appetite, and liver function. Phenolics (chicoric, chlorogenic, and caffeic) and flavonoids (luteolin and quercetin) increase antioxidant capacity, reduce TOS/OSI/MDA/NOx, and scavenge ROS/RNS. Taraxasterol/ursolic acid improves UC healing and microbiota by activating Nrf2/HO-1 and suppressing JNK/Bax/NF-κB/TNF-α/IL-1β/TLR4. Unlike S. aureus, B. subtilis, and E. coli (ethanol extracts work best), sesquiterpenes, flavonoids, and phenolics interfere with membranes, enzymes, and quorum sensing. efficiently cures E. coli UTIs in DAPAD and improves the milk microbiota in mastitis. ^69-74.

3. Ginger (Zingiber officinale Roscoe): contains zingiberene, shogaols, and gingerols ([6/8/10]) with neuroprotective, anti-inflammatory, antioxidant, and antibacterial properties: scavenges DPPH/superoxide/OH, suppresses ROS/NO/PGE2, reduces TNF-α/MDA, maintains CAT/GSH, and prevents NF-κB/lipoxygenase/protein denaturation ^[75–76]. 6-gingerol and 6-shogaol improve gastric emptying and prokinetics, reduce dyspepsia, nausea, and bloating, and suppress 5-HT3 ^[78].Bacterial membranes, biofilms, and quorum sensing are disrupted by phenolics and terpenes (strong vs. S. aureus, P. aeruginosa, S. mutans/sobrinus) ^[79–81]. promotes Lactobacillus spp./L. reuteri/rhamnosus (1.13–2.25 mg/mL), moderate Bifidobacterium; clinically, 3 g/day eliminates H. pylori, 730 mg gingerol helps IBD, and mixes lessen pain, bloating, and depression.^79-81

4. Fennel (Foeniculum vulgare Mill.): Fruits and seeds high in trans-anethole, fenchone, estragole, and terpenes (α/β-pinene, myrcene, γ-terpinene, limonene) exhibit carminative/spasmolytic gastrointestinal effects (flatulence, bloating, pain, newborn colic) through suppression of IL-17–IL-10–NF-κB ^[82–85]. Flavonoids (quercetin, rutin, and kaempferol) and phenolics (caffeic, quinic, and chlorogenic acids) have antioxidant properties (SOD/catalase, lipid peroxidation) ^[86–87].Through monoterpenes (65.64%) and phenylpropanoids (30.36%), essential oils have antimicrobial properties (MIC 250 µg/mL vs. E. coli/S. aureus/B. cereus; 3.13/6.25 mg/mL vs. C. albicans/A. niger; 50 mg/mL vs. S. aureus; 50% M. smegmatis biofilm inhibition at 5 µL Lactobacillus/Bifidobacterium. Clinically, CU-FEO improves QoL and decreases IBS pain/IBS-SSS in 211 real-world patients in 121 RCTs (30 days).^88-90

5. Green Tea (Camellia sinensis (L.) Green tea catechins: Epigallocatechin-3-gallate (50–60% of flavonoids, most potent), epicatechin, and epicatechin gallate scavenge free radicals; inhibit hydroxy-3-methyl-glutaryl-coenzyme A reductase, xanthine oxidase, glucose transporters, and lipid peroxidation; upregulate tight junction proteins (claudin-1, claudin-4, and occludin); and shield the intestinal barrier from damage caused by interferon-gamma and tumor necrosis factor-alpha.^91–100While quercetin, kaempferol, caffeic acid, and syringic acid stabilize nuclear factor-kappa B and prevent reactive oxygen species and lipid peroxidation, these catechins reduce nuclear factor-kappa B, inducible nitric oxide synthase, tumor necrosis factor-alpha, and interleukin-6.¹⁰¹ The protein kinase B/inhibitor of kappa B kinase/nuclear factor-kappa B pathway is blocked by saponins (theaflavin, 21-O-angeloyltheasapogenol E3). Catechins (epigallocatechin-3-gallate and epicatechin gallate > epigallocatechin) primarily target Gram-positive bacteria, damage bacterial membranes, and inhibit dihydrofolate reductase. Polyphenols travel through the colon.¹⁰²

Celosia Cristata: This Unani and pharmacologically recognized medicinal plant has antimicrobial, anti-inflammatory, antioxidant, tissue-regenerating, and immunomodulatory effects due to the abundance of flavonoids, phenolic acids, triterpenoid saponins, betacyanins, sterols, and glycoproteins found throughout all plant parts; flowers are richest in flavonoids and phenolics, while seeds contain high levels of triterpenoid saponins and phytosterols, supporting activity against infection, inflammation, and cellular damage. Despite having a robust profile, Celosia cristata has not yet been studied in models of experimental gut microbiota dysbiosis. The current author is doing a preclinical investigation using flower extract to close this gap.¹⁰³

Parts of Plants with a Chemical Composition

· The entire Celosia cristata plant contains sterols and betanin, which give the plant its red color and increase membrane activity.

· Amarantin, isoamarantin, celosianin, and isocelosianin are among the pigments with antioxidant potential found in the inflorescence.

· Myristic, palmitic, lauric, stearic, oleic, linoleic, and linolenic acids, together with a documented alkaloid, are abundant in the fixed oil found in seeds.

· Alpha-aminobutyric acid, hexadecadienoic acid, tricosanoic acid, and other minor compounds are found in aqueous root extract.

· All main amino acids, dietary fiber, and vitamins B1, B2, C, E, and beta-carotene are present in dried plant material, which has significant nutritional value for supporting intestinal health. ^[103]

· Although Celosia cristata has not yet been investigated in dysbiosis models, the combination of these nutrients and phytochemicals suggests potential antioxidant, antibacterial, and gut-protective benefits; your continued study will fill this gap.

Despite this powerful phytochemical profile, Celosia cristata has not yet been evaluated in experimental gut dysbiosis or microbiota models, so its role in restoring gut balance remains unexplored and is now being addressed by the present author’s ongoing study.

Figure 1: Celosia cristata

Table 4: Biological origin ¹⁰³

Kingdom	Plantae
subkingdom	Viridiplantae
Super division	Spermatophyta
Division	Magnoliophyta
Class	Magnoliopsida
Subclass	Caryophyllidae
Order	Caryophyllales
Family	Amaranthaceae
Subfamily	Amaranthoideae
Tribe	Celosieae
Genus	Celosia
Subgenus	Celosia
Species	Celosia Cristata/Celosia Argentea

Research Gap and Future Research Opportunities (Review Context):

The phytochemical components and pharmacological characteristics of Celosia cristata, such as hemostatic, anti-inflammatory, antibacterial, antioxidant, and metabolic activity, have been thoroughly investigated. Its multi-target potential is demonstrated by recent thorough evaluations, such as the 2024 Journal of Ethnopharmacology network pharmacology analysis; nevertheless, these analyses are currently mostly limited to host-centered molecular and metabolic pathways.

Recent experimental studies provide additional evidence for the biological role of C. cristata in metabolic regulation. For instance, Hyeon-Jun Kim et al. (2024) demonstrated that C. cristata flower extract suppressed adipogenesis and reduced weight gain and hepatic lipid accumulation in high-fat diet animals. Similarly, downregulating PPARγ and related genes decreased the production of adipocytes, according to Li et al. (2013). Although gut microbial imbalance is intimately linked to inflammation and metabolic illnesses, none of the present study has looked at the makeup of the gut microbiota, microbial metabolites, or dysbiosis-related mechanisms.

Crucially, because Celosia cristata lacks living bacteria, it cannot be categorized as a probiotic. However, its high concentration of fermentable bioactive components, dietary fibers, and polyphenols indicates a substantial potential to function as a gut microbiota regulator or prebiotic-like agent. No published review or original study has yet thoroughly examined or assessed Celosia cristata's possible biotic-related role (prebiotic, synbiotic-supporting, or non-classical microbiota modulator).

Therefore, our study is the first to compile the available evidence and specifically propose gut dysbiosis as a unique molecular framework for understanding the therapeutic potential of Celosia cristata. The study establishes the foundation for further experimental research, including in vitro, in vivo, and microbiome-based studies, to verify the plant's involvement in dysbiosis-related illnesses.

By Altering Bacterial Communities and Their Metabolic Processes, Phytochemicals from Several Sources Affect the Regulation of the Gut Microbiota:

Phytochemicals and gut microbiota: Polyphenols, flavonoids, flavones, flavanones, isoflavones, anthocyanins, curcumin, phenolic acids (hydroxybenzoic and hydroxycinnamic acids), stilbenes (piceatannol, resveratrol), lignans, tannins (condensed tannins/proanthocyanidins), and carotenoids (astaxanthin, lutein, and lycopene) are examples of phytochemicals ^104.

1. Flavonoids:

Flavones, flavanones, flavanols (flavan-3-ols), flavonols, flavanonols, isoflavones, and anthocyanins comprise the biggest subclass of polyphenols (>6,000 plant compounds). These substances are powerful scavengers of free radicals and are commonly found as plant pigments. Each of these compounds has a unique biological action.¹⁰⁵

2. Lignans:

Many plant parts, including oilseeds (particularly flaxseed) and bran-rich cereals, include dietary phytoestrogens in the form of aglycones or glycosides. Ruminococcus lactaris, Ruminococcus bromi, and Methanobrevibacter,¹⁰⁶Lactobacillus–Enterococcus, which transforms lignans into enterolactone and enterodiol, are linked to the gut microbiota of the colon ^[107]. Human enterolignan profiles and fecal microbiota are changed by lignan-rich diets, but further research is required to create long-term modulation techniques.

3. Carotenoids:

Carotenes (lycopene, alpha-carotene, and beta-carotene) and xanthophylls (zeaxanthin, lutein, and meso-zeaxanthin) are fat-soluble pigments that give food its red, orange, and yellow hues. Carotenoids must be consumed because people are unable to produce them on their own. They have a limited bioavailability (10–40%) and go to the colon, where the gut flora ferments them. Carotenoids exhibit antioxidant qualities at low dosages but may be dangerous at high dosages in clinical studies, despite the fact that their precise intestinal and microbial metabolic activities are still unknown.^108–111

4. Curcumin:

Using solvent techniques, curcumin—a member of the polyphenol subgroup utilized in traditional medicine and cooking—is extracted from the rhizomes of Curcuma longa and crystallized. In animal models of colitis, it increases butyrate-producing bacteria and fecal butyrate levels with 0.2% (w/w) nanoparticles while inhibiting NF-κB and inflammatory mediators in epithelial cells; in rats fed a high-fat diet, it increases anti-inflammatory Lactobacilli and Bifidobacteria while decreasing pro-inflammatory Enterococci and Enterobacteria. Individuals treated with curcumin and turmeric saw time-dependent, unique alterations in their colonic microbiota in double-blind, randomized, placebo-controlled pilot research. These modifications reduced 71 and 56 taxa, respectively, and significantly increased beneficial microbes.^112-115

Figure 2: Chemical structure of curcumin¹³⁰

5. Phenolic Acids:

Berries, wine, and whole grains are rich sources of phenolic acids, the second major polyphenol subgroup with a phenyl ring and carboxylic group produced by the shikimate pathway. These acids can be divided into two groups: hydroxycinnamic and hydroxybenzoic.¹¹⁶

6. Hydroxybenzoic Acids:

Gallic, protocatechuic, syringic, vanillic, and p-hydroxybenzoic acids are examples of hydroxybenzoic acids, which are manufactured or naturally occurring derivatives of benzoic acid. White grapes, bran, brown rice, gooseberries, olive oil, onions, plums, and almonds are rich sources of protocatechuic acid (3,4-dihydroxybenzoic acid).¹¹⁷ restores dysbiotic gut ecosystems in mouse models by lowering inflammatory Helicobacter, Mucispirillum, and Lachnospiraceae.¹¹⁸by Trianthema portulacastrum fractions. It increases the variety of microbiota in broilers by lowering pro-inflammatory Proteobacteria and Bacteroidetes and raising beneficial Firmicutes and Actinobacteria.^119-120

7. Tannins:

(Protein-precipitating polyphenols are classified as either hydrolyzable (HTs, like ellagitannins) or condensed (CTs); HTs hydrolyze to ellagic acid and are gut-metabolized to urolithins, which have antibacterial properties in vitro but may not affect the colon in vivo.^[121]In vitro, Bialonska et al. (2009) discovered that 0.01% pomegranate extract/0.05% components decreased S. aureus/Clostridia without influencing Bifidobacteria/Lactobacilli.¹²²In fecal cultures, pomegranate extract increased Enterococcus, Bifidobacterium, Lactobacillus, and total bacteria (but not C. histolyticum); in rats, urolithin and ellagitannins increased Bifidobacterium and Lactobacillus.^123–124

According to Li et al. (2015), four weeks of 1 g pomegranate extract raised Actinobacteria/Akkermansia muciniphila, decreased Firmicutes/Collinsella in urolithin A synthesis, and increased genera.¹²⁵ On the other hand, tannic acid caused microbiota modification, overgrowth, weight loss, and toxicity; meals high in tannin raised Enterobacteriaceae/ Prevotella/ Bacteroides/ Porphyromonas and decreased low G+C Gram-positives.^126–129

CONCLUSION:

IBD and genetic anomalies are among the many diseases that can be brought on by dysbiosis, or an imbalance in the gut microbiota. Dysbiosis can be more readily identified utilizing a variety of assays that can detect changes in microbial flora, whereas biomarkers refer to the identification of basic indicators of gut microbiota imbalance using tests on blood or feces (such as SCFAs, LPS, and TNF-α). This imbalance in the gut flora can be corrected by herbal treatments that employ phytochemical-rich plants with anti-inflammatory or antibacterial properties. Despite having comparable effects, several plants or their phytochemical components have not been employed in dysbiosis research. One such plant is Celosia cristata, whose flowers and seeds contain flavonoids, saponins, and other compounds that have been demonstrated to have antibacterial and anti-inflammatory qualities in a number of traditional and experimental studies. However, these compounds have not yet been studied using gut dysbiosis models. To bridge this gap, the author is conducting an ongoing study of Celosia cristata flower and leaf extract in dysbiosis.

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Received on 21.01.2026 Revised on 17.02.2026

Accepted on 14.03.2026 Published on 13.04.2026

Available online from April 15, 2026

Asian J. Pharm. Tech. 2026; 16(2):207-218.

DOI: 10.52711/2231-5713.2026.00030

This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License. Creative Commons License.

Category	Organ System	Related Illnesses (Examples)	Modified Microbe Examples (Dysbiosis Signature)
Gut	Cardiovascular	Atherosclerosis and hypertension	Lactobacillus plantarum, Lactobacillus rhamnosus, and Akkermansia muciniphila ^[6-7]
Non-gut	Respiratory	Pneumonia, fibrosis, asthma, and COPD	↑ Pseudomonas aeruginosa, Neisseria, Klebsiella, Moraxella, Streptococcus pneumoniae, and Haemophilus influenzae ^[8-9]
Non-gut	Central Nervous System	Parkinson's disease, stroke, and meningitis	Neisseria meningitidis and Streptococcus pneumoniae together ^[10]
Non-gut	Skin	Psoriasis, dermatitis, and eczema	Modified Bifidobacterium, Bacteroidetes, and Bacteroides ^[11-12]
Gut	Endocrine and metabolic autoimmune	Rheumatoid Arthritis, Systemic Sclerosis, Sjögren’s Syndrome, Antiphospholipid Syndrome Obesity	Bifidobacterium, Peptostreptococcus, and Faecalibacterium are modified anaerobes ^[13].

Biomarker	Sample Type	Class	Detection Method	Key threshold	Inflammation Type	Associated Disease
Cytokines (IL-6)	Plasma	Signal that promotes inflammation	ELISA (enzyme-linked immunosorbent assay)	N/A	N/A	Cancer of the colon (CRC)
Cytokines (TNF-α)	Serum	Signal that promotes inflammation	ELISA	>46.10ng/L	Chronic	Obesity and MDD
Cytokines (IL-10)	Serum	Signal that reduces inflammation	ELISA	<133.70 ng/L	Chronic	Obesity and MDD
C-reactive protein (CRP)	Serum/plasma/blood	Acute sign of inflammation	Turbidometric analysis, ELISA, and biochemistry analyzer	>0.60mg/(chronic)L;>96.8mg/L(severe)	Systemic/chronic	Obesity, Major Depressive Disorder (MDD), Metabolic Syndrome, Colorectal Cancer (CRC), Severe COVID-19, and post-COVID-19
Calprotectin	Serumorfecal	Neutrophil-derived protein	ELISA	>9.74 mcg/mL (serum); >92.06 mcg/g (fecal); >70.14 pg/mL (fecal)	Systemic/chronic	Ankylosing spondylitis, ulcerative colitis, gestational diabetes mellitus, and Parkinson's disease (PD)
LPS-binding protein	Serum	Binder for bacterial toxins	ELISA	>16.82ng/mL	Chronic	Diabetes mellitus during pregnancy
Zonulin	Serumorfecal	Protein of the gut barrier	ELISA	>3.80 ng/L (serum); >21.99 ng/mL (serum); >50.56 ng/mL (fecal)	Chronic	MDD with Obesity, Gestational Diabetes Mellitus, and Sporadic Parkinson's Disease
Lipopolysaccharide (LPS)	Serumorfecal	Toxin produced by bacteria	ELISA	>203.30 EU/L (serum); >117.31 ng/L (fecal)	Chronic	Obesity and MDD, Gestational Diabetes Mellitus

Biomarkers	What it shows	For diagnosis	For treatment check
SCFAs	By product of intestinal bacteria	Active, healthy bacteria	Microbes are fixed by diet.
Fecal calprotectin	Indication of edema in the stomach	inflammation caused by pathogenic microbes	tracks the reduction in edema
Bacterial DNA	Significant bacterial footprints	Overpopulation or lack of species	notices the reappearance of germs.
Cytokines	The body's alarm proteins	Immune confusion caused by dysbiosis	Immunological balance restoration
LPS (bacterial poison)	The intestines release bacteria.	Toxins can pass through barrier holes.	Check for gut seal repair.
Dysbiosis score	The sum of the bacterial errors	How severe the imbalance is	The score rises with treatment.

Plant or extract	Principal phytochemicals	The approximate proportion of the plant or extract	Primary activity related to the gut
Aloe vera	Fructooligosaccharides, acemannan, aloin, and aloesin	Leaf pulp (gel), used as juice or gel	Acemannan and related polysaccharides have a powerful mucosal/gut-healing effect and are strong anti-inflammatories, mild antioxidants, and moderate prebiotics (derived from fructooligosaccharides/fructans).
Dandelion (Taraxacum officinale)	Taraxacin (sesquiterpene lactone), taraxasterol (triterpenoid), luteolin, quercetin, chlorogenic acid, and fructooligosaccharides	Roots and leaves	Strong antioxidant and anti-inflammatory qualities. The prebiotic effect of fructooligosaccharides is mild. Insufficient direct antimicrobial action has strong effects on bile flow stimulation and hepatoprotection (choleretic/cholagogue).
Ginger (Zingiber officinale)	Ascorbic acid (vitamin C), zingiberene, gingerol, shogaol, and alpha-tocopherol (vitamin E)	The rhizome	Strong anti-inflammatory and antioxidant qualities slight antimicrobial action Moderate prokinetic/digestion-supporting activity (mobility, symptom alleviation)
Fennel (Foeniculum vulgare)	Dietary fiber (including fructooligosaccharides), quinic acid, chlorogenic acid, caffeic acid, fenchone, estragole, quercetin, rutin, kaempferol, and trans-anethole	Fruit seeds	Moderate spasmolytic/antispasmodic and carminative effects Flavonoids and phenylpropanoids have weak antioxidant and anti-inflammatory qualities. Fructooligosaccharides and dietary fiber have a slight prebiotic effect. Insufficient direct antimicrobial action
Green tea (Camellia sinensis)	Caffeine, kaempferol, gallic acid, epicatechin, epigallocatechin gallate, and quercetin	Leaves	Strong antioxidant and anti-inflammatory properties mild antibacterial activity (mostly against certain microbes); Moderate effects on microbiota and prebiotics
Garlic (Allium sativum)	Alliin, fructooligosaccharides, allicin, ajoene, S-allyl cysteine, and inulin	Cloves, or bulbs	Strong antioxidant and anti-inflammatory properties Inulin and fructooligosaccharides have substantial antibacterial activity and a powerful prebiotic effect against gut-related illnesses.
Celosia cristata, or cockscomb	Saponin, betacyanins, cristatein, cochliophilin, triterpenoids, fatty acids, etc.	Seeds, leaves, inflorescences/flowers, and aerial parts	Scavenge free radicals to lessen oxidative stress. Antimicrobial, hemostatic, and anti-inflammatory ¹⁰³